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Hepatotoxicity of Cadmium and Roles of Mitigating Agents

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Abstract

There are increasing reports on cadmium associated hepatotoxicity, due to these reports this study reviewed relevant literature on cadmium associated hepatotoxicity with emphasis on doses, route of administration, salt forms (cadmium compounds) and the roles of mitigating agents. Reports have shown that continuous exposure of the liver to cadmium has led to hepatotoxicity. Humans are generally exposed to cadmium by two main routes, inhalation and ingestion. In this study, evaluation of relevant literature showed that irrespective of route of administration and salt forms cadmium hepatotoxicity is dose and time dependent. Cadmium associated hepatotoxicity manifested through impaired functions of hepatic biomarkers (transaminases), enzymatic and non enzymatic antioxidants. Histopathological damage to liver architecture manifested as swelling of hepatocytes, focal necrosis, hepatocytes degeneration, dilatation of ribosomes, damage of membrane-bounded lysosomes, nuclear pyknosis and cytoplasm vacuolization. Deterioration of mitochondrial cristae, deposition of collagen fibrils, hypertrophy of kuffer cells, congestion in central veins and sinusoids, infiltration of mixed inflammatory cells and peripheral hemorrhage also occurred. Hepatotoxic effect of cadmium was mitigated by Vitamin C, Vitamin E, Manganese (11) Chloride, N-acetylcysteine and Selenium. Extracts of plant origin including Solanum tuberosum, Calycopteris floribunda Hibiscus sabdariffa mitigated cadmium induced hepatotoxicity. Chemical substances of animal origin including honey and camel milk were reported to have ameliorated cadmium induced hepatotoxicity. One of the mechanisms of cadmium induced hepatotoxicity is reported to be associated with the up regulation of reactive oxygen species (oxidative stress) which caused oxidative damage to lipid contents of membranes and direct liver injury. Conclusion cadmium is dose and time dependently hepatotoxic irrespective of route of administration, salt form and is ameliorated by some antioxidants and extracts of plant and materials of animal origin which may require further evaluation for clinical application.

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... The modification of chitosan nanoparticle has received much attention in relation to their potential application, especially from a pharmaceutical viewpoint. [15][16] Nanoparticle chitosan has attracted attention due to its biodegradability, biocompatibility, cost-effectiveness, high permeability and non-toxic property. Moreover, its ability to enhance the penetration of large molecules across a mucosal surface and its recognition as muco adhesivity chitosan. ...
... Moreover, its ability to enhance the penetration of large molecules across a mucosal surface and its recognition as muco adhesivity chitosan. 13,16 However, the gastroprotective effect of chitosan nanoparticles has seldom been reported elsewhere. The unique character of chitosan nanoparticles for their small size and quantum size effect could make chitosan nanoparticles exhibit superior activities. ...
... Chitosan nanoparticle very interesting to be developed as a new therapeutic drug because it has a good biodistribution, high sensitivity and low pharmacological toxicity. [15][16] It has been reported that antioxidant activity or inhibition of generation of free radicals plays a crucial role in protection against cadmium toxicity. So, can be claimed that protective agents, such as antioxidants, may be useful therapeutic for against free radicals on heavy metal toxicity in gastric. 2 It has been reported that chitosan has an antioxidant effect. ...
Article
Full-text available
Objective: This study was carried to investigate the role of chitosan nanoparticle in protecting against cadmium chloride-induced gastric toxicity in the rat. Methods: The 50 male rats were divided into 5 group: negative control (Rats were given daily with aquadest); positive control (Rats were given daily with cadmium chloride 5 mg/kg BW orally once in a day for 28 days) and the treatment group (Rats were given the chitosan nanoparticle 150 mg; 300 mg; 600 mg/kg BW orally once in a day for 32 days and on 4th day, were given cadmium chloride 5 mg/kg BW one hour after the chitosan nanoparticle administration for 28 days). On day 32, the rats were sacrificed, and gastric tissues were collected to measure Malondialdehyde (MDA), Superoxide Dismutase (SOD), Glutathione Peroxidase (GPx) and histological evaluations. Results: Oral administration of cadmium chloride 5 mg/kg BW for 28 days significant induced gastric mucosal hemorrhagic lesions, increase MDA, decrease SOD and GPx, and also caused necrosis of gastric mucosal epithelial cell in the rat. Treatment with the chitosan nanoparticle 600 mg/kg BW but not 150 mg/kg BW and 300 mg/kg BW significantly improved gastric injury, decreased MDA, increase in SOD and GPx levels, and also improved necrosis of gastric mucosal epithelial cell as compared to positive control group. Conclusion: From the results of this study concluded that the chitosan nanoparticle could be a potent natural product provide a promising gastroprotective effect against cadmium chloride induced gastric toxicity in rats.
... Upon acute exposure to cadmium, hepatotoxicity is indicated by changes such as swelling of hepatocytes, fatty changes, focal necrosis, hepatocytes degeneration and impaired functions of biomarkers of liver function such as aspartate aminotransferase (AST) and alanine aminotransferase (ALT). On electron microscopy, changes such as dilatation of ribosomes, damage of membrane-bounded lysosomes, nuclear pyknosis, were reported [9], [10]. ...
... Over-production of ROS normally induces oxidative stress unless it was scavenged with endogenous antioxidants. Thus, overproduction of ROS could be attributed to the depletion of antioxidants or to the direct action of cadmium on peroxidation reaction and iron-mediated peroxidation [10]. ...
... The hepatotoxicity of cadmium has also been attributed to the formation of toxic metabolites when it is activated by hepatic cytochrome P-450 to a highly active metabolite N-acelyl-P-benzooquinone imine. Furthermore, interference with essential metals could be one of the mechanisms employed by cadmium mediated toxicological effects [10]. ...
... These results indicated that cadmium at the administered dose in the study produced severe oxidative damage in liver. This is in agreement with many authors who reported the toxicity of Cd on the liver24252627. Mahran et al. [28] found that the Cd can cause vacuolar degeneration and increased density of nuclear chromatin with very compact nuclear structure found in hepatocytes. ...
... Similarly, Renugadevi, and Prabu [4] found that the levels of serum hepatospecific enzymes such as AST, ALT, ALP, γ-GT and the level of total bilirubin were significantly increased in cadmium treated rats. Cadmium associated hepatotoxicity manifested through impaired functions of hepatic biomarkers (transaminases) [25,26]. These results may indicate degenerative changes and hypofunction of liver [44,45] as well as hepatic cell necrosis [46] which increase the releasing of these enzymes in the blood stream [47]. ...
... A water extract of Fenugreek seeds concurrently during 60 days of alcohol ingestion was associated with a reduction in the rise of oxidation and liver enzymes noted in the serum of rats given ethanol alone, suggesting protective effects [60]. It was observed that some antioxidants, extracts of plant origin including Solanum tuberosum, Calycopteris floribunda and Hibiscus sabdariffa, and chemical substances of animal origin including honey and camel milk were reported to have ameliorated Cd induced hepatotoxicity through normalization of biochemical parameters and histopathological changes induced by cadmium [26]. The administration of naringenin in cadmium treated rats counteracted the oxidative hepatic dysfunction attributed by cadmium. ...
Article
Hepatotoxic agents can react with the basic cellular components and consequently induce almost all types of liver lesions. Objective: The present work aimed to evaluate effectiveness of fenugreek seeds, rosemary and cinnamon against cadmium induced hepatotoxicity in guinea pigs from the histological and biochemical aspects. Materials and methods: 48 guinea pigs were used for this study and divided into 8 groups. The first 4 groups were control groups, the 5th group was the experimental and administered oral cadmium chloride at a dose of 5 mg/kg. body weight./day for 28 days, the 6th, 7th, and 8th groups co-administered cadmium with aqueous extracts of fenugreek seeds, rosemary and cinnamon at a dose of 150 mg, 220 mg, and 200 mg/ kg body weight /day, respectively. The livers were dissected out, weighted and specimens were taken and processed for light microscopic examinations. Blood samples were obtained for assessment of serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, γ- glutamyltransferase activities, and serum total and direct bilirubin. Results: In cadmium treated animals, there were severe structural damage in the liver. Most of hepatocytes appeared fused together forming eosinophilic syncytial masses. The hepatocytes appeared irregularly arranged with disorganization of hepatic architecture. The hepatocytes appeared large with light and foamy cytoplasm filled with numerous vacuole-like spaces. The nuclei appeared with pyknotic nuclei. The central vein appeared dilated and congested with massive hemorrhage extending to the nearby cells. Mild periductal fibrosis around bile duct in the portal area were observed. Also, there were focal degenerative and necrotic changes along with inflammatory cell infiltration. Decrease in body weight and increase in liver weight were observed. Biochemically, the serum alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase), and γ- glutamyltransferase activities, serum total and direct bilirubin were elevated. Co-adminstration of fenugreek, rosemary and cinnamon significantly improved the structural changes in the liver and also all the above mentioned biochemical parameters were significantly declined. Conclusion: It can be concluded that, the cadmium had adverse effects on the liver. Aqueous extracts of different natural materials as Fenugreek, rosemary and cinnamon were able to attenuate these effects. So, the populations of high risk to cadmium should be advised to take one of these materials.
... These results indicated that cadmium at the administered dose in the study produced severe oxidative damage in liver. This is in agreement with many authors who reported the toxicity of Cd on the liver [24][25][26][27]. Mahran et al. [28] found that the Cd can cause vacuolar degeneration and increased density of nuclear chromatin with very compact nuclear structure found in hepatocytes. ...
... Similarly, Renugadevi, and Prabu [4] found that the levels of serum hepatospecific enzymes such as AST, ALT, ALP, γ-GT and the level of total bilirubin were significantly increased in cadmium treated rats. Cadmium associated hepatotoxicity manifested through impaired functions of hepatic biomarkers (transaminases) [25,26]. These results may indicate degenerative changes and hypofunction of liver [44,45] as well as hepatic cell necrosis [46] which increase the releasing of these enzymes in the blood stream [47]. ...
... It was observed that some antioxidants, extracts of plant origin including Solanum tuberosum, Calycopteris floribunda and Hibiscus sabdariffa, and chemical substances of animal origin including honey and camel milk were reported to have ameliorated Cd induced hepatotoxicity through normalization of biochemical parameters and histopathological changes induced by cadmium [26]. The administration of naringenin in cadmium treated rats counteracted the oxidative hepatic dysfunction attributed by cadmium. ...
... According to Wang et al. (2023), Zou et al. (2021), Andujar et al. (2010), Yu et al. (2010) and Buxbaum and Pfaff (2005), cadmium has many common industrial applications including being a key component in battery and plastic production, and its use in electroplating and nuclear fission. In spite of its many useful industrial applications, cadmium, in its various forms, has detrimental effects on humans and animals, as they have been found to be carcinogenic (Souza-Arroyo et al., 2022;Ankit et al., 2021;Adikwu et al., 2013;Godt et al., 2006). According to Liu et al. (2022), Naksen et al. (2022), Zou et al. (2020) and ATSDR (2014), cadmium has also been found to be a contributor of many cardiovascular, neurological, gastrointestinal, renal, reproductive, respiratory and developmental disorders. ...
... Although, according to Bernard (2008), no known compound has been approved for the treatment of cadmium toxicity, many plant extracts and animals products have been evaluated in the treatment of cadmium, one of which is honey, as several studies (Eze and Asomugha, 2022;Quddus et al., 2021;Atagana and Asagba, 2015;Abdelaziz et al., 2013;Abdel-Moneim and Ghafeer, 2007) on the protective effect of honey on different organs and tissues such as the blood, liver, kidney, lungs, testes of rats exposed to cadmium toxicity have been conducted. The protective effect of other therapeutic agents on cadmium-induced toxicity in different organs and tissues such as the liver, kidney, lungs, testes, as well as the heart and brain of rats have also been extensively studied (Amr et al., 2023;Orororo et al., 2018;Brzoska et al., 2016;Alpsoy et al., 2014;Adikwu et al., 2013;Obioha et al., 2009). However, there is paucity of information on the effect of honey on cadmium-induced brain injury. ...
Article
Full-text available
Cadmium (Cd) toxicity has led to the search for possible ameliorators, which is an interesting area of research currently being explored worldwide. This research investigated the effect of honey on some biochemical parameters in the brain tissues of rats following acute and sub-chronic Cd exposures. Thirty adult Wistar rats were divided into 6 groups (A-F): control, sub-chronic Cd exposure, sub-chronic Cd exposure plus honey, acute Cd exposure, acute Cd exposure plus honey and honey only, respectively. Cadmium chloride (CdCl2) was administered at a dosage of 2 mg/kg body weight by intraperitoneal injection (IP), every two days interval, for a period of 4 weeks (for the sub-chronic study) and a dosage of 4 mg/kg body weight by IP, 12 hours before sacrifice (for the acute study). Honey was administered at a dose of 1 ml/kg body weight orally, once daily for 4 weeks. The study revealed that groups B and D showed significantly higher lipid peroxidation and acid phosphatase (ACP) activity in the brain tissues than that of group A; as well as significantly lower catalase (CAT), superoxide dismutase (SOD), alanine aminotransferase (ALT), aspartate aminotransferase (AST) and alkaline phosphatase (ALP) activities. However, administration of honey to Cd-exposed rats ameliorated the Cd-induced changes by causing a reduction in lipid peroxidation and maintaining the activities of these enzymes in the brain tissues within levels significantly similar to that of the control group. This suggests that honey produces an ameliorative effect on Cd-induced injuries in the brain tissues at acute and sub-chronic levels.
... There are increasing reports on cadmium associated hepatotoxicity; these reports have shown that continuous exposure of the liver to cadmium has led to hepatotoxicity (Adikwu et al., 2013).In Ilorin Nigeria, Adeniji and Anjorin, (2002) identified cirrhosis and hepatocellular carcinoma as causes of chronic liver disease. Humans are generally exposed to cadmium by two main routes, inhalation and ingestion. ...
... This is in line with Ahmetn et al, (2006) who conducted a study on evaluation of the effects of cadmium on rat liver using 18 albino rats (10weeks old), exposed to 15ppm of Cadmium via consumption of water daily for 30days, revealing great distortion to liver histo-architecture with the central vein normal. This also agrees with Adikwu et al, (2013) who conducted a research on the hepatotoxicity of Cadmium and roles of mitigating agents revealing that cadmium exposure causes histopathological damage to the liver architecture such as swelling of hepatocytes, deposition of collagen fibrils, hypertrophy of kupffer cells, congestion in central vein and sinusoids and peripheral haemorrhage. also discovered that the central vein of the animals treated with CdCl 2 were congested in their research on the effect of cadmium on liver and amelioration by aqueous extracts of fenugreek seeds, rosemary and cinnamon in guinea pigs (histological and biochemical study) which also agrees with the present findings. ...
... Consistently, it has been reported that the serum content of AST and ALT was significantly increased in rats treated with CdCl 2 [54,55]. Elevation of ALT and AST were noted in workers who exposed to CdCl 2 [56]. ...
... In the present study, histopathological examination revealed prominent changes in the structure of the liver tissues following CdCl 2 administration. Several studies have shown severe histological changes in the liver of CdCl 2 treated rats [41,[56][57][58]. Our findings are in agreement with the results of Mohammad et al., which reported cadmium bromide-induced degeneration of hepatocytes, inflammatory infiltrated leucocytes, and dilation of blood sinusoid lumens in cadmium treated female rat liver [59]. ...
Article
Aims Cadmium chloride has various industrial applications and considered an industrial and environmental pollutant. The aim of this study was to evaluate the effect of atorvastatin on Cadmium chloride-induced hepatotoxicity in male rats. Materials and methods Fifty-six adult male rats, randomly were divided into 8 groups. Groups 1–3 were received atorvastatin (20 mg/kg) intragastrically for 15 days during which Cadmium chloride (1, 2, and 3 mg/kg) were given intraperitoneally from days 8 to 15. Groups 4–6 were as first three groups but animals were received vehicle of atorvastatin. Group 7 was received vehicle of atorvastatin and vehicle of Cadmium chloride and Group 8 was received atorvastatin and vehicle of Cadmium chloride according to timeline of other groups. On day 16, under full anesthesia, blood sampling was prepared from heart, and livers were dissected out to analyses the biochemical and histopathology studies. Key findings Cadmium chloride significantly increased aspartate transaminase (AST), alanine transaminase (ALT), and alkaline phosphatase (ALP) in the serum. Malondialdehyde (MDA) significantly increased and superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione (GSH) significantly decreased the in the liver following Cadmium chloride administration. Atorvastatin significantly improved the levels of MDA, SOD, GPx, GSH, but not ALT, AST, and ALP in Cadmium chloride-treated rats. In histopathological studies, atorvastatin could not improve injured liver tissues induced by Cadmium chloride. Significance Atorvastatin has beneficial effects in improving Cadmium chloride-induced antioxidative enzymes disturbance which may be contribute to improving liver function in male rats.
... There are increasing reports on cadmium associated hepatotoxicity; these reports have shown that continuous exposure of the liver to cadmium has led to hepatotoxicity (Adikwu et al., 2013).In Ilorin Nigeria, Adeniji and Anjorin, (2002) identified cirrhosis and hepatocellular carcinoma as causes of chronic liver disease. Humans are generally exposed to cadmium by two main routes, inhalation and ingestion. ...
... This is in line with Ahmetn et al, (2006) who conducted a study on evaluation of the effects of cadmium on rat liver using 18 albino rats (10weeks old), exposed to 15ppm of Cadmium via consumption of water daily for 30days, revealing great distortion to liver histo-architecture with the central vein normal. This also agrees with Adikwu et al, (2013) who conducted a research on the hepatotoxicity of Cadmium and roles of mitigating agents revealing that cadmium exposure causes histopathological damage to the liver architecture such as swelling of hepatocytes, deposition of collagen fibrils, hypertrophy of kupffer cells, congestion in central vein and sinusoids and peripheral haemorrhage. also discovered that the central vein of the animals treated with CdCl 2 were congested in their research on the effect of cadmium on liver and amelioration by aqueous extracts of fenugreek seeds, rosemary and cinnamon in guinea pigs (histological and biochemical study) which also agrees with the present findings. ...
Article
Full-text available
This study investigated the hepatoprotective role of ethanolic extract of Moringa oliefera (M.O) on liver function (Biomarkers) in cadmium chloride (CdCl2)-induced hepatotoxicity on the liver of albino Wistar rats. Sixty-six adult male albino wistar rats weighing between 130g – 180g were used. LD50 was determined for both CdCl2and MO using twenty-six (26) rats, while 40 rats were used for the experiment proper. The experimental rats were distributed into eight groups –A (control) and B, C, D, E, F, G and H, served as the treatment groups that received graded doses of CdCl2or MOor both simultaneously or at separate periods. The animals were then euthanized for sample collection and analysis using standard methods. The results showed significant increase (P<0.05) in the serum levels of Alanine aminotransferase (ALT) (430.50 ± 149.20), Aspartate aminotransferase (AST) (421.10 ± 8.34) and Alkaline Phosphatase (ALP) (515.60 ± 21.78) of animals in group B, but some protective effect of MO in the treatment groups with significant decreases in ALT, AST and ALP levels. The study therefore concludes that ethanolic extract of Moringa oleifera showed appreciable hepatoprotective values on liver functions (biomarkers) in CdCl2hepatotoxicity. Key words: Liver Functions, Cadmium, Moringa oleifera, Hepatoprotective, Hepatotoxiciy
... Macroscopically, individual and prolonged exposure to Cd lead to liver enlargement and ischemia compared with the control, which is consistent with previous reports on Cd-induced liver inflammation processes that involve Kupffer cells activation and neutrophil infiltration 28 . Cd treatment also caused an increase in serum aminotransferases (AST and ALT) ( Table 5), probably causing substantial leakage of hepatic enzymes into the bloodstream 21,56 . On the other hand, DSF treatment did not affect serum aminotransferases activity (Table 5), which is not in line with the previous reports on moderately elevated aminotransferases serum level during chronic DSF exposure 57 . ...
... Examination of liver from Cd21 and Cd42 groups, showed infiltration of neutrophils, which indicates the presence of inflammation (Figure 4(B,C)). Inflammation process is consistent with previous reports 22,56,58 . Focal necrosis is also present in Cd21 group (Figure 4(B)), which is consistent with previous report indicating appearance of hepatic necrosis at the similar applied i.p. dose of CdCl 2 59 . ...
Article
Full-text available
Examination of cadmium (Cd) toxicity and disulfiram (DSF) effect on liver was focused on oxidative stress (OS), bioelements status, morphological and functional changes. Male Wistar rats were intraperitoneally treated with 1 mg CdCl2/kg BW/day; orally with 178.5 mg DSF/kg BW/day for 1, 3, 10 and 21 days; and co-exposed from 22nd to 42nd day. The co-exposure nearly restored previously suppressed total superoxide dismutase (SOD), catalase (CAT) and increased glutathione peroxidase (GPx) activities; increased previously reduced glutathione reductase (GR) and total glutathione-S-transferase (GST) activities; reduced previously increased superoxide anion radical (O2·−) and malondialdehyde (MDA) levels; increased zinc (Zn) and iron (Fe), and decreased copper (Cu) (yet above control value), while magnesium (Mg) was not affected; and decreased serum alanine aminotransferases (ALT) levels. Histopathological examination showed signs of inflammation process as previously demonstrated by exposure to Cd. Overall, we ascertained partial liver redox status improvement, compared with the formerly Cd-induced impact.
... Consistent with our results, previous studies have shown that Cd causes severe histological changes in rat liver [60][61][62]. Here, histopathological data clearly showed that Morin significantly corrected the observed Cd-induced hepatic damage. ...
Article
Full-text available
Cadmium (Cd) is a toxic heavy metal with significant environmental health hazards. It enters the body through various routes with tissue accumulation. The relatively longer half-life with slow body clearance significantly results in hepatotoxicity during its liver detoxification. Therefore, researchers are exploring the potential use of herbal-derived phytocomponents to mitigate their toxicity. Here, we investigated, for the first time, the possible ameliorative effect of the phytochemical Morin (3,5,7,29,49-pentahydroxyflavone) against acute Cd-induced hepatotoxicity while resolving its underlying cellular mechanisms in a rat animal model. The study involved 50 adult male Sprague–Dawley rats weighing 200–250 g. The animals were divided into five equal groups: control, Cd, Morin100 + Cd, Morin200 + Cd, and Morin200. The 2nd, 3rd, and 4th groups were intraperitoneally treated with Cd (6.5 mg/kg), while the 3rd, 4th, and 5th groups were orally treated with Morin (100 and 200 mg/kg) for 5 consecutive days. On the 6th day, hepatic function (serum ALT, AST, ALP, LDH enzyme activities, and total bilirubin level) testing, transcriptome analysis, and immunohistochemistry were performed to elucidate the ameliorative effect of Morin on hepatotoxicity. In addition to restoring liver function and tissue injury, Morin alleviated Cd-induced hepatic oxidative/endoplasmic reticulum stress in a dose-dependent manner, as revealed by upregulating the expression of antioxidants (SOD, GSH, Gpx, CAT, and Nrf2) and decreasing the expression of ER stress markers. The expression of the proinflammatory mediators (TNF-α, IL-1-β, and IL-6) was also downregulated while improving the anti-inflammatory (IL-10 and IL-4) expression levels. Morin further slowed the apoptotic cascades by deregulating the expression of pro-apoptotic Bax and Caspase 12 markers concomitant with an increase in anti-apoptotic Blc2 mRNA expression. Furthermore, Morin restored Cd-induced tissue damage and markedly suppressed the cytoplasmic expression of JNK and p-PERK immunostained proteins. This study demonstrated the dose-dependent antioxidant hepatoprotective effect of Morin against acute hepatic Cd intoxication. This effect is likely linked with the modulation of upstream p-GRP78/PERK/ATF6 pro-apoptotic oxidative/ER stress and the downstream JNK/BAX/caspase 12 apoptotic signaling pathways.
... Among heavy metals of concern is Cadmium (Cd), which is a non-essential element (WHO, 2011). Cd is commonly found together in ores with other metals such as zinc, lead and copper (Elias et al., 2013;Song et al., 2015). Arising from increased industrial, volcanic and agricultural activities and its nonbio-degradable nature, Cd is present in the environment in toxic levels, from where humans are generally exposed through inhalation and ingestion (WHO, 2011;Nordberg et al., 2011;Satarug et al., 2017). ...
Article
Full-text available
The liver and kidney are prime targets of cadmium (Cd) toxicity and the search for antidotes of Cd-induced hepato-renal toxicity is an important area of research. This research was designed to assess the impact of anthocyanins from Hibiscus sabdarrifa L. on cadmium-induced hepato-nephro toxicity in rats following acute and chronic Cd exposure. Fifty adult male Wistar rats were shared into ten (10) groups (A-E): Naive control, Cd control, anthocyanins control, Cd (3g/body weight) + anthocyanins (/3mg/kg body weight) pre-treatment and Cd+anthocyanins post-treatment. Five groups were used for 5days acute toxicity study while the other five groups were used for the 15days chronic toxicity study. The organ/body weight ratio for the liver and kidney were considerably (p<0.05) reduced in rats after acute and sub-chronic exposure to Cd The administration of Cd to rats in both modes of exposure significantly (p<0.05) increased AST activity in serum with a corresponding decrease in the liver, but the changes were improved by pre and post treatment of Cd-exposed rats with HSA. Similarly, acute and chronic exposure to Cd significantly increased ALT activity in serum with a corresponding decrease in the liver. Pre-treatment and post-treatment of Cd-exposed rats with HSA considerably lowered serum creatinine and urea equated to rats exposedto Cd alone. The results showed that administration of cadmium to rats altered liver and kidney function indices. However, pre-treatment and post-treatment of Cd-exposed rats with H. sabdariffa anthocyanins meaningfully reversed these effects indicating that HS anthocyanins can ameliorate Cd-induced hepato-renal toxicity in Wistar rats.
... In another study using animal model, it was also observed that mercury intoxication elevated serum total bilirubin concentration (41). Cadmium caused an increased level of bilirubin in conjunction with ALT, AST, ALP and Y-GT (42). In the current study, total bilirubin and conjugated bilirubin were elevated with conjugate bilirubin been significant compared with the control subjects. ...
Article
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Solid wastes are infectious and toxic to humans and the environment. This study was aimed at evaluating hepatic function and oxidative stress markers of solid waste management workers in Yenagoa Metropolis, Bayelsa State.Blood samples was collected from apparently healthy male subjects aged 20-40 years. Biochemical parameters: AST, ALT, Total protein, Albumin, Total and conjugated bilirubin, catalase, glutathione, superoxide dismutase and malondialdehyde were analyzed using spectrophotometer. Results showed statistically significant (p<0.05) increase in conjugated bilirubin (6.95±3.89) and AST (14.17 ±4.22) among test sample compared with the control (2.30±1.14 and9.08±2.15 respectively).STotal protein (69.60±5.58) and albumin (37.39±4.89) showed a statistically significant (p<0.05) reduction in the exposed subjects when compared with the control (69.60±5.58 and 44.84±5.29 respectively).Furthermore, there was a statistically significant (p<0.05) elevation in Total bilirubin (15.53±5.99), conjugated bilirubin (6.95±3.89), and AST (15.53±5.11) among subjects with ≥2years duration compared with <2years (10.01±7.55, 3.92±3.14 and 12.08± 2.09).The antioxidant enzymes glutathione (20.6±4.20) was statistically (p<0.001) elevated, whereas Catalase (66.2±19.3) and Superoxide Dismutase (61.9±0.97) showed non-significantly (p>0.05) reduction compared with the control (15.7±0.99, 75.7±21.7 and 62.5±7.02 respectively) as well on job duration. Malondialdehyde (7.37±1.57) showed a statistically significant (p<0.001) increase when compared with the control group (5.88±0.42). Solid wastes have a negative effect on the liver function and oxidative stress markers in prolonged exposure
... Cadmium induced hepatotoxicity resulting in increased activities of AST, ALT and ALP has been reported by other authors. [43,44] The reversal of the activities of these enzymes by ethanol leaf extract of Pterocarpus mildbraedii would imply that this extract has protective activity against cadmium induced hepatotoxicity by conferring stability on the membranes of cells thereby preventing passage of the marker enzymes into circulation from the liver. [45] . ...
... Histologically, the results indicate that Cd injection resulted in severe oxidative damage in the liver tissues, which was evidenced by the appearance of necrotic alterations, along with inflammatory cell infiltration. This result agreed with the previous study that reported the hazards of Cd on the liver [34]. Previous studies have suggested that Cd generates reactive oxygen species (ROS), causes oxidative damage to membrane lipids, disturbs membranes integrity, and involves cytotoxic and inflammatory mediators in the liver [4,35]. ...
Article
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Heavy metals intoxication causes several health problems that necessitate finding new protective and therapeutic approaches. This study aimed to evaluate the impact of Musa sp. leaves extract (MLE) on hepato-renal toxicities induced by cadmium (Cd) in male mice. The phytochemical screening, metal chelating activity (MCA), and the median lethal dose (LD50) of MLE were determined. Fifty CD-1 male mice were used and intraperitoneally (i.p.) injected with MLE (1000 to 5000 mg/kg b.wt) for MLE LD50 determination. Another 50 mice were used for evaluating the effect of MLE on Cd toxicity. Blood samples were collected for hematological, liver, and kidney functions assessments. Liver tissue homogenates were used for determination of oxidant/antioxidant parameters. Liver and kidney tissues were harvested for histopathological and molecular investigations. MLE showed potent in vitro antioxidant activities. The MCA and LD50 of the MLE were 75 µg/mL and 3000 mg/kg b.wt, respectively. MLE showed beneficial therapeutic activity against hepato-renal toxicities in Cd-intoxicated mice, evidenced by improving the hematological, biochemical, histopathological, and molecular alterations.
... As the evaluation of the activity of the enzymes AST and ALT is important for evaluating the function of cells of some tissues, especially the liver, it is known that both are present in hepatocytes, renal, muscle, and others. Therefore, their high activity outside the cell indicates the presence of functional impairment or the presence of damage to the cells of these tissues [23] , So the treatment with cadmium chloride to the use of radicals and active oxygen species (ROS) , which worked on loading neurons, [24] , And the increase in the level of these two enzymes explained the effect of cadmium in changing the permeability of the membranes of the liver cells, which leads to the leakage of these enzymes into the blood, or due to the occurrence of Hepatocellular necrosis that occurs as a result of toxic substances or the occurrence of liver cirrhosis and also leads to leakage of these Enzymes from broken cells and their arrival into the blood [25,26] . ...
Poster
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The study designed for the toxic role of cadmium chloride on the liver of mice from both a physiological and histological aspects. The animals were treated with a dose of 5 mg/kg of body weight for 30 days. And the protective role of Brassica nigra seed extract against cadmium chloride toxicity. This pilot study was conducted on 20 adult white rats divided into 4 equivalent groups including the control group: Animals in this group received a dosed of distilled water for 30 days. The placebo group was treated with cadmium chloride at a dose of 5 mg/kg of body weight for 30 days and returned as an infected control group. While in the third group, animals treated with cadmium chloride were dosed with Brassica nigra seed extract at a dose of 200 mg/kg of body weight for 30 days. The fourth group was dosed with Brassica nigra seed extract at a dose of 200 mg/kg of body weight for 30 days. After 30 days, liver enzymes including aminotransferase (AST), alanine aminotransferase (ALT) and alkaline phosphatase (ALP) were measured by spectrophotometric method. In addition to making tissue sections of the liver. The treatment of rats led to a significant increase (P≤0.05) in liver enzymes compared with the control group. It also led to histopathology in the liver tissue, while the Brassica nigra seed extract acted as a protective role against the toxicity of cadmium chloride.
... direct ingestion of water and accidentally soil, and consumption of food grown in contaminated fields, inhalation of dust and dermal contact of soil and water (Wu et al., 2016). Notwithstanding that the factors like route, quantity and rate of exposure determine the clinical fate of Cd toxicity, toxic exposure may lead to renal tubular dysfunction, osteoporosis, endocrine disruption, respiratory tract irritation, hypertension, anemia, hepatotoxicity and even pancreatic or lung cancer (Adikwu et al., 2013;Bernhoft, 2013;Hossain et al., 2018). Moreover, Cd also exerts severe adverse effects on the normal functioning of the nervous system because of its high blood-brain barrier permeability (Wang and Du, 2013). ...
Article
Cadmium (Cd2+) is a heavy metal that can induce cytotoxicity leading to many chronic diseases. Ajwain (Trachyspermum ammi L.) is a popular spice with diverse pharmacological properties. It is used for the remedy of many pathological conditions that could be manifested by Cd2+ exposure e.g. inflammatory, toxic, neurological, genital or respiratory tract disorders. To reduce the Cd2+-induced cytotoxicity and apoptosis, PC12 cells were exposed/co-exposed to Cd2+ (5 or 10 µM) with/without non-toxic dose (240 µg/mL) of ethanolic extract of ajwain (AE) for 24 h. The cytotoxicity and apoptosis were evaluated by cell viability, lactate dehydrogenase (LDH) activity, glutathione levels, genomic DNA fragmentation and expressions of Bax, Bcl-2, Bcl-xL, NF-КB, cytosolic cytochrome c and caspase-3. Cd2+ reduced the cell viability significantly 24 h after exposure; however, the co-exposure of AE with Cd2+ reduced the cell death. The co-exposure also raised up glutathione levels, and decreased LDH activity. AE lessened the DNA fragmentation caused by Cd2+. AE suppressed the Cd2+-induced increased expression of apoptotic protein Bax, and promoted suppressed expressions of anti-apoptotic proteins Bcl-2, Bcl-xL and NF-КB. Moreover, it reduced the cytosolic cytochrome c levels and the caspase-3 expressions increased by Cd2+. Thus, it was suggested that AE reduced cytotoxicity and apoptosis was caused by Cd2+ in P12 cells. It inhibited Cd2+-induced apoptosis through intrinsic pathway possibly boosting up the antioxidant defense. Therefore, AE can be a candidate for a potential agent against metal and/or other toxicants. Additionally, this study validated the ethno-pharmacological therapeutic uses of ajwain in various pathological conditions.
... The exposure to lead originates from numerous sources, including contaminated water, food, air, and soil. When exposed to lead, it enters the body system and accumulates in various internal organs, including the liver and kidneys (Adikwu et al., 2013). Nowadays, lead poisoning is treated by using antidotes commonly known as chelators. ...
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Lead is a multisystemic toxicant when it accumulates and is hazardous to health. This study was conducted to determine the effect of Caulerpa lentillifera aqueous extract on lead accumulation in the internal organs and liver functions of lead-intoxicated rats. Sprague Dawley rats (n = 24) were divided into four groups (n = 6). Group I was healthy rats treated with saline (2 ml/kg bwt) daily for 28 days. Group II was healthy rats treated with C. lentillifera aqueous extract (500 mg/kg bwt) daily for 28 days. Group III was intoxicated with lead acetate (20 mg/kg bwt) daily for 4 days and then treated with saline (2 ml/kg bwt) for another 24 days. Group IV was intoxicated with lead acetate (20 mg/kg bwt) daily for 4 days and then treated with C. lentillifera aqueous extract (500 mg/kg bwt) for another 24 days. Lead accumulation in the internal organs was measured by the atomic absorption spectrophotometer and the liver function markers were determined using assay kits. Lead intoxication significantly (p < 0.05) increased lead accumulation in the rats’ internal organs and affected their liver functions. C. lentillifera aqueous extract supplementation to leadintoxicated rats significantly (p < 0.05) decreased lead accumulation in the rats’ internal organs and protected their liver functions. This study concludes that C. lentillifera aqueous extract possesses the capability of a chelating agent and attenuates the effect of lead on lead-intoxicated rats.
... Although the concentrations of dietary Cu, Zn, and Pb in the impact zone are high, their toxic load on the body is not significant due to the removal of excess HMs through the digestive tract. This barrier is less effective against Cd [38], and an increased Cd intake with food leads to its accumulation in the liver. Such a dependence has been described for small mammals of different trophic groups [39][40][41]. ...
Article
Long-term changes in the contents of heavy metals (Cu, Zn, Cd, Рb) in the food and liver of bank voles (Myodes glareolus) inhabiting areas exposed to pollution from the Middle Ural Copper Smelter (MUCS) in the period of reduction of its emissions (1990–2015). The results show that 50-fold reduction of emissions has not resulted in an equivalent decrease in the dietary and body concentrations of metals: in the impact zone (1–2 km from the MUCS), Cu, Zn, and Pb concentrations remain unchanged, while Cd concentrations have increased twofold by the end of the observation period; in the background zone (20 km), Cu, Zn, and Cd concentrations remain unchanged, while Pb concentrations have decreased by a factor of 1.7–2.5; and no directed changes have been revealed in moderately polluted plots (4–6 km). The accumulation of heavy metals in the animal body depends primarily on the contents of these elements in food and on the system of elementspecific homeostatic barriers providing effective protection from the toxic effect of heavy metals.
... Несмотря на высокие концентрации Cu, Zn и Pb в корме в импактной зоне, их токсическая нагрузка на организм незначительна вследствие выведения избыточных количеств ТМ через желудочно-кишечный тракт. Для Cd этот барьер не столь эффективен [38], поэтому повышенное поступление элемента с кормом приводит к его накоплению в печени. Подобная зависимость была показана для ММ разных трофических групп [39][40][41]. ...
Article
Анализировали многолетние (1990–2015 гг.) изменения содержания тяжелых металлов (Cu, Zn, Cd, Рb) в корме и печени особей рыжей полевки (Myodes glareolus), населяющих территории в зоне действия Среднеуральского медеплавильного завода в период снижения его выбросов. Показано, что сокращение выбросов (в 50 раз за 25 лет) не привело к эквивалентному снижению концентраций металлов в корме и организме животных: на импактных участках (1–2 км от завода) содержание Cu, Zn и Pb не изменилось, концентрации Cd к концу наблюдений возросли в 2 раза; в фоновой зоне (20 км) не изменилось содержание Cu, Zn и Cd, концентрации Pb снизились в 1.7–2.5 раза; на умеренно загряз- ненных участках (4–6 км) четких направленных изменений не выявлено. Ключевая роль в накоплении тяжелых металлов в организме животных принадлежит содержанию элементов в корме и системе элементоспецифичных гомеостатических барьеров, позволяющих эффективно защищать организм от токсического воздействия металлов.
... In addition, damage to mitochondrial cristae, hypertrophy of Kupffer cells, and infiltration of mixed inflammatory cells occurred as a result of Cd exposure. 29,30 Human liver cells and rat liver cells in in vitro studies showed parallel results with regard to Cd-induced oxidative stress, dose-related cellular stress, protein responses and apoptosis. 31,32 Studies on normal and immortalized human liver cells showed damage and loss of mitochondrial membrane potential (Delta Psi) with activation of caspase-9 and caspase-3, which was associated with the development of apoptosis over a concentration range of 1-100 μmol L −1 . ...
Article
Cadmium (Cd) is a highly toxic heavy metal and has spread widely in the environment in recent decades. This review summarizes current knowledge about Cd contamination of leafy vegetables, its toxicity, exposure, health risks, and approaches to reducing its toxicity in humans. Leafy vegetable consumption has been identified as a dominant exposure pathway of Cd in the human body. An overview of Cd pollution in leafy vegetables as well as the main sources of Cd is given. Notable estimated daily intakes and health risks of Cd exposure through vegetable consumption for humans are revealed in occupational exposure areas and even in some reference areas. Vegetable consumption is one of the most significant sources of exposure to Cd, particularly in occupational exposure regions. Therefore, numerous approaches have been developed to minimize the accumulation of Cd in leafy vegetables, among which the breeding of Cd pollution-safe cultivars is one of the most effective tools. Furthermore, dietary supplements from leafy vegetables perform positive roles in alleviating Cd toxicity in humans with regard to the effects of essential mineral elements, vitamins and phytochemicals taken into the human body via leafy vegetable consumption.
... Cd has been found to accumulate in endothelial cells leading to necrosis and denudation of hepatic sinusoids. Thus will disrupt the glucose metabolism [27]. ...
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Objective: The present study was undertaken to investigate the ameliorative effect of the bark and leaves of Nothaphoebe coriacea (gemor) on Cadmium (Cd) induced glucose metabolism alteration in liver homogenate in vitro. Methods: Glucose metabolism alteration in liver homogenate was induced by the administration of Cadmium Sulphate (CdSO4) at a dose 3 mg/l. Ameliorative effect of the leaves and bark extracts was determined by assessing the concentration of glycogen, glucose and Methylglyoxal (MG). Dubois hydrolytic method was used for liver glycogen and glucose concentration estimation. Modified Dinitro Phenyl Hydrazine (DNPH) method was used for MG concentration estimation. Results: The results of this present studies showed that treatment with CdSO4 significantly decreased the levels of glycogen and MG concentration, and increased the level of glucose in liver homogenate compared to control. The aqueous extracts of bark and leaves of gemor significantly increased the levels of glycogen and MG concentration, and decreased the level of glucose in liver homogenate compared to control. The aqueous extracts of the bark of gemor in comparison with CdSO4 treatment group showed the significant effect to maintain the glycogen, glucose, and MG concentration in liver homogenate. However, when compared to the aqueous extracts of leaves of gemor the result was not significant. The results suggest aqueous extracts of the bark of gemor was more effective to prevent the glucose metabolism alteration induced by CdSO4 than the aqueous extracts of leaves of gemor. Conclusion: The present study demonstrated Cd could induced the glucose metabolism alteration in liver homogenate, and the aqueous extracts of bark and leaves of gemor showed the ameliorative effect to prevent this alteration. In addition, the bark was more effective than leaves of gemor to prevent the glucose metabolism alteration induced by Cd. © 2015, International Journal of Pharmacy and Pharmaceutical Science. All rights reserved.
... The stimulation of alk. phosphatase in our study indicated increases in permeability damage or necrosis of hepatocytes [43]. Acid phosphatase and alk. ...
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The present work is aimed to investigate the toxicity of 1/20 LD50 of cadmium chloride (CdCl2) on male albino rats by oral ingestion and to determine the hepatoprotective effect of Solanum nigrum Linn (SN) dried fruits and their ethanolic extract against CdCl2 toxicity using biochemical parameters. Rats were divided into six groups; the first group is control, second group is CdCl2-intoxicated rats, third group is fed with a semi-modified diet with S. nigrum fruits, fourth group rats ingested with dried extract, and intoxicated rats (groups 5 and 6) were treated with fruits and ethanolic extract of S. nigrum, respectively. The results showed that rats exposed to CdCl2 induced remarkable decrease in body weight gain, feed efficiency, and Hb, Hct, RBC, and WBC count and MCHC, but increase in MCV and MCH values. In the case of plasma enzymes, there were significant stimulations observed in ALT and AST, acid phosphatase, alkaline phosphatase, and LDH activities of CdCl2-intoxicated rats (group 2) compared to control (group 1). Plasma protein profile showed decreases in total soluble protein and albumin; also globulin content was decreased by CdCl2 ingestion. Under the same condition, plasma total bilirubin and glucose levels were increased in group 2. In addition, lipid peroxidation and antioxidative system (GSH, catalase, and SOD) of liver were harmed by CdCl2 ingestion. Whereas, normal rats treated with SN showed insignificant changes in groups 3 and 4 as compared to control (group 1). The treatment with dried fruits and their ethanolic extract in CdCl2-intoxicated rats (groups 5 and 6) ameliorated and improved these harmful effects in all above parameters either for blood or liver. The results of this study suggest the protective effect of S. nigrum against liver injury happened by CdCl2 which may be attributed to its hepatoprotective activity and thereby.
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In recent decades, cadmium pollution has emerged as a core issue around the globe, rendering it of severe and fundamental concern to the scientific community. Against this background, several removal methods have been proposed and implemented to address environmental pollution and sustainable and eco-friendly development. Among them, biosorption has been extensively utilized for cadmium removal from the contaminated aqueous systems. The use of microalgae as biosorbent for Cd²⁺ removal has been widely used by researchers owing to its cost-effectiveness, simple and robust process, high efficiency, reusable, high growth rate, high surface to volume ratio, no generation of lethal products, can be used in both batch and continuous system, high binding capacity, and applicable to remove pollutants even at low concentration. The review further evaluated the mechanisms (extracellular and intracellular) adapted by microalgae encountered with Cd²⁺ ions in the contaminated aqueous system. This review will provide insightful knowledge for the development of cost-effective, efficient and sustainable microalgae-based technology for the heavy metal removal.
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Cadmium is extremely toxic heavy metal and there is no specific, safe and efficacious therapeutic management of cadmium toxicity. Scientific literature reveals several medicinal plants and natural products alleviate experimentally induced cadmium toxicity in animals. The present review attempts to collate those experimental studies on medicinal plants and plant derived natural products with cadmium toxicity ameliorative effects. Literature survey was carried out by using internet and the studies for the last two decades were considered. Minerals and semi-synthetic or synthetic analogs of natural products were excluded. Literature study revealed that 36 medicinal plants and 16 natural products exhibited significant protection from cadmium toxicity in experimental animal models i.e., pre-clinical studies. Clinical studies were not found in literature. Relevant research in this field could lead to development of a potentially useful agent in therapeutic management of cadmium toxicity in humans.
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This study investigated the hepatoprotective role of ethanolic extract of Moringa oliefera (M.O) on liver function (Biomarkers) in cadmium chloride (CdCl 2)-induced hepatotoxicity on the liver of albino Wistar rats. Sixty-six adult male albino wistar rats weighing between 130g-180g were used. LD 50 was determined for both CdCl 2 and MO using twenty-six (26) rats, while 40 rats were used for the experiment proper. The experimental rats were distributed into eight groups-A (control) and B, C, D, E, F, G and H, served as the treatment groups that received graded doses of CdCl 2 or MOor both simultaneously or at separate periods. The animals were then euthanized for sample collection and analysis using standard methods. The results showed significant increase (P<0.05) in the serum levels of Alanine aminotransferase (ALT) (430.50 ± 149.20), Aspartate aminotransferase (AST) (421.10 ± 8.34) and Alkaline Phosphatase (ALP) (515.60 ± 21.78) of animals in group B, but some protective effect of MO in the treatment groups with significant decreases in ALT, AST and ALP levels. The study therefore concludes that ethanolic extract of Moringa oleifera showed appreciable hepatoprotective values on liver functions (biomarkers) in CdCl 2 hepatotoxicity.
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Mixed contamination of benzo[a]pyrene (B[a]P), arsenic (As), cadmium (Cd), and lead (Pb) is a major environmental and human health concern. The mixture toxicity data on these co-contaminants are important for their risk assessment. In this study, we have determined the mixture toxicity of As, Cd and Pb, and B[a]P with As, Cd or Pb in HepG2 cells. The binary mixtures of Cd + As, Cd + Pb and As + Pb and B[a]P + metals (B[a]P + As, B[a]P + Cd and B[a]P + Pb) were evaluated for their interaction on the cytotoxicity using the MTS assay. A full factorial design (4 × 5) was used to determine the interaction toxicity and all the six mixtures showed significant interaction on the cytotoxicity. We further investigated the role of oxidative stress (reactive oxygen species (ROS) generation) and antioxidant defense mechanism (total glutathione (GSH) level) with the observed cytotoxicity. The mixtures of metals reduced the total GSH level and increased the ROS generation, respectively. In the case of mixtures of B[a]P and metals, both total GSH level and ROS generation were increased. Overall, the binary mixtures of metals and B[a]P with metals caused a dose dependent toxicity to HepG2 cells. The results also showed a significant contribution of oxidative stress to the observed toxicity and the potential protective role of the total GSH level against this mixture toxicity. The findings of interaction between B[a]P and metals might have an impact on the potential human health risk of this mixtures at contaminated sites.
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The aim of this study was to evaluate the health benefits associated with apple consumption following cadmium exposure. A total of 15 Wistar rats were distributed into three groups (n=5), as follows: control group (non-treated group, CTRL); cadmium group (Cd) and apple juice group (Cd+AJ). The results showed a decrease in the frequency micronucleated cells in bone marrow and hepatocytes in the group exposed to cadmium and treated with apple juice. Apple juice was also able to reduce the 8OHdG levels and to decrease genetic damage in liver and peripheral blood cells. Catalase (CAT) was decreased following apple juice intake. Taken together, our results demonstrate that apple juice seems to be able to prevent genotoxicity and oxidative stress induced by cadmium exposure in multiple organs of Wistar rats. Copyright © 2015 Elsevier GmbH. All rights reserved.
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Cadmium (C d) and zinc (Zn) are an industrial and environmental pollutant of aquatic system has attracted the attention of research's all over the world. In the present study the toxic effects of zinc (Zn) and Cadmium (C d) on the liver of male mice. Male Balb /c mice weighing 32-34 gm, 70 days old, were treated orally with (1-10 mg/kg body wt. CdCl 2 and 1-8 mg/kg body wt. ZnCl 2). The body weight, liver weight, histological examination of liver, along with DNA ladder for apoptosis was studied. Cadmium and zinc induced both a time, and dose dependent increase in apoptotic, severity of necrosis. Liver weight, body weight decreased with increase of dose. It has been concluded that cadmium and zinc caused necrotic effect in liver and apoptotic as well as decrease body weight and liver weight.
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In this study, 4 experimental groups and 1 control group containing adult mice (Mus musculus var. albinos) were used to examine the effects of 2 different cadmium compounds, namely cadmium para hydroxybenzoate, which was newly synthesized, and cadmium chloride the liver of mice. In various test concentrations, both cadmium compounds were intraperitoneally injected into dult mice everyday for 15 days. With standard histological techniques samples were obtained from the livers of the mice. Slides were prepred and examined with light microscopy (Nikon Eclipse E600) and histopathological structures were observed.
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Background: Cadmium is one of the most toxic heavy metals in our environment having a very strong ability to accumulate in body organs, especially in kidney. The present study was done to determine the genotoxicity and cytotoxicity in kidneys of rats exposed to cadmium. Methods: Male rats (n=30), kept in standard conditions were used in this study. The animals were randomly divided into 2 groups (control and treatment). The treatment group was intraperitoneally injected with Cd (300µm/kg) at hours 0, 6, 12, 24, 48. Twenty four hours after the last injection, the rats were sacrificed and their kidneys were obtained. Then oxidative stress markers, malondialdehide (MDA), glutathione (GSH), and superoxide dismutase (SOD), were assayed in homogenized kidney for studying their cytotoxicity. For genotoxicity and DNA damage studies, Comet assay was run on isolated kidney cells. Data analysis was done by t-test and ANOVA using SPSS software version 15. Results: MDA and GSH concentrations in normal and Cd exposed kidney cells were 287.01±37.30nmol/g.pr and 15.61±3.89µmol/g.pr and 609.24±87.87nmol/g.pr and 28.52±5.22µmol/g.pr, respectively. In addition, SOD activity in normal and Cd exposed kidney cells were 77.75±4.12 and 218.91±5.40 U/mg.pr, respectively. Comet assay results (content comet length, tail length, and head diameter) showed DNA breakage in the treatment group that was stimulated by Cd which was not seen in the control group. Conclusion: The results demonstrated the genotoxicity effect of Cd on kidney cells as well as the ability of Cd to producing cytotoxicity.
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Cadmium (Cd) is an environmental and industrial pollutant known to be highly toxic to large number of tissues in the body. In this study, the protective effects of aqueous extract of potato (Solanum tuberosum) against the hepatotoxic effect of Cadmium (Cd) were investigated in a set of female Wistar rats. The rats were given oral administrations of potato extract for 3 weeks at a dose of 250 mg kg(-1) body weight prior to one week intraperitoneal exposure to 4 mg kg(-1) Cadmium (Cd) as Cadmium Chloride (CdCl2). Liver damage were monitored using markers of hepatocellular injury such as serum (GOT, Glutamate Oxaloacetate Transaminase; GPT, Glutamate Pyruvate Transaminase; theta GT, Gamma-Glutamyl Transpeptidase and ALP, Alkaline Phosphatase). The levels of reduced glutathione (GSH), GST activity, lipid peroxidation and the expressions of HO-1 and NQO1 were also determined in order to evaluate the antioxidant status of the liver after Cd exposure. The results show that the presence of aqueous extract of Solanum tuberosum significantly reduced the activities of all the serum enzymes in the presence of Cd. The level of GSH and the activity of GST were also significantly increased in the presence of the extract plus Cd when compared with rats exposed to Cd alone. The extract also attenuates lipid peroxidation induced by Cd indicating decrease oxidative damage. Western blot results show addictive effect of the extract and Cd on the expressions of HO-1 and NQO1. Taken together, the presence work shows that aqueous extract of Solanum tuberosum contains active agents that are potent in preventing Cd-induced liver damage in exposed rats.
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Abdel-Moneim & Ghafeer ment that occurs naturally in ores together with zinc, lead and copper or is emitted into the air through the process of volcanic INTRODUCTlON Cadmium (Cd) is a relatively rare ele- ABSTRACT The therapeutic properties of natural honey once considered a form of folk or preventive medicine. It is important for the treatment of acute and chronic free radical mediated diseases and toxicity. Oxidative stress can play a key role in cadmium-induced dysfunction. The aim of this work was to study the effect of natural honey on cadmium-induced liver and kidney damage. A total of 30 adult male rats were divided into three groups. Group I animals served as control were injected daily I.P. by 1 ml saline. Group II an-imals were injected daily I.P. with 0.5mg/kg cadmium chloride dissolved in 1 ml saline for 4 weeks. Ani-mals of group III were treated with 0.5 mg /kg cadmium chloride I.P. and 0.05ml of natural honey mixed with water orally concurrently for 4 weeks. Liver function (SGOT),(SGPT), (ALP) and kidney function (creatinine and urea nitrogen) tests were measured. In addition lipid peroxidation,reduced glutathione (GSH) and glutathione peroxidase (GPx) were estimated in liver and kidney tissues samples. Light and transmission electron microscopic examination were used for histological changes. The results revealed that treatment with Cd caused marked elevation in the level of free radicals (lipid peroxidation) and kid-ney and liver enzymes, and a decline in GPx activity and GSH level. Administration of honey with Cd in-duced improvement in all examined parameters. On the other hand, light microscopic examination of kid-ney cortex of Cd treated group revealed swelling of the cells lining the convoluted tubules and vaculation of their cytoplasm. Variable degrees of glomerular degeneration were present. The liver showed different degrees of cell degeneration, necrosis, dilatation and congestion of blood vessels. Results obtained by EM examination revealed that there were affection of mitochondria and partial loss of microvilli of some kidney tubules. Furthermore, electron dense mitochondrea, depletion of glycogen granules in a rarified vaculated cytoplasm were seen in the hepatocytes. It is noticed that concurrent administration of honey with cadmium improved histological changes in both kidney and liver by light and electron microscope. It could be concluded that honey via its antioxidant activity has the ability to protect against cadmium-induced hepatotoxicity and nephrotoxicity.
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Cadmium is a widely distributed environmental pollutant and toxicant. The present study was carried out to evaluate the effects of vitamins C and E on cadmium-induced serum levels of alkaline phosphatase (ALP), urea, creatinine, progesterone, LH and FSH in the female guinea pig. Animals were given single doses of vitamins C (1.5 mg/kg) and E (50 mg/kg) per oral and (0 -8 mg Cd/kg ip) for 24 h. Animals were sacrificed and the serum levels of the above parameters were measured. Also, the effects of pretreatments with vitamins C and E on Cd-induced serum levels of the parameters were determined. Serum levels of all parameters were significantly (p 0.05) decreased in a dose-dependent manner in vitamins-treated animals, while they were increased in cadmium-treated animals, compared to the control animals. Furthermore, pretreatments with vitamins C, E and combination of both vitamins reduced the cadmium-induced serum levels of all parameters, which was most pronounced in animals pretreated with a combination of both vitamins, especially on ALP and progesterone levels. These results may be due to the oxidative and anti-oxidative properties of cadmium and the vitamins (C and E) respectively, acting through calcium and protein kinase C signal transduction pathways.
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The effect of chronic exposure to cadmium (Cd) on the mechanical properties of femoral diaphysis and femoral neck was investigated on a rat model of human exposure. Three-week-old female Wistar rats were exposed to Cd in drinking water at concentrations of 1, 5, 50, or 100 mg/L for 12 months. Biomechanical properties of the femoral diaphysis were evaluated in a three-point bending test and those of the femoral neck in a bending test with vertical loading of the head. Bone mineral content (BMC) and bone mineral density (BMD) at the whole femur, and BMD at the diaphysis and proximal femur (head and neck region) of the Cd-treated rats decreased in a dose-dependent manner, except for the diaphyseal BMD at a Cd concentration of 1 mg/L. Exposure to Cd concentrations of 1 and 5 mg/L had only little effect on the diaphyseal mechanical properties (decreased yield load with unchanged bending strength, stiffness, yield stress, ultimate stress, and Young modulus), whereas the bending strength and stiffness of the neck decreased and the yield load clearly tended to decline or declined. The effect of Cd at the two locations was more marked in the 50 and 100 mg/L groups, and changes in the bone geometry were observed in these animals. The results clearly revealed that chronic, even low-level, exposure to Cd results in demineralization and weakening of the femur. The femoral neck seems to be more vulnerable than the diaphysis to failure from Cd. We conclude that environmental exposure to Cd may be an important risk factor for femoral neck fracture.
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Curcumin, a biologically active compound from turmeric, and vitamin C act as a natural antioxidant and potent chemopreventive agent. The objective of the study was to investigate whether the combined pretreatment with curcumin and vitamin C offers more beneficial effects than that provided by either of them alone in reversing cadmium (Cd)- induced hepatotoxicity. For this purpose, 64 adult male Wistar rats, equally divided into control and seven treated groups, received either Cd (as CdCl2 5 mg/kg), curcumin 400 mg/kg, curcumin 200 or 400 mg/kg + CdCl2, vitamin C 100 mg/kg + CdCl2, curcumin 200 or 400 mg/kg + vitamin C + CdCl2. All groups were treated by gavage for 27 days. The results showed that Cd treatment increased significantly lipid peroxidation levels,decreased significantly the glutathione levels, increased significantly on metallothionein (MT) expressions including the degenerative changes of liver histological tissues were observed. The treatment of Cd-exposed rats with curcumin or vitamin C alone could not reverse Cd-induced the above changes. The combined treatment with curcumin along with vitamin C before Cd intoxication was more effective than that with either of them alone in reducing such changes and reverse the changes almost similar to that of control. In conclusion, the results demonstrated that the combined pretreatment with curcumin along with vitamin C could recover the alterations and offer more protection than curcumin or vitamin C alone against Cd hepatotoxicity.
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The present study was conducted to investigate the protective potentials of methanolic extract of the leaf of Momordica charantia (MC) against cadmium randomly divided into three groups (A, B and C) of ten rats each. Group A rats served as the control and received normal saline orally. Group B rats were treated with cadmium c while group C rats were pre-treated orally with extract of MC 300 mg/kg bwt before treating with cadmium chloride 2.5 mg/kg bwt subcutaneously. The rats were treated every other day regularly for six weeks. Blood samples were collected by ocular puncture and five rats each per group were sacrificed at third week and six week post-treatment intervals. Serum total protein, albumin, alanine aspartate-amino transferase (AST) were evaluated. Histop challenged rats, compared to control, total protein and albumin levels were significantly reduced while ALT activity was significantly raised at the two hepatotoxicity. However, the toxic effect of cadmium was significantly controlled in the rats pre methanolic extract of MC at the two time intervals. 1.0 Introduction Liver is an abdominal organ which plays a vital role in detoxification and excretion of many endogenous and exogenous substances. The liver is a natural chemical factory which aids anabolism of complex molecules from simple substances absorbed from the gastro which aids fat digestion and removes toxins through the bowels (Buraimoh and intoxication of liver to different t dysfunction (Nithya et al., 2012). Hepatic dysfunction due to exposure to environmental toxic agents is increasing worldwide. Among the various known hepatoxins, cadmium (Cd) preferentially l and causes liver injury. Cadmium is known for its deleterious effects on hepatocytes among which are enhancement of lipid peroxidation and oxidative damage through free radicals generation (Manca Alhazza, 2008). Management of liver disease is still a challenge to the modern medicine and conventional medicine is now pursuing the use of natural products such as herbs to complement the liver needs (Gayatri different plants are being evaluated on d against different chemical-induced liver damage in experimental animals. Momordica charantia is a tendril bearing economically important medicinally vine belonging to the family cucurbitaceae (Paul and Raychaudhuri, 2010; Bakare et al., 2010). It is a vegetable widely cultivated in tropical areas including West Africa, East Africa, Amazon, and the Carribean, both as medicine and fruit. All the plant parts including flower, leaves, stem, fruits and seeds have been used traditionally to treat array of conditions like diabetes, hypertension, cancers, ulcers, asthma, Gastrointestinal problems, fever, inflammation, erectile dysfunction, bacteria and viral infections (Kumar and Bhowmik, 2010) the hepatoprotective potentials of the methanolic leaf extract of albumin, aspartate amino transferase (AST), alanine amino transferase (ALT), and histology of cadmium-induced liver damage.
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The present study was undertaken to examine the attenuative effect of Piper betle leaf extract (PBE) against cadmium (Cd) induced oxidative hepatic dysfunction in the liver of rats. Pre-oral supplementation of PBE (200 mg/kg BW) treated rats showed the protective efficacy against Cd induced hepatic oxidative stress. Oral administration of Cd (5 mg/kg BW) for four weeks to rats significantly (P > 0.05) elevated the level of serum hepatic markers such as serum aspartate transaminase (AST), serum alanine transaminase (ALT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), gamma-glutamyl transpeptidase (GGT), bilirubin (TBRNs), oxidative stress markers viz., thiobarbituric acid reactive substances (TBARS), lipid hydroperoxides (LOOH), protein carbonyls (PC) and conjugated dienes (CD) and significantly (P > 0.05) reduced the enzymatic antioxidants viz., superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione S-transferase (GST), glutathione reductase (GR) and glucose-6-phosphate dehydrogenase (G6PD) and non-enzymatic antioxidants Viz., reduced glutathione (GSH), total sulfhydryls (TSH), vitamin C and vitamin E in the liver. Pre-oral supplementation of PBE (200 mg/kg BW) in Cd intoxicated rats, the altered biochemical indices and pathological changes were recovered significantly (P > 0.05) which showed ameliorative effect of PBE against Cd induced hepatic oxidative stress. From the above findings, we suggested that the pre-administration of P. betle leaf extract exhibited remarkable protective effects against cadmium-induced oxidative hepatic injury in rats.
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Problem statement: Cadmium is one of the most dangerous occupational and environmental toxins. It is found in drinking water , atmospheric air and even in food. Cadmium is reported to be very toxic to biological systems. Un til now in treating intoxication with this metal, chelating Compounds have been used, burdened with numerous undesirable symptoms. For this reason, many researches are carried out in many cou ntries to find natural-made compounds that help in the protection against cadmium induced toxicity wit h fewer or no side effects. This study was conducted to demonstrate the effect of daily oral C amel's milk administration against Cadmium chloride induced toxicity in white albino rats. Approach: White albino rats of both sexes (230-250 g) were housed in standard metal cages (6 rats/cage). The experimental rats (6 in each group) distributed into two experimental groups with a shared control group received only normal saline orally (Group 1). In experimental first group a daily dose (10 mg kg 1 body weight) of cadmium chloride was orally administrated to the rats for 21 days and named Cad mium chloride treated rats. In experimental second group, the same concentrations of cadmium chloride was dissolved in 2 mL of early morning fresh Camel's milk and the whole solution was administered into the experimental rats for 21 days and named Camel's milk cadmium chloride treated group. Water and food were provided ad libitum . Results : The data indicated that, in experimental Cadmium c hloride treated rats, serum albumin, calcium and blood hemoglobin were decreased compared with control group received normal saline only. Moreover, Camel's milk administration with ca dmium chloride showed a significant improvement of albumin, hemoglobin and calcium levels in the serum of the rats compared with cadmium chloride treated rats. Serum iron, sodium, chloride and urea levels were significantly increased in cadmium chloride treated rats compared with control group, while the addition of camel's milk to cadmium chloride decreased the high levels of these serum parameters in the treated rats. The enzyme activities of serum Alanine Aminotransferase (ALT), Aspartate Aminotransferase (AST) and serum Alkaline Phaospatase (ALP) were significantly increased by orally administration of cadmium chloride compared with control group, while adding Camel's milk to cadmium chloride decreased the high levels of these enzymes comparing with the cad mium chloride treated rats. Cadmium chloride administration resulted in a high concentration of lipid peroxidation markers; TBARS and Hydroperoxides in comparison to control group, adding camel's milk to the cadmium chloride restored the levels of these markers to their normal levels in comparing to Cadmium chloride treated rats. Also treatment with cadmium chloride alone caused a significant decrease in both the enzymatic and non- enzymatic markers of oxidative stress (superoxide d ismutase and catalase) and reduced glutathione, respectively in the liver tissues of treated rats, while the administration of camel's milk with cadmi um chloride increased and restored their levels to nea r normal in comparing with cadmium chloride treated rats. These results demonstrated that camel's milk had a protective effect against the toxicity induce d by cadmium chloride. Conclusion : the above results indicated a protective effect of camel's milk oral administration against cadmium induced toxicity in white albino rats.
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To investigate the protective effect of Lithium against the toxic effect of Cadmium in the rat testes. Twenty four adult male Sprague-Dawley rats were treated with four different regimens: Cadmium only, Cadmium and lithium, lithium only and controls. Rats were sacrificed after 6 weeks and testicular levels of pro-inflammatory cytokine (IL-4), anti-inflammatory cytokine (TNF-α), Pro-apoptotic protein (Bax) and anti-apoptotic protein (Bcl-2) were measured by ELISA while serum levels of FSH, LH, Prolactin and Testosterone were measured using the Vidas parametric system. Antioxidant status (MDA, SOD) was also assessed in serum. Histopathological changes of testes were examined using light and electron microscopy. Immunohistochemical staining for Bax, Bcl-2 and Caspase 3 were performed. Treatment with lithium was associated with significant reduction in the toxic effects of Cadmium as shown by reduced testicular levels of TNF-α, serum levels of Malondialdehyde and testicular level of Bax, and increased levels of IL-4, Zn-Cu SOD, Bcl-2 and Testosterone. Testicular histopathology showed that Cadmium produced an extensive germ cells apoptosis and the addition of lithium in Cadmium-treated rats significantly reduced cadmium-induced testicular damage. Lithium has a protective effect against cadmium-induced testicular apoptosis in the rat.
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Although it is well known that cadmium (Cd) causes adverse effects on male rat reproductive organs, few studies have quantified alterations caused by its low doses. Quantification of these alterations, especially in the testis, was measured using morphometry. A single dose of cadmium chloride (1 or 1.2 mg/kg BW) was injected i.p. in adult rats, killed after 7 or 56 days. The lower dose caused slight alterations as measured by morphometrical analysis. The higher dose caused significant reduction in testis and epididymis weight, gonadossomatic index and length of seminiferous tubule (ST) after 7 and 56 days. Cadmium significantly reduced the ST diameter after 56 days. Decreased volume density of ST, after 7 and 56 days, was accompanied by an increase in interstitium volume density. The damage caused by the dose of 1.2 mg/kg can be clearly observed with light microscope. After 7 days, the tubule lumens were filled with degenerated germ cells and multinucleated spermatid aggregates. Vacuolization of the seminiferous epithelium was also observed. After 56 days, increased damage resulted in vacuolated ST, consisting only of Sertoli cells. Scanning electron microscopy examination of the testis showed that, in the group cadmium treated (1.2 mg/kg) and killed after 56 days, the interstitial tissue presents a compact and fibrous appearance with absence of fenestrae. The seminiferous epithelium height diminished and the absence of spermatozoa can be noted. The results show that a very small difference of Cd dose causes a sudden increase in testicular damage, apparently overpowering this tissue's natural defences.
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The infl uence of lead (5mg/kg b.w) and cadmium (2mg/kg b.w) after chronic treatment of the rabbits on serum protein is investigated. Signifi cantly raised content of the cholesterol, ASAT and ALAT; hypo-albuminemia and hyperbetaglobulinemia of the background of one hypoproteinemia and low A/G coeffi cient are established. On basis of obtained result can to show degree of liver parenchyma damage and as trial for used the hyperbeta-globulinemia (at chronic treatment with cadmium is stronger markedly) as indicator for delimitation of enteral from parenteral toxication, at that is noted hypergamma-globulinemia.
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This study was designed to examine the protective role of vitamin C (VC) against oxidative stress and morphological changes induced by chronic exposure to cadmium chloride (CdCl 2) in the lungs and brain. Male adult rats received CdCl 2 (5 mg/kg body weight) daily for forty days. Vitamin C (VC) at a dose of 100 mg/kg body weight was given concomitantly with CdCl 2 to the rats. Three animal groups were used in this experiment (control, CdCl 2 and CdCl 2 +VC). The concentration of malondialdehyde (MDA), activity of superoxide dismutase (SOD) enzyme and concentration of glutathione (GSH) were measured in the lung and brain homogenates. Also, histopathological investigations were carried out in lung and brain tissues. CdCl 2 administration significantly increased the levels of MDA and decreased the activity of SOD and GSH concentration in the lungs and brain versus those of control rats. Administration of vitamin C counteract the changes of all measured parameters and appear nearly like those of controls. Light microscopy revealed marked changes in the structure of the studied tissues of CdCl 2 administered animals. Again, vitamin C restored the damage of tissues associated with CdCl 2 administration. The present results suggest that vitamin C administration attenuated the oxidative damage and morphological changes induced by CdCl 2 in the lungs and brain of rats.
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This study was designed to evaluate the Hepatoprotective effect of Ethanolic leave Extract of Moringo Oleifera on the Histology of the liver of wistar rats. Fifteen (15) female adult wistar rats were divided into three (3) groups. Group I was the Control group that received distilled water only, group II was the negative control that received 1 g/kg of paracetamol on the 10th day, and group III received 500 mg/kg of the extract for duration of ten (10) days. Group III was pre-treated with 500 mg/kg of the ethanolic leave extract of Moringa oleifera before inducing the liver damage on the 10th day with 1 g/kg of paracetamol. Twelve (12) h after administration, the rats were sacrificed and the liver was fixed immediately in Formalin. The liver tissues was processed and stained in Haematoxylin and Eosin (H&E).The histological observations showed that the leave extract of Moringa oleifera was hepatoprotective.
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Cadmium bioaccumulation and its effects on the changes of some hematological parameters in carp, Cyprinus carpio L., was studied. Carp was exposed 24 h to acute concentration of cadmium (0.5 mg Cd/dm3 water) at 27°C. Particularly the greatest accumulation of cadmium was in gills, kidneys, alimentary canal, hepatopancreas, and with lesser degree in spleen and vertebral column; while in skin and muscles accumulated only low levels of cadmium. Hematologically, cadmium bioaccumulation significantly raised erythrocytes count, hemoglobin content, hematocrite value and blood glucose, but decreased leukocytes count in comparison to control samples. Histologically, cadmium caused pathological alterations in the gill filaments and respiratory lamellae, hepatopancreas and kidney but did not affecting the skin. In addition, cadmium disturbed the metal contents (Cu, Zn, Fe and Mg) in organs in which it accumulated.
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Ethanolic leaf extract of Calycopteris floribunda was investigated for hepatoprotective activity against cadmium induced liver damage. Various biochemical parameters, serum glutamate oxalo acetate transaminase (SGOT), serum glutamate pyruvate transaminase (SGPT), serum alkaline phosphatase and total protein were determined to assess the effect of the leaf extract on the cadmium induced hepatic damage. The animals treated with cadmium recorded elevated concentration indicating severe hepatic damage by cadmium, whereas the blood samples from the animals treated with 200 mg/kg (b.w) and 400 mg/kg (b.w) of ethanolic leaf extract of Calycopteris floribunda showed significant reduction in the serum markers indicating the effect of the leaf extract in restoring the normal functional ability of the hepatocytes. Silymarin (100 mg/kg, p.o.) was given as reference drug. The present study concluded that the ethanolic leaf extract of Calycopteris floribunda showed significant hepatoprotection against cadmium-induced hepatocellular injury.
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It is known that cadmium induces a variety of functional disorders, especially liver and kidney dysfunction. The main mechanism involved in cadmium hepatotoxicity is its binding to sulfhydryl groups and initiation of inflammation. Additionally, oxidative stress, due to a decrease in antioxidative capacity, plays a role in chronic cadmium hepatotoxicity. The role of oxidative stress in acute cadmium intoxication is still not clear. The aim of our study was to investigate the role of reactive oxygen species and efficiency of antioxidant protection in rat liver in acute cadmium intoxication. Male Wistar rats (n=16) were divided into the following groups: 1. control group (n=7), treated with saline, 2. cadmium-treated (n=9) with a single dose of 2.5 mg/kg intraperitoneally. After administration (24 hours), blood samples from the right side of the heart and liver samples were collected for the determination of oxidative stress parameters. In our study malondialdehyde concentration was elevated both in plasma and liver after cadmium administration (p<0.01). Moreover, superoxide dismutase activity was increased in the cadmium-treated group, mainly due to increasean in copper/zinc superoxide dismutase activity (p<0.01). Reduced glutathione level in liver and plasma and concentration of sulfhydryl groups were not significantly changed by cadmium. The present study suggests that lipid peroxidation plays an important role in acute cadmium-induced liver injury. Antioxidant capacity of hepatocytes is partly increased due to an adaptive increase of superoxide dismutase activity.
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Cadmium is an extremely toxic metal which has no known necessary function in the body. Industrial use and agricultural fertilizers are the major source of its environmental contamination. It principally affects lung, liver, kidney and testes following acute intoxication. The present study pertains to the protective role of rutin against cadmium (Cd)-induced hepatotoxicity in mice. Rutin is a naturally occurring citrus flavanone which has been reported to have a wide range of pharmacological properties. In the present investigation cadmium (5 mg kg -1) was administered orally for 4 weeks to induce hepatotoxicity. Cadmium treatment enhanced the lipid peroxidation in liver significantly (p<0.001). Cadmium treatment also decreased the amount of non-enzymatic antioxidant viz., reduced glutathione (GSH) significantly. Cadmium treatment decreased the level of enzymatic antioxidant enzymes viz., super oxide dismutase (SOD), catalase (CAT) and Glutathione-S-Transferase (GST). Two different doses of rutin (80 and 20 mg kg -1 b.wt.) were given to the mice along with the cadmium. High dose treatment of rutin (80 mg kg -1 b.wt.) resulted in significant decrease in lipid peroxidation (p<0.001). It also restored the amount of reduced glutathione significantly (p<0.001). Administration of high dose of rutin also brought the activities of cellular antioxidant enzymes viz., SOD (pO.OOl), CAT (pO.Ol) and GST (pO.OOl) significantly to normal. The study result suggested that rutin may be beneficial in ameliorating the cadmium-induced oxidative damage in the liver of mice.
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The main threats to human health from heavy metals are associated with exposure to lead, cadmium, mercury and arsenic. These metals have been extensively studied and their effects on human health regularly reviewed by international bodies such as the WHO. Heavy metals have been used by humans for thousands of years. Although several adverse health effects of heavy metals have been known for a long time, exposure to heavy metals continues, and is even increasing in some parts of the world, in particular in less developed countries, though emissions have declined in most developed countries over the last 100 years. Cadmium compounds are currently mainly used in re-chargeable nickel-cadmium batteries. Cadmium emissions have increased dramatically during the 20th century, one reason being that cadmium-containing products are rarely re-cycled, but often dumped together with household waste. Cigarette smoking is a major source of cadmium exposure. In non-smokers, food is the most important source of cadmium exposure. Recent data indicate that adverse health effects of cadmium exposure may occur at lower exposure levels than previously anticipated, primarily in the form of kidney damage but possibly also bone effects and fractures. Many individuals in Europe already exceed these exposure levels and the margin is very narrow for large groups. Therefore, measures should be taken to reduce cadmium exposure in the general population in order to minimize the risk of adverse health effects. The general population is primarily exposed to mercury via food, fish being a major source of methyl mercury exposure, and dental amalgam. The general population does not face a significant health risk from methyl mercury, although certain groups with high fish consumption may attain blood levels associated with a low risk of neurological damage to adults. Since there is a risk to the fetus in particular, pregnant women should avoid a high intake of certain fish, such as shark, swordfish and tuna; fish (such as pike, walleye and bass) taken from polluted fresh waters should especially be avoided. There has been a debate on the safety of dental amalgams and claims have been made that mercury from amalgam may cause a variety of diseases. However, there are no studies so far that have been able to show any associations between amalgam fillings and ill health. The general population is exposed to lead from air and food in roughly equal proportions. During the last century, lead emissions to ambient air have caused considerable pollution, mainly due to lead emissions from petrol. Children are particularly susceptible to lead exposure due to high gastrointestinal uptake and the permeable blood-brain barrier. Blood levels in children should be reduced below the levels so far considered acceptable, recent data indicating that there may be neurotoxic effects of lead at lower levels of exposure than previously anticipated. Although lead in petrol has dramatically decreased over the last decades, thereby reducing environmental exposure, phasing out any remaining uses of lead additives in motor fuels should be encouraged. The use of lead-based paints should be abandoned, and lead should not be used in food containers. In particular, the public should be aware of glazed food containers, which may leach lead into food. Exposure to arsenic is mainly via intake of food and drinking water, food being the most important source in most populations. Long-term exposure to arsenic in drinking-water is mainly related to increased risks of skin cancer, but also some other cancers, as well as other skin lesions such as hyperkeratosis and pigmentation changes. Occupational exposure to arsenic, primarily by inhalation, is causally associated with lung cancer. Clear exposure-response relationships and high risks have been observed.
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Cyclophosphamide (CP) is one among the important therapeutic chemotherapy drug used worldwide. Damage to normal tissues due to toxic metabolites limits the usage of CP efficiently for treating various cancers. In the present study, hepatoprotective effect of Momordica charantia Linn. (Cucurbitaceae) against CP induced hepatotoxicity in rats was evaluated. Hepatocellular damage in rats was induced by injecting CP i.p. (total of 200 mg kg -1, b.wt.) for 2 days. Momordica charantia fruit aqueous extract (MCE) (300 mg kg -1 b.wt.) was administered orally for 12 days for treatment. Protective effect of MCE was evaluated by assessing the liver marker enzymes such as AST, ALT, ALP, LDH and γ-GT in serum, AST and ALT in Hver tissues and biochemical parameters such as total protein, urea, creatinine, uric acid, total and direct bilirubin. Liver marker enzymes and clinical chemistry parameters were significantly altered in CP intoxication. These alterations were significantly normalized in animals administered with MCE. Protective effect of MCE could be due to radical-scavenging and antioxidant properties of the MCE. MCE could had been demonstrated these properties due to the presence of phytochemical components that include polyphenols, alkaloids, terpenoids, glycosides and tannins. Present findings supported that the treatment with MCE could be helpful against hepatocellular damage, owing to its hepatoprotective property.
Article
Cadmium (Cd) is a dangerous occupational and environmental toxin. Exceeding its permissible weekly uptake in meals is a disturbing phenomenon. The aim of this study is to assess the effect of long-term uptake of cadmium chloride on selected biochemical parameters and oxidative stress biomarkers in animal models. Long-term intoxication with cadmium chloride elevated blood serum concentration of urea, creatinine, glucose, AspAT and A1AT activity as well as TBARS and protein carbonyl group concentrations; TBARS concentration in erythrocytes was also elevated as well as 8-hydroxy-2'-deoxyguanosine excretion with urine.
Article
Cadmium induced testicular damage has been investigated in -tocopherol (Vitamin E) pretreated and non-pretreated male rats exposed to a single sub-lethal dose of cadmium in form of CdCl 2. Graded doses of vitamin E (75, 150, and 750 mg kg -1 body wt.) were administered daily to rats in separate groups by gavage for 4 weeks while 3 mg Cd kg-1 body wt was administered subcutaneously, 24 hr to the termination of the study. Relative to the Cd -free control rats, cadmium significantly (P < 0.05) increased total cholesterol (CHL) levels in the testes and prostate but did not change its level in plasma. It also decreased TPL/CHL and phosphatidylcholine (PC) / phosphatidylethanolamine (PE) ratios in testes and increased sphingomyeline (SPM) / phosphatidylethanolamine (PE) ratios in the testes. However, cadmium administration increased the PC/PE and SPM/PE ratio but reduced the TPL/CHL ratio in the prostate. It appears that increased cholesterol levels within the testes and prostate and attendant membrane rigidity may be one mechanism by which cadmium causes damage to the testes and prostate. It also appears that low -medium doses of -tocopherol can effectively protect the testes and prostate against Cd -induced damage.
Article
The susceptibility to cadmium (Cd)-induced toxicity in male Long-Evans (LE) rats was compared with that in male Fischer 344 (Fischer) and Wistar-Imamichi (WI) rats, which are sensitive and resistant, respectively, to Cd toxicity. All rats of the LE and WI strains survived for 7 days after the treatment with a toxic dose of Cd (6.5mg/kg b.w.). However, all rats of the Fischer strain died by the following day. The strong resistance to Cd toxicity in the LE strain was confirmed to be independent of metallothionein synthesis induced by Cd. The hepatic and renal Cd contents after its administration were significantly lower in the LE strain than in the Fischer strain. Furthermore, the hepatic and renal zinc (Zn) contents after its administration were significantly lower in the LE strain than in the Fischer strain. These limited data suggest that the strong resistance to Cd toxicity in male LE rats results from, at least in part, the lower accumulation of the metal in the liver and kidney, in a similar mechanism as the lower Zn accumulation.
Article
Since occupational and environmental exposure to the heavy metal Cadmium (Cd) affects human health this study investigated the effects of exposure to a single, or multiple, sub-toxic Cd concentrations on sub-confluent and confluent human osteoblast growth and expression of specific bone differentiation markers. RT-PCR quantified gene expression of type I collagen, metalloprotease (MMP13), runt-related transcription factor-2 (RUNX2), osterix, osteocalcin, osteonectin, alkaline phosphatase, integrins and bone sialoprotein (BSP). Expression of fibroblast growth factors 1 and 2 (FGF1, FGF2), transforming growth factor-beta(3) (TGFbeta(3)) and bone morphogenetic protein-2 (BMP2) were also evaluated to determine whether Cd-related effects were mediated by an imbalance in expression. Depending on osteoblast concentration and maturation stages, Cd inhibited or stimulated cell growth, decreased type I collagen, increased MMP13, FGF1 and BMP2 gene expression and stimulated the mineralization process only in continuously exposed cultures. These results suggest that in vivo, acute or chronic exposure to sub-toxic Cd concentrations may affect bone formation differently and support the hypothesis that Cd-induced bone disorders may involve downstream changes in growth factor expression. The results are of interest in forensic and occupational medicine in establishing preventive measures to reduce professional exposure risks.
Article
Objectives: This study was undertaken to investigate copper, zinc, iron, and selenium in a rat model of cadmium toxicity and effects of antioxidant substances such as taurine, melatonin and N-acetylcysteine.Materials and Methods: Ninety male Sprague Dawley rats were divided into nine groups. Group 1 received tap water comprising the controls; the remaining eight groups received 200 µg/ml cadmium chloride (CdCl2) for three months. Group 2 had CdCl2. Groups 3, 4, and 5 were administered taurine, melatonin and N-acetylcystein for three months together with CdCl2. Groups 6, 7, 8, and 9 had CdCl2 for three months and then only water as the second control or antioxidants for seven days. Cadmium, copper, zinc, iron, and selenium levels of heart and brain were measured by atomic absorption spectrophotometer.Results: Cadmium accumulated in significant amounts in brain and heart tissues when compared with controls. CdCl2 levels in Group 1 and Group 2 were 2.56±0.77 and 27.2±5.82 in the heart, 46.16±14.81 and 300.34±58.19 in the brain, respectively (p<0.001). We found that melatonin was more effective in brain tissue (p<0.05) whereas N-acetylcysteine was more effective in heart tissue (p<0.001) against cadmium accumulation.Conclusion: We suggest that taurine, melatonin and N-acetylcysteine have some protective effects in brain and heart tissues against cadmium accumulation. Furthermore, trace element levels were restorated in different degrees after taurine, melatonin and N-acetylcysteine administration.
Article
The effect of different doses of cadmium [CD] on some biochemical, hormonal and histopathological parameters of the liver, kidney and testes of the Wistar rate were investigated. Cadmium in the dose range 0-40 mg/kg while causing a time-and dose-dependent decrease of the basal serum levels of alkaline phosphatase [ALP] also caused a dose-dependent increase in the serum concentration of the acid and prostatic acid phosphatases. The value of the ALP changed from 148.7+/-1.0 IU/L in the control to 53.7+/-0.098 at 40 mg/kg of cadmium. While the ACP and ACPT changed from 32.6+/-0.72 and 7 Units in the control to 54 and 17 units respectively at 40 mg/kg of CD. Furthermore cadmium also caused positively correlated dose-and time-dependent destruction of the histology of the liver, kidney and testes. These were characterized by vascular congestion, vacuolation, destruction of the seminal epithelial layers, focal necrosis of nucleus, oedema of the seminal epithelia layers, focal necrosis of nucleus, oedema of the seminiferous tubules and reduction of spermatogenesis. CD also caused granular and eosinophilic cytoplasm, enlargement of sinusoids with kupffer cells, haemorrhage and apoptosis of cells. Finally pre-treatment with vitamin C [0.0015/kg], vitamin E [1.51/g] and selenium [0.25 mg] which on their own had little or no effects on the serum basal phosphatases, hormonal and histological stability caused a reversal of the cadmium-induced biochemical, hormonal and histological toxicities of the liver, kidney and testes. These results may be explained by the oxidational/antioxidational properties of these xenobiotics and their mechanisms of actions.