Research Items (25)
- Apr 2018
The worldwide consumption of energy drinks (EDs) has increased in recent years. EDs have several side effects and can be linked to liver injury, kidney damage and risk-seeking behavior. The impact of perinatal consumption of EDs on the newborns has not been previously investigated. In this study, we evaluated the effects of perinatal exposure to a caffeinated ED on the liver, kidney, brain, locomotor activity and anxiety in mice newborns. Pregnant mice received 2.5 or 5 ml ED by oral gavage from the first day of pregnancy until day 15 after birth. Perinatal exposure to the ED induced a significant increase in lipid peroxidation and declined antioxidant defenses in the liver, kidney, cerebrum, cerebellum and medulla oblongata of the newborns at days 21 and 35 after birth. ED induced several histological alterations, including vacuolations and lipid infiltration of hepatocytes, developing and degenerated glomeruli and dilated urinary spaces in the renal cortex, pyknosis and chromatolysis of the cerebral and medullary neurons, and degenerated and abnormal Purkinje cells in the cerebellum. In addition, ED increased the locomotion and induced anxiety-like behavior in mice newborns. In conclusion, perinatal exposure to EDs induces oxidative stress, tissue injury and behavioral alterations in the mice newborns. Therefore, the consumption of EDs during pregnancy and lactation has a negative impact on the newborns and should be treated as a significant health problem that warrants attention.
- Jan 2018
Cadmium considers one of non-essential toxic heavy metals which affects biological tissues and produces major pathological disorders. Thus, in this study, metanolic extract of olive leaf was analyzed for antioxidant activity, antifibrotic, and hepatoprotective activity against cadmium toxicity inducing liver cell fibrosis in rats. Male wistar rats were classified into four equal groups of ten rats each; group I (control), group II (Cd-treated), group III (OLE + Cd), group IV (vit E + Cd). Cd, OLE, and vitamin E in a doses of 5.6 mg/kg bw and 300 mg/kg bw for both OLE and vit. E were administrated orally for six weeks. Hepatic, oxidative, and fibrogentic biomarkers as well as cadmium traces were estimated in blood and liver tissues following six weeks of treatments. Also, OLE active constituents were estimated using HPLC and colorimetric assays. Compared to Cd-intoxicated rats, hepatic and oxidative biomarkers; AST, ALT, ALP, bilirubin, albumin, MDA, and TAC were significantly improved following administration of OLE and vitamin E in doses of 300 mg/kg bw. In addition, the expression of HYP as measures of fibrogenesis and collagen synthesis showed significant reduction in OLE and vit E treated rats in comparison with Cd-treated rats. The data of HYP were positively correlated with hepatic biomarkers, fibrosis scores, and negatively with MDA and TAC. The antifibrotic and antioxidant property of OLE were significantly related to its phenolic contents especially oleuropein. Cd induces marked oxidative stress and multiple liver cell damage via initiation of oxidative stress and fibrogensis mechanisms and finally liver cell fibrosis. Treatment strategies with olive leaf extracts or vitamin E significantly reduce free radical oxidative stress damage, fibrogenesis of liver cells and finally may help in reversing liver fibrosis. Thus, Olive as dietary supplements could be a promising anti-fibrotic and hepatoprotective agent especially in the highly Cd-polluted environment. [Al-Basher G. Anti-fibrogentic and hepatoprotective potential of methanolic olive extract on cadmium induced toxicity in rats. Life Sci J 2018;15(7):1-11].
- Mar 2018
Hepatic encephalopathy (HE) is a serious neuropsychiatric complication that occurs as a result of liver failure. Umbelliferone (UMB; 7-hydroxycoumarin) is a natural product with proven hepatoprotective activity; however, nothing has yet been reported on its protective effect against hyperammonemia, the main culprit behind the symptoms of HE. Here, we evaluated the effect of UMB against ammonium chloride (NH4Cl)-induced hyperammonemia, oxidative stress, inflammation and hematological alterations in rats. We demonstrated the modulatory role of UMB on the glutamate-nitric oxide (NO)-cGMP pathways in the cerebrum of rats. Rats received intraperitoneal injections of NH4Cl (3 times/week) for 8 weeks and concomitantly received 50 mg/kg UMB. NH4Cl-induced rats showed significantly elevated blood ammonia and liver function markers. Lipid peroxidation and NO were increased in the liver and cerebrum of rats while the antioxidant defenses were declined. UMB significantly reduced blood ammonia, liver function markers, lipid peroxidation and NO, and enhanced the antioxidant defenses in NH4Cl-induced rats. UMB significantly prevented anemia, leukocytosis, thrombocytopenia and prolongation of PT and aPTT. Hyperammonemic rats showed elevated levels of cerebral TNF-α, IL-1β and glutamine as well as increased activity and expression of Na+/K+-ATPase, effects that were significantly reversed by UMB. In addition, UMB down-regulated nitric oxide synthase and soluble guanylate cyclase in the cerebrum of hyperammonemic rats. In conclusion, this study provides evidence that UMB protects against hyperammonemia via attenuation of oxidative stress and inflammation. UMB prevents hyperammonemia associated hematological alterations and therefore represents a promising protective agent against the deleterious effects of excess ammonia.
Objective: Perinatal nicotine exposure induces malformations and imbalances the prooxidant/antioxidant status. The present study aimed to investigate the possible protective effects of green tea extract against perinatal nicotine-induced alterations in mice newborns. Materials and Methods: Pregnant mice received 0.25 mg k–1 nicotine on gestational day 12 to postnatal day 15. A control group received an equal volume of saline. Both control and nicotine exposed mice received 50 mg k–1 green tea on gestational day 1 to postnatal day 15. Results: Mice born to nicotine-exposed dams showed significantly decreased body weight at days 10, 15 and 20 after birth. Nicotine administration provoked chromatolysis in cerebral neurocytes and oxidative stress, evidenced by elevated lipid peroxidation and declined antioxidants, in newborn mice. Green tea supplementation significantly prevented body weight reduction, histological alterations and oxidative stress. In addition, nicotine significantly increased blood glucose and cholesterol, erythrocytes, leukocytes and platelets, an effect that was significantly reversed following green tea supplementation. Conclusion: Green tea protects against perinatal nicotine-induced oxidative stress and hematologic, histologic and metabolic alterations. Therefore, green tea may be considered a potential candidate for attenuating smoking/nicotine-induced alterations in newborns.
- Apr 2019
Androgenetic alopecia is the most common type of alopecia, and it affects humans of both genders. Finasteride is a type II selective 5α-reductase inhibitor that is administered orally to treat androgenetic alopecia and benign prostatic hyperplasia in human males. However, its effect on the vital organs of females is unknown. This study was designed to investigate the effects of finasteride on the vital organs such as liver, kidney, and heart of female mice. To study the prospective effects of finasteride, female mice were orally administered two doses of finasteride (0.5 and 1.5 mg/kg) once daily for 35 days, and serum levels of various biochemical parameters and histopathology of various organs were examined. The results showed that serum levels of alkaline phosphatase were significantly increased by both high- and low-dose finasteride, whereas cholesterol was significantly increased by the high dose only. Creatine kinase was significantly increased by the high and low doses, whereas glucose was significantly decreased by both doses. Histopathological analysis and DNA damage assays showed that finasteride has adverse effects within both the short and the long periods in female mice. In addition, the proapoptotic genes Bax and caspase-3 were significantly increased by high dose finasteride, whereas the antiapoptotic gene Bcl-2 was significantly decreased by the low and high doses. In conclusion, finasteride is not currently approved for therapeutic use in females, and the findings in this study suggest caution in any future consideration of such use.
Cadmium exposure induces nephrotoxicity by mediating oxidative stress, inflammation, and apoptosis. The purpose of this study was to examine the protective effect of royal jelly on Cd-induced nephrotoxicity. Adult male mice were distributed randomly into 4 clusters: untreated, royal jelly-treated (85 mg/kg, oral), CdCl2-treated (6.5 mg/kg, intraperitoneal), and pretreated with royal jelly (85 mg/kg) 2 h before CdCl2 injection (6.5 mg/kg, intraperitoneal) for seven consecutive days. Cd concentration in the renal tissue and absolute kidney weight of the Cd-treated mice were significantly higher than those of control group. The levels of kidney function markers, kidney injury molecules-1 (KIM-1), metallothionein, lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1β, and the apoptosis regulators Bax and caspases-3 also increased significantly in the renal tissue of Cd-treated mice, whereas the levels of glutathione, antioxidant enzyme activities, and the apoptosis inhibitor Bcl-2 were significantly reduced in the renal tissue of Cd-treated group. Histopathological studies showed vacuolation and congested glomeruli in the kidney tissue of Cd-treated mice. However, all aforementioned Cd-induced changes were attenuated by pretreatment with royal jelly. We therefore concluded that royal jelly attenuated Cd-induced nephrotoxicity and it is suggested that this nephroprotective effect could be linked to its ability to promote the nuclear factor erythroid 2–related factor 2 (Nrf2)/antioxidant responsive element (ARE) pathway.
- Mar 2019
Nephrotoxicity is a common adverse effect of treatment with cisplatin (CDDP). This study was performed to evaluate the antioxidant and nephroprotective efficacy of ceftriaxone (CTX) to vitamin E (Vit.E), alone and in combination against CDDP-induced acute renal injury. Fifty-six male albino rats were equally divided into seven groups, receiving (I) normal saline, (II) CTX (100 mg/kg, intraperitoneal [i.p] injection), (III) Vit.E (100 mg/kg orally), (IV) CDDP (5 mg/kg i.p injection), (V) CDDP plus CTX, (VI) CDDP plus Vit.E, and (VII) CDDP plus CTX in combination with Vit.E. All treatments were administered daily for 10 days except CDDP, which was given as a single dose at the sixth day of the study. Compared to normal control rats, CDDP-injected rats showed significantly (p < 0.05) higher serum levels of renal injury biomarkers (uric acid, urea, and creatinine) and tumor necrosis factor-α (TNF-α), as well as increased renal tissue concentration of malondialdehyde, nitric oxide, and TNF-α. Moreover, CDDP administration was associated with significantly lower (p < 0.05) renal tissue levels of reduced glutathione and activities of endogenous antioxidant enzymes (glutathione peroxidase, superoxide dismutase, and catalase) and total antioxidant capacity. All these alterations were significantly ameliorated in CDDP-injected rats, receiving CTX and/or Vit.E, compared to rats receiving cisplatin alone. Interestingly, the antioxidant and anti-inflammatory effects were more marked in the CTX-Vit.E combination group, compared to groups receiving either drug alone. In conclusion, CTX and Vit.E (especially in combination) could counteract the nephrotoxic effect of CDDP, probably through their antioxidant activities. Key words: Ceftriaxone, Cisplatin, Rats, α-Tocopherol, Vitamin E
- Feb 2019
We sought to elucidate if the perennial lifestyle per se, or lifeform, enhances independence of soil nutrient availability. We measured parameters of CO2 fixation and electron transport, stomatal conductance, P and N nutrition, as well as integrative water relations (δ¹³C abundance) of an overstory tree (Snow Gum; Eucalyptus pauciflora, Sieber ex Spreng.) and a perennial understory shrub (Alpine Shaggy-pea; Podolobium alpestre F. Muell.) at two Australian field sites with different soil nutrient availability, but otherwise similar environmental conditions. Snow Gums are renowned for their longevity, including the ability to re-sprout profusely after fire, while Alpine Shaggy-pea has a relatively short lifespan, and regenerates from seed after fire. Photosynthesis parameters of P. alpestre were more sensitive to soil properties than for E. pauciflora. P and N status of leaves and roots of E. pauciflora were comparable at both sites, whereas P and N status of P. alpestre reflected their availability in the soil. Differences in δ¹³C abundance of the two species studied indicated the use of different water sources at both field sites. These results suggest that long-lived plants with the capability to recycle nutrients from woody tissues, can grow largely independent of soil P and N availability.
The current study examined the efficacy of royal jelly (RJ) against cadmium chloride (CdCl2)-induced testicular dysfunction. A total of 28 Swiss male mice were allocated into four groups (n = 7), and are listed as follows: (1) the control group, who was intraperitoneally injected with physiological saline (0.9% NaCl) for 7 days; (2) the RJ group, who was orally supplemented with RJ (85 mg/kg daily equivalent to 250 mg crude RJ) for 7 days; (3) the CdCl2 group, who was intraperitoneally injected with 6.5 mg/kg for 7 days; and (4) the fourth group, who was supplemented with RJ 1 h before CdCl2 injection for 7 days. Cd-intoxicated mice exhibited a decrease in serum testosterone, luteinizing hormone (LH), and follicle stimulating hormone (FSH) levels. A disturbance in the redox status in the testicular tissue was recorded, as presented by the increase in lipid peroxidation and nitrate/nitrite levels and glutathione (GSH) depletion. Moreover, the activities of glutathione peroxidase (GPx), glutathione reductase (GR), superoxide dismutase (SOD), catalase (CAT), and nuclear factor (erythroid-derived 2)-like-2 factor (Nrf2) and their gene expression were inhibited. In addition, interleukin-1ß (IL-1β) and tumor necrosis factor-α (TNF-α) levels were elevated. Furthermore, Cd triggered an apoptotic cascade via upregulation of caspase-3 and Bax and downregulation of Bcl-2. Histopathological examination showed degenerative changes in spermatogenic cells, detachment of the spermatogenic epithelium from the basement membrane, and vacuolated seminiferous tubules. Decreased cell proliferation was reflected by a decrease in proliferating cell nuclear antigen (PCNA) expression. Interestingly, RJ supplementation markedly minimized the biochemical and molecular histopathological changes in testes tissue in response to Cd exposure. The beneficial effects of RJ could be attributed to its antioxidative properties.
Introduction The communication between a substance and a cell may depend on whether the cell is normal or pathological. The disease cells and drug interaction may occasionally overcome beneficial action of the drug; subsequently, it is important to investigate the effect of the drug in both the normal and target cells. This study aimed to evaluate the methotrexate (MTX) antiproliferative effect and explore the mechanistic approach to investigate the cell death index in SKOV-3 ovarian cells during treatment with MTX. Methods In vitro studies of SKOV-3 cells were examined by tetrazolium assay after exposure to various concentrations of MTX. Moreover, reactive oxygen species (ROS) generation, mitochondrial membrane potential, DNA damage, and AO/EtBr staining morphological analysis of necrotic/apoptotic cells were detected; cellular impairment in mitochondria and DNA was confirmed by JC-1 mitotracker/DAPI, respectively, and cell death pathway markers; bax/bcl-2 were analyzed. Results A dose-dependent antiproliferative effect of MTX treatment was observed in SKOV-3 cells; the prominent inhibitory concentration was 40 µM of MTX (P<0.01). The growth inhibition rates of the cancer cells reached 24.07% in MTX. The MTX showed increase in ROS generation and mitochondrial depolarization, and DNA integrity cells collectively advocated the apoptotic cell death at higher concentration. In addition, the results of reverse transcription polymerase chain reaction also supported the apoptosis by upregulating the bax and downregulating the bcl-2 (P<0.01). Thus the MTX moderately provokes apoptosis. Conclusion Our findings suggest that MTX acts on SKOV-3 cancer cells by increasing intracellular ROS levels, leading to DNA damage and altering the MMP along with apoptotic gene upregulation. This mechanism may provide new therapeutic targets to improve tumor treatment.
- Nov 2018
This study aimed to evaluate the potential neuroprotective effect of royal jelly (RJ) against Cd-induced neuronal damage. Twenty-eight adult mice were placed equally into four groups. The control group received intraperitoneal (IP) injections of normal saline; the cadmium chloride (CdCl2) group was IP-injected 6.5 mg/kg (mg per kg of bodyweight) CdCl2; the RJ group was gavaged 85 mg/kg RJ; and the RJ + CdCl2 group was orally administered 85 mg/kg RJ 2 h before receiving IP-injections of 6.5 mg/kg CdCl2. All groups were treated for seven consecutive days and the mice were decapitated 24 h after the final dose. Cd accumulation was recorded in the cortical homogenates, accompanied by elevated levels of lipid peroxidation, nitric oxide, tumor necrosis factor-α, interleukin-1β, and the pro-apoptotic mRNA Bax and caspase-3. Meanwhile, significantly decreased levels of detoxifying antioxidant enzymes including GSH-Px, GSH-R, SOD, and CAT, anti-apoptotic mRNA Bcl-2, and monoamines such as norepinephrine, dopamine, and serotonin were also observed, along with reduced gene expression of Nrf2-dependent antioxidants. Interestingly, in mice pretreated with RJ, the assessed parameters remained near normal levels. Our data provide evidence that RJ treatment has the potential to protect cortical neurons in Cd-intoxicated mice via its antioxidant, anti-inflammatory, anti-apoptotic, and neuromodulatory activity.
Background and Objective: Impaired wound healing was seriously associated with diabetes. More complications such as microbial infections, delay in fibrogenesis is process and collagen deposition were shown to be linked with hyperglycemia. In this study, an aqueous extract of olive leaf was analyzed for antioxidant activity, wound healing property and then its effect on the activity and expression of tTG was tested in vivo by applying on the wounds of rats with streptozotocin (STZ)-induced diabetes. Methodology: Fifty healthy male wistar rats were treated intravenously with STZ (55 mg kgG¹ body weight) to induce diabetes. To evaluate wound healing activity of olive leaf extracts, animals with diabetic wounds were treated topically twice daily with ointments of olive extracts at doses of 2 and 5% (w/w). Wound closer, epithelialization, hydroxyproline (HPX), tissue transglutaminase (tTG) and total antioxidant capacity (TAC) were estimated as parameters of wound healing capacity of olive extracts in diabetic treated and non-treated rats. Also, in vitro phytochemical screening analyses were performed to estimate active constituents present in OLE. Results: In diabetic group, wound healing time was found to be (18.8±0.61) and (16.8±1.3) in OLE wound treated rats at a doses of 2 and 5% compared to non-treated (27.9±0.96) and standard drug (21.5±0.6) respectively. Wound contraction, scar formation and epithelialization processes positively correlated with the increase in the levels of HPX, tTG as markers of collagen deposition and TAC activity and negatively with diabetes (HbA1c)in treated wound tissues. Due to antioxidant and anti-diabetic activity of OLE constituents, particularly oleuropein, collagen deposition and accelerated epithelialization processes were estimated in diabetic wound healing. Conclusion: Finally, the data showed that OLE as ointment in doses of 2 and 5% efficiently accelerates wound healing process via promoting antioxidant capacity, expression of both HPX and tTG, which are essential for collagen deposition and re-epithelialization process. These findings suggested that methanolic extract olive leaf enriched with of oleuropein could be a suitable therapeutic agent for diabetic wound healing.
- Jul 2018
Exposure to heavy metal-containing dust arising from stone quarrying may cause severe health problems. The aim of this study was to evaluate the impact of stone quarrying in Riyadh (Saudi Arabia) on the Libyan jird Meriones libycus. Soil samples and jirds were collected from four sites located at different distances from the quarrying area. Soil from the first (500 m away from the quarry) and second (1800 m away) sites showed a significant increase in cadmium (Cd), lead (Pb), nickel (Ni), and vanadium (V) when compared with the reference site (38,000 m away). Jirds at these sites exhibited significant increases in liver, kidney, lung, and fur levels of Cd, Pb, Ni, and V. Serum transaminases, creatinine, and malondialdehyde (MDA) levels were significantly increased in jirds, whereas reduced glutathione (GSH) levels decreased. Liver, kidney, and lung tissues of jirds, collected from the first and second sites, showed significantly increased MDA and decreased GSH levels. Additionally, animals at both sites showed altered hematological parameters and several histopathological changes in their liver, kidney, and lung. Soil and animals at the third site (7300 m away) showed no significant changes. Thus, our study showed the impact and hazardous effects of quarrying on the liver, kidney, lung, and hemogram of M. libycus. These findings can provide scientific evaluation for studying the impact of quarrying on the workers and communities living close to the studied area.
- May 2018
Hepatic encephalopathy (HE) is a serious neuropsychiatric complication that occurs as a result of liver failure. Umbelliferone (UMB; 7-hydroxycoumarin) is a natural product with proven hepatoprotective activity; however, nothing has yet been reported on its protective effect against hyperammonemia, the main culprit behind the symptoms of HE. Here, we evaluated the effect of UMB against ammonium chloride (NH 4 Cl)-induced hyperam-monemia, oxidative stress, inflammation and hematological alterations in rats. We demonstrated the modulatory role of UMB on the glutamate-nitric oxide (NO)-cGMP pathways in the cerebrum of rats. Rats received intraperi-toneal injections of NH 4 Cl (3 times/week) for 8 weeks and concomitantly received 50 mg/kg UMB. NH 4 Cl-induced rats showed significantly elevated blood ammonia and liver function markers. Lipid peroxidation and NO were increased in the liver and cerebrum of rats while the antioxidant defenses were declined. UMB significantly reduced blood ammonia, liver function markers, lipid peroxidation and NO, and enhanced the antioxidant defenses in NH 4 Cl-induced rats. UMB significantly prevented anemia, leukocytosis, thrombocytopenia and prolon-gation of PT and aPTT. Hyperammonemic rats showed elevated levels of cerebral TNF-α, IL-1β and glutamine as well as increased activity and expression of Na + /K +-ATPase, effects that were significantly reversed by UMB. In addition, UMB down-regulated nitric oxide synthase and soluble guanylate cyclase in the cerebrum of hyper-ammonemic rats. In conclusion, this study provides evidence that UMB protects against hyperammonemia via attenuation of oxidative stress and inflammation. UMB prevents hyperammonemia associated hematological alterations and therefore represents a promising protective agent against the deleterious effects of excess ammonia.
- Aug 2017
Iron overload toxicity was shown to associate with chronic liver diseases which lead to hepatic fibrosis and subsequently the progression to cancer through oxidative stress and apoptotic pathways. Green tea potential activity as chelating, anti-oxidative, or anti-apoptotic mechanisms against metal toxicity was poorly clarified. Here, we are trying to evaluate the anti-oxidant and anti-apoptotic properties of green tea in the regulation of serum hepcidin levels, reduction in iron overloads, and improve of liver fibrosis in iron overloaded experimental rats. Three groups of male adult rats were randomly classified into three groups and treated as follows: control rats, iron treated rats for two months in drinking water followed by either vehicle or green tea extract (AGTE; 100 mg/kg) treatment for 2 more months. Thereafter, we studied the effects of AGTE on iron overload-induced lipid peroxidation, anti-oxidant depletion, liver cell injury and apoptosis. Treatment of iron-overloaded rats with AGTE resulted in marked decreases in iron accumulation within liver, depletion in serum ferritin, and hepcidin levels. Iron-overloaded rats had significant increase in malonyldialdehyde (MDA), a marker of lipid peroxidation and nitric oxide (NO) in liver when compared to control group. Also, significant change in cytochrome c and DNA content as apoptotic markers were reported in iron treated rats. The effects of iron overload on lipid peroxidation, NO levels, cytochrome c and DNA content were significantly reduced by the intervention treatment with AGTE (P
Hyperammonemia is a serious complication of liver disease and may lead to encephalopathy and death. This study investigated the effects of Commiphora molmol resin on oxidative stress, inflammation, and hematological alterations in ammonium chloride- (NH 4 Cl-) induced hyperammonemic rats, with an emphasis on the glutamate-NO-cGMP and Nrf2/ARE/HO-1 signaling pathways. Rats received NH 4 Cl and C. molmol for 8 weeks. NH 4 Cl-induced rats showed significant increase in blood ammonia, liver function markers, and tumor necrosis factor-alpha (TNF- α ). Concurrent supplementation of C. molmol significantly decreased circulating ammonia, liver function markers, and TNF- α in hyperammonemic rats. C. molmol suppressed lipid peroxidation and nitric oxide and enhanced the antioxidant defenses in the liver, kidney, and cerebrum of hyperammonemic rats. C. molmol significantly upregulated Nrf2 and HO-1 and decreased glutamine and nitric oxide synthase, soluble guanylate cyclase, and Na ⁺ /K ⁺ -ATPase expression in the cerebrum of NH 4 Cl-induced hyperammonemic rats. Hyperammonemia was also associated with hematological and coagulation system alterations. These alterations were reversed by C. molmol . Our findings demonstrated that C. molmol attenuates ammonia-induced liver injury, oxidative stress, inflammation, and hematological alterations. This study points to the modulatory effect of C. molmol on glutamate-NO-cGMP and Nrf2/ARE/HO-1 pathways in hyperammonemia. Therefore, C. molmol might be a promising protective agent against hyperammonemia.
Nicotine exposure during pregnancy induces oxidative stress and leads to behavioral alterations in early childhood and young adulthood. The current study aimed to investigate the possible protective effects of green tea (Camellia sinensis) against perinatal nicotine-induced behavioral alterations and oxidative stress in mice newborns. Pregnant mice received 50 mg/kg C. sinensis on gestational day 1 (PD1) to postnatal day 15 (D15) and were subcutaneously injected with 0.25 mg/kg nicotine from PD12 to D15. Nicotine-exposed newborns showed significant delay in eye opening and hair appearance, and declined body weight at birth and at D21. Nicotine induced neuromotor alterations in both male and female newborns evidenced by the suppressed righting, rotating and cliff avoidance reflexes. Nicotine-exposed newborns exhibited declined memory, learning and equilibrium capabilities, as well as marked anxiety behavior. C. sinensis significantly improved the physical development, neuromotor maturation and behavioral performance in nicotine-exposed male and female newborns. In addition, C. sinensis prevented nicotine-induced tissue injury and lipid peroxidation, and enhanced antioxidant defenses in the cerebellum and medulla oblongata of male and female newborns. In conclusion, this study shows that C. sinensis confers protective effects against perinatal nicotine-induced neurobehavioral alterations, tissue injury and oxidative stress in mice newborns.
- Nov 2016
Background: Vitamin D levels play a pivotal role in most biological processes and differ according to age. A deficiency of vitamin D in chronic hepatitis C (CHC) patients has been shown to be linked with the severity of liver fibrosis, but little is known about the mechanism of this association. Objective: In this study, we evaluate the potential interrelation between vitamin D levels, oxidative stress, and apoptosis, based on liver fibrosis in geriatric patients infected with hepatitis C virus (HCV) genotype 4. Subjects and methods: A total of 120 adult individuals aged 30–68 years were recruited in this study. Of these, 20 healthy subjects (15 men and five women) with a mean age of 48.3±6.1 years were selected as controls, and 100 patients with a mean age of 47.8±4.9 years with chronic HCV (CHC) who had undergone liver biopsy (80 men and 20 women) were included in this study. Based on liver radiographic (computed tomography, magnetic resonance imaging) and histological Metavir system analyses, the CHC patients were classified into three groups: asymptomatic CHC carriers (n=30), fibrosis (n=25), and cirrhosis (n=45). HCV RNA, HCV genotypes, inflammatory cytokines AFP and TNFα, 25-hydroxyvitamin D (25[OH]D) levels, apoptotic markers single-stranded DNA (ssDNA) and soluble Fas (sFas), and oxidative stress markers nitric oxide (NO) and total antioxidant capacity (TAC) were estimated by using molecular, immunoassay, and colorimetric techniques. Results: Approximately 30% of the study population (n=30) were diagnosed as asymptomatic CHC carriers, and 70% of the study population (n=70) had severe fibrosis; these were classified into fibrosis and cirrhosis. There was a significant reduction in 25(OH)D levels and TAC activity, along with an increase in levels of NO, AFP, TNFα, ssDNA, and sFas in fibrosis and cirrhosis subjects compared with those of asymptomatic CHC carriers and health controls. The deficiency in 25(OH)D levels correlated positively with sFas, ssDNA, AFP, TNFα, NO, and TAC, and negatively with age, sex, liver function, body mass index, homeostatic model assessment – insulin resistance, HCV RNA, and viral load. Significant intercorrelation was reported between serum 25(OH)D concentrations and apoptotic and oxidative markers, which suggested progression of liver pathogenesis and fibrogenesis via oxidative and apoptotic mechanisms. Conclusion: The data showed that vitamin D status was significantly correlated with pathogenesis and fibrogenesis of the liver in geriatric patients infected with HCV genotype 4. The deficiency in 25(OH)D levels was shown to have a pivotal role in the pathogenesis of liver via apoptotic, oxidative stress, and inflammatory mechanistic pathways. The data point to adequate vitamin D levels being recommended for a good response to treatment strategies, especially in older CHC patients. Keywords: 25(OH)D, HCV, apoptosis, Fas an
- Apr 2016
Abstract Background: Parsley was employed as an experimental probe to prevent the behavioral, biochemical and morphological changes in the brain tissue of the albino mice following chronic cadmium (Cd) administration. Methods: Non-anesthetized adult male mice were given parsley juice (Petroselinum crispum, Apiaceae) daily by gastric intubation at doses of 10 and 20 g/kg/day. The animals were divided into six groups: Group A, mice were exposed to saline; Groups B and C, were given low and high doses of parsley juice, respectively; Group D, mice were exposed to Cd; Groups E and F, were exposed to Cd and concomitantly given low and high doses of parsley, respectively. Results: Cd intoxication can cause behavioral abnormalities, biochemical and histopathological disturbances in treated mice. Parsley juice has significantly improved the Cd-associated behavioral changes, reduced the elevation of lipid peroxidation and normalized the Cd effect on reduced glutathione and peroxidase activities in the brain of treated mice. Histological data have supported these foundations whereas Cd treatment has induced neuronal degeneration, chromatolysis and pyknosis in the cerebrum, cerebellum and medulla oblongata. Conclusion: The low dose (5 g/kg/day) of parsley exhibited beneficial effects in reducing the deleterious changes associated with Cd treatment on the behavior, neurotransmitters level, oxidative stress and brain neurons of the Cdtreated mice. Keywords: Heavy metal, Cerebellum, Cerebrum, Medulla oblongata, Neurotransmitter
Parsley was employed as an experimental probe to prevent the behavioral, biochemical and morphological changes in the brain tissue of the albino mice following chronic cadmium (Cd) administration. Non-anesthetized adult male mice were given parsley juice (Petroselinum crispum, Apiaceae) daily by gastric intubation at doses of 10 and 20 g/kg/day. The animals were divided into six groups: Group A, mice were exposed to saline; Groups B and C, were given low and high doses of parsley juice, respectively; Group D, mice were exposed to Cd; Groups E and F, were exposed to Cd and concomitantly given low and high doses of parsley, respectively. Cd intoxication can cause behavioral abnormalities, biochemical and histopathological disturbances in treated mice. Parsley juice has significantly improved the Cd-associated behavioral changes, reduced the elevation of lipid peroxidation and normalized the Cd effect on reduced glutathione and peroxidase activities in the brain of treated mice. Histological data have supported these foundations whereas Cd treatment has induced neuronal degeneration, chromatolysis and pyknosis in the cerebrum, cerebellum and medulla oblongata. The low dose (5 g/kg/day) of parsley exhibited beneficial effects in reducing the deleterious changes associated with Cd treatment on the behavior, neurotransmitters level, oxidative stress and brain neurons of the Cd-treated mice.
Selenium is an essential element with a narrow margin between beneficial and toxic effects. The learning and sensory motor reflexes-changes were studied after the perinatal exposure of mice to acute toxic doses of sodium selenite. Atomic absorption as well as the behavioral observations were employed. Adult pregnant mice was assigned into three groups: the first group was remained as a control group; the second and the third groups were orally administrated sodium selenite at doses of 1 mg/Kg (1 ppm) and 4 mg/kg (4 ppm) of the diet, respectively started from the 7th day of gestation to the 15th day of birth. Results revealed that body weight gain came significantly lower in pups born to treated mothers than those of the control pups. The appearance of body hair and opening of eyes of the pups from treated mothers were delayed in a dose-dependent manner. Selenite also inhibited the sensory motor reflexes in all elements in a dose dependent manner. The active avoidance test indicated that selenite exposure was associated with learning impairment. Acetylcholine recorded a significant decrease in treated pups. Significant high concentrations of selenium in the brain, liver and kidney was detected, indicating active transfer of selenium from mothers during pregnancy and lactation periods.
Selenium is an essential element with a narrow margin between beneficial and toxic effects. This study was aimed to determine the neurobehavioral changes resulted from the prenatal exposure of mice to high doses of sodium selenite during fetal and early postnatal development. Atomic absorption for monitoring the placental transfer of selenium to offspring was employed. The developmental observations as well as the behavioral tests, such as sensory motor reflexes, and learning and memory test in automatic reflex conditioner (shuttle box) (active avoidance responses) were applied. Adult mice was assigned into three groups: the first group was remained as a control group given phosphate buffered saline; the second and the third groups were orally administrated sodium selenite at doses of 1 mg/kg and 4 mg/kg of the diet, respectively started from the 7th day to the end of the gestation period. Appearance of body hair and opening of eyes of the pups from treated mothers were delayed in a dose-dependent manner. The body weight gain came significantly lower than those of the control especially at the higher dose. Selenite also inhibited the sensory motor reflexes in all elements of acts and postures in a dose dependent manner. The active avoidance training-test indicated that selenite exposure was associated with learning impairment. Acetylcholine recorded a significant decrease in almost all the period of this study. By using atomic absorption, we found a significant high concentration of selenium in the brain, liver and kidney until the 40th postnatal day, indicating active transfer of selenium from mothers to embryos. Key wordsselenium–atomic absorption–acetylcholine–learning–sensory motor reflexes