Mokhtar I Yousef

Alexandria University, Al Iskandarīyah, Alexandria, Egypt

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Publications (68)146.92 Total impact

  • Hasan Turkez, Fatime Geyikoglu, Mokhtar I Yousef
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    ABSTRACT: The 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant toxicant that mediates carcinogenic effects associated with oxidative DNA damage. Docosahexaenoic acid (DHA) with antioxidant functions has many biochemical, cellular, and physiological functions for cells. The present study assessed, for the first time, the ameliorative effect of DHA in alleviating the toxicity of TCDD on primary cultured rat hepatocytes (HEPs). In vitro, isolated HEPs were incubated with TCDD (5 and 10 μM) in the presence and absence of DHA (5, 10, and 20 μM) for 48 h. The cell viability was detected by 3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay and lactate dehydrogenase (LDH) release. DNA damage was analyzed by liver micronucleus assay and 8-oxo-2-deoxyguanosine (8-OH-dG) level. In addition, total antioxidant capacity (TAC) and total oxidative stress (TOS) were assessed to determine the oxidative injury in HEPs. The results of MTT and LDH assays showed that TCDD decreased cell viability but not DHA. On the basis of increasing treatment concentrations, the dioxin caused significant increases of micronucleated HEPs and 8-OH-dG as compared to control culture. TCDD also led to significant increases in TOS content. On the contrary, in cultures treated with DHA, the level of TAC was significantly increased during treatment in a concentration-dependent fashion. DHA showed therapeutic potential against TCDD-mediated cell viability and DNA damages. As conclusion, this study provides the first evidence that DHA has protective effects against TCDD toxicity on primary cultured rat hepatocytes.
    Toxicology and Industrial Health 09/2014; · 1.56 Impact Factor
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    ABSTRACT: The present study was designed to investigate genotoxic and cytotoxic effects and oxidative damage of increasing concentrations of nano-hydroxyapatite (5, 10, 20, 50, 75, 100, 150, 300, 500 and 1000 ppm) in primary human blood cell cultures. Cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay and lactate dehydrogenase release, while total antioxidant capacity and total oxidative stress levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by sister chromatid exchange, micronuclei, chromosome aberration assays and 8-oxo-2-deoxyguanosine level as indicators of genotoxicity. The results of [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] and lactate dehydrogenase assays showed that the higher concentrations (150, 300, 500 and 1000 ppm) of hydroxyapatite nanoparticles (HAP NPs) decreased cell viability. HAP NPs led to increases of total oxidative stress (300, 500 and 1000 ppm) levels and decreased total antioxidant capacity (150, 300, 500 and 1000 ppm) levels in cultured human blood cells. On the basis of increasing concentrations, HAP NPs caused significant increases of sister chromatid exchange, micronuclei, chromosome aberration rates and 8-oxo-2-deoxyguanosine levels as compared to untreated culture. In conclusion, the obtained in vitro results showed that HAP NPs had dose-dependent effects on inducing oxidative damage, genotoxicity and cytotoxicity in human blood cells. Copyright © 2013 John Wiley & Sons, Ltd.
    Journal of Applied Toxicology 04/2014; 34(4):373-9. · 2.60 Impact Factor
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    ABSTRACT: Objectives The objective of this research was to assess ability of biodegradable implantable 5-Fluorouracil dosage forms, to maximize the regional exposure of the drug while limiting its systemic toxicity in rats with induced liver cancer. Methods Liver cancer was successfully induced in male Wistar rats using a selected protocol followed by surgical implantation of prepared 5-FU biodegradable implant. Rats were sacrificed at selected time intervals and the pooled blood was used to perform the different tests and the implant was retrieved, and analyzed to calculate the amount of drug left in the implant. The amount of 5-FU in blood was quantified using high pressure liquid chromatography (HPLC). Gross examination of rat liver, calculation of liver to body weight percentage, and complete blood picture analysis were also performed. Liver biopsies were examined to assess signs of liver necrosis. Results Localized necrotic areas were noted in rat liver biopsies after 5 days with a perimeter of 0.3 to 0.6 cm around the implants indicating the localized 5-FU therapeutic effect. Sustained drug release was detected in rats for about 2 months and the amount of 5-FU released from the implant into the systemic circulation was found to represent less than 13%. Conclusion PLA coated injection molded implants loaded with 5-FU could present a promising dosage form for liver cancer treatment.
    Journal of Taibah University Medical Sciences. 01/2013;
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    ABSTRACT: The purpose of this study was to evaluate the effect of carotenoid astaxanthin (ASTA) on cultured primary rat hepatocytes treated with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the cell viability (3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide, MTT), lactate dehydrogenase (LDH) activity, 8-oxo-2-deoxyguanosine (8-OH-dG), total antioxidant capacity (TAC), and total oxidative stress (TOS) levels, and liver micronucleus rates. ASTA (2.5, 5, and 10 µM) was added to cultures alone or simultaneously with TCDD (5 and 10 µM) for 48 h. The results of MTT and LDH assays showed that both doses of TCDD caused significant decrease in cell viability. Also, TCDD significantly increased TOS and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the dioxin caused significant increase in micronucleated hepatocytes) and 8-OH-dG level as compared to control culture. The presence of ASTA with TCDD minimized its effects on primary hepatocytes cultures and DNA damages.
    Toxicology and Industrial Health 07/2012; · 1.56 Impact Factor
  • Heba M Abdou, Hend M Hussien, Mokhtar I Yousef
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    ABSTRACT: The involvement of reactive oxygen species (ROS) has been implicated in the toxicity of various pesticides. Our study was designed to investigate the induction of oxidative stress by cypermethrin; a Type II pyrethroid in rat liver and kidney. In addition, the protective role of sesame oil against the toxicity of cypermethrin was investigated. Animals were divided into four equal groups; the first group used as control while groups 2, 3 and 4 were treated with sesame oil (5 mL/kg b.w), cypermethrin (12 mg/kg b.w) and the combination of both sesame oil (5 mL/kg b.w) plus cypermethrin (12 mg/kg b.w), respectively. Rats were daily administered with their respective doses for 30 days by gavage. Repeated oral administration of cypermethrin was found to reduce the level of glutathione (GSH) and the activities of the antioxidant enzymes. While, the level of TBARS was elevated indicating the presence of oxidative stress. The activities of LDH, AST and ALT were decreased in the liver extract while increased in the plasma of the cypermethrin-treated group. Also, the levels of urea and creatinine were significantly increased after treatment with cypermethrin. Liver and kidney injury was confirmed by the histological changes. In conclusion, the administration of sesame oil provided significant protection against cypermethrin-induced oxidative stress, biochemical changes, histopathological damage and genomic DNA fragmentation.
    Journal of Environmental Science and Health Part B Pesticides Food Contaminants and Agricultural Wastes 04/2012; 47(4):306-14. · 1.10 Impact Factor
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    ABSTRACT: The most potent of the dioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is a persistent and ubiquitous environmental contaminant. And the health impact of exposure to TCDD is of great concern to the general public. Recent data indicate that L: -glutamine (Gln) has antioxidant properties and may influence hepatotoxicity. The objective of the present study was undertaken to explore the effectiveness of Gln in alleviating the hepatotoxicity of TCDD on primary cultured rat hepatocytes. Gln (0.5, 1 and 2 mM) was added to cultures alone or simultaneously with TCDD (0.005 and 0.01 mM). The hepatocytes were treated with TCDD and Gln for 48 h. Then cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC), total glutathione (TGSH) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (MN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD decreased cell viability but not L: -glutamine. TCDD also increased TOS level in rat hepatocytes and significantly decreased TAC and TGSH levels. On the basis of increasing doses, the dioxin in a dose-dependent manner caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG as compared to control culture. Whereas, in cultures exposured with Gln alone, TOS levels were not changed and TAC and TGSH together were significantly increased in dose-dependent fashion. The presence of Gln with TCDD modulated the hepatotoxic effects of TCDD on primary hepatocytes cultures. Noteworthy, Gln has a protective effect against TCDD-mediated DNA damages. As conclusion, we reported here an increased potential therapeutic significance of L: -glutamine in TCDD-mediated hepatic injury for the first time.
    Cytotechnology 03/2012; · 1.32 Impact Factor
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    ABSTRACT: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) induces hepatic damage. Propolis exhibits antioxidant properties and several studies suggest that supplementations with antioxidants can influence hepatotoxicity. Therefore, the aim of the current study was to explore the effectiveness of propolis in alleviating the toxicity of TCDD in the liver of rats. Animals were divided into six groups, namely, TCDD (0.75 and 8 µg/kg body weight (bw)), propolis (50 mg/kg bw), TCDD (0.75 and 8 µg) plus propolis (50 mg/kg bw), and control, respectively. Rats were intraperitoneally administered with their respective doses daily for 21 days. In rats that received a high dose of TCDD, the antioxidant enzymes were significantly decreased and the serious pathological findings were established. Also, the rate of hepatocyte micronucleus (HMN) was increased after treating with TCDD. The reactions of enzymes in control and low-dose group were weak. The frequencies of HMN and liver histology were similar to both the groups. The presence of propolis with TCDD alleviated its pathological effects in hepatic tissue. Propolis also prevented the suppression of antioxidant enzymes in the livers of animals exposed to TCDD and displayed a strong protective effect against HMN. It can be concluded that propolis has beneficial influences and was able to antagonize TCDD toxicity in the liver.
    Toxicology and Industrial Health 03/2012; · 1.56 Impact Factor
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    ABSTRACT: Xenobiotics such as insecticides are metabolized to more or less toxic metabolites by drug-metabolizing enzymes including cytochrome P450 (Cyp P450), cytochrome b5 (Cyp b5), NADPH-cytochrome c reductase (Cyt.c R), N-nitrosdimethylamine-N-demethylase I (NDMA-dI), glutathione (GSH), glutathione s-transferase (GST), and glutathione reductase (GR). Therefore, the present study showed the influence of oral administration of cypermethrin (6 and 12 mg/kg/day) and dimethoate (1.6 and 3.2 mg/kg/day) for 63 consecutive days on the activities of the above mentioned enzymes in the livers of male sheep. Low and high-treatments of sheep with cypermethrin significantly increased the levels of Cyp P450 by 56% and 98%, Cyp b5 by 65% and 80%, GSH by 68% and 74%, and Cyt.c R by 67% and 98%, respectively in a dose-dependent manner. However, low dose of cypermethrin increased the activities of GST and GR by 56% and 91% respectively. In addition, low and high dose-treatments with dimethoate increased the hepatic contents of Cyp P450 by 27% and 40%, GSH by 259% and 132%, whereas NDMA-dI decreased by 27 and 55% respectively, and no change in the content of Cyp b5 and the activity of Cyt.c-R at any given dose of this compound. It is concluded that exposure to cypermethrin and dimethoate significantly changed the hepatic activity of phases I & II drugmetabolizing enzymes in sheep, and these changes are mainly dependent on the administred dose, and also on the type of the tested insecticides. Also, such changes should be considered when therapeutic drugs administered to people exposed to such insecticides.
    Drug metabolism letters. 02/2012; 6(1):2-6.
  • Hasan Turkez, Fatime Geyikoglu, Mokhtar I Yousef
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    ABSTRACT: Exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) represents a potential health risk and hepatotoxicity. Astaxanthin (ASTA) exhibits antioxidant properties and can influence hepatotoxicity. Therefore, the present study was carried out for using ASTA against hepatotoxicity induced by TCDD in the liver of rats. Animals were treated intraperitoneally daily with TCDD (8 µg/kg body weight (b.w.)), ASTA (12.5 mg/kg b.w. and 25 mg/kg b.w.) and TCDD plus ASTA (12.5 and 25 mg/kg b.w.) for 21 days. TCDD significantly decreased the activities of antioxidant enzymes and resulted in serious pathological findings. Moreover, the rate of micronucleus (MN) in hepatocytes increased after treating with TCDD. The activities of enzymes, frequencies of MNs and liver histology in lower dosage group of ASTA remained unchanged compared with the control group. In rats treated with ASTA, at higher dosage alone, the MNs remained unchanged and the activities of antioxidant enzymes significantly increased. The presence of ASTA (except for lower dose) with TCDD alleviated its pathological effects in hepatic tissue. ASTA also prevented the suppression of antioxidant enzymes in the livers of animals exposed to TCDD and displayed a strong protective effect against MNs. Thus, the present findings might provide new insight into the development of therapeutic and preventive approaches of TCDD toxicity.
    Toxicology and Industrial Health 02/2012; · 1.56 Impact Factor
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    ABSTRACT: Xenobiotics such as insecticides are metabolized to more or less toxic metabolites by drug-metabolizing enzymes including cytochrome P450 (Cyp P450), cytochrome b5 (Cyp b5), NADPH-cytochrome c reductase (Cyt.c R), N-nitrosdimethylamine-N-demethylase I (NDMA-dI), glutathione (GSH), glutathione s-transferase (GST), and glutathione reductase (GR). Therefore, the present study showed the influence of oral administration of cypermethrin (6 and 12 mg/kg/day) and dimethoate (1.6 and 3.2 mg/kg/day) for 63 consecutive days on the activities of the above mentioned enzymes in the livers of male sheep. Low and high-treatments of sheep with cypermethrin significantly increased the levels of Cyp P450 by 56% and 98%, Cyp b5 by 65% and 80%, GSH by 68% and 74%, and Cyt.c R by 67% and 98%, respectively in a dose-dependent manner. However, low dose of cypermethrin increased the activities of GST and GR by 56% and 91% respectively. In addition, low and high dose-treatments with dimethoate increased the hepatic contents of Cyp P450 by 27% and 40%, GSH by 259% and 132%, whereas NDMA-dI decreased by 27 and 55% respectively, and no change in the content of Cyp b5 and the activity of Cyt.c-R at any given dose of this compound. It is concluded that exposure to cypermethrin and dimethoate significantly changed the hepatic activity of phases I & II drug-metabolizing enzymes in sheep, and these changes are mainly dependent on the administred dose, and also on the type of the tested insecticides. Also, such changes should be considered when therapeutic drugs administered to people exposed to such insecticides
    Drug Metab Lett. 02/2012;
  • Drug Metabolism Letters 02/2012;
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    [Show abstract] [Hide abstract]
    ABSTRACT: Abstract: Xenobiotics such as insecticides are metabolized to more or less toxic metabolites by drug-metabolizing enzymes including cytochrome P450 (Cyp P450), cytochrome b5 (Cyp b5), NADPH-cytochrome c reductase (Cyt.c R), N-nitrosdimethylamine-N-demethylase I (NDMA-dI), glutathione (GSH), glutathione s-transferase (GST), and glutathione reductase (GR). Therefore, the present study showed the influence of oral administration of cypermethrin (6 and 12 mg/kg/day) and dimethoate (1.6 and 3.2 mg/kg/day) for 63 consecutive days on the activities of the above mentioned enzymes in the livers of male sheep. Low and high-treatments of sheep with cypermethrin significantly increased the levels of Cyp P450 by 56% and 98%, Cyp b5 by 65% and 80%, GSH by 68% and 74%, and Cyt.c R by 67% and 98%, respectively in a dose-dependent manner. However, low dose of cypermethrin increased the activities of GST and GR by 56% and 91% respectively. In addition, low and high dose-treatments with dimethoate increased the hepatic contents of Cyp P450 by 27% and 40%, GSH by 259% and 132%, whereas NDMA-dI decreased by 27 and 55% respectively, and no change in the content of Cyp b5 and the activity of Cyt.c-R at any given dose of this compound. It is concluded that exposure to cypermethrin and dimethoate significantly changed the hepatic activity of phases I & II drug- metabolizing enzymes in sheep, and these changes are mainly dependent on the administred dose, and also on the type of the tested insecticides. Also, such changes should be considered when therapeutic drugs administered to people exposed to such insecticides.
    Drug Metabolism Letters 01/2012; 6(6):2-6.
  • Hend M Hussien, Heba M Abdou, Mokhtar I Yousef
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    ABSTRACT: The protective effect of sesame oil against cypermethrin-induced brain toxicity was studied. Female rats were orally treated with cypermethrin, sesame oil and their combination for 30 consecutive days. The results showed that cypermethrin increased thiobarbituric acid-reactive substances (TBARS), and decreased glutathione (GSH) and the activities of the antioxidant enzymes. Brain injury was confirmed by histopathological changes and DNA damage. Also, the reduction in the activities of acetylcholinesterase and monoamine oxidase (AChE & MAO), total protein, albumin and body weight, and the induction in triacylglycerol and cholesterol have been observed due to cypermethrin toxicity. Animals treated with sesame oil and cypermethrin together showed that brain TBARS and plasma triacylglycerol and cholesterol returned to the control level which indicating a protective effect of sesame oil. Also, sesame oil was able to attenuate the decrease in total protein, albumin, triacylglycerol and cholesterol, GSH, AChE and antioxidant enzymes induced by cypermethrin. In addition, sesame oil protected the brain histological changes and fragmentation of genomic DNA in animals treated with cypermethrin. The present results showed a protective effect of sesame oil against the cypermethrin induced brain toxicity and this could be associated mainly with the attenuation of the oxidative stress and the preservation in antioxidant enzymes.
    Brain research bulletin 11/2011; · 2.18 Impact Factor
  • Hasan Türkez, Fatime Geyikoglu, Mokhtar I Yousef
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    ABSTRACT: The aim of this study was to explore the effectiveness of L-glutamine (Gln) in alleviating the toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in liver of rats. Rats were intraperitoneally administered Gln and TCDD doses daily for 21 days. In the liver of rats, the biochemical tests, pathological examination and micronucleus (MN) test were performed. TCDD significantly decreased the activities of antioxidant enzymes and serious pathological findings. Moreover, the rate of MNs in hepatocytes increased after treatment with dioxin. In rats treated with Gln alone, the MNs remained unchanged, but the ratio of glutathione (GSH) and the activity of glutathione peroxidase (GSH-Px) were significantly increased. Gln also prevented the suppression of GSH-Px (except for superoxide dismutase and catalase) and GSH in the livers of animals exposed to TCDD and displayed a strong protective effect against MNs. Thus, our findings for Gln might provide new insight into the development of therapeutic and preventive approaches in TCDD toxicity.
    Toxicology and Industrial Health 10/2011; 28(7):663-72. · 1.56 Impact Factor
  • Hasan Türkez, Fatime Geyikoglu, Mokhtar Ibrahim Yousef
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    ABSTRACT: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that leads to the development of hepatotoxicity. Docosahexaenoic acid (DHA) has been proposed to counteract oxidative stress and improve antioxidant status, and several studies suggest that supplementations with antioxidants can influence hepatotoxicity. The aim of the current study was to explore the role of DHA in modulating the toxicity of TCDD in the liver of Sprague-Dawley rats. Animals were assigned to four groups (n = 5): control (only dimethyl sulfoxide (DMSO)), 8 μg/kg body weight (b.w.) TCDD in DMSO solution; 250 mg/kg b.w. DHA and TCDD plus DHA; respectively. Rats were intraperitoneally administered their respective doses daily for 21 days. On day 21, the animals were killed, and then biochemical tests, pathological examination, and micronucleus (MN) assay were performed in the liver. Our results showed that the activities of antioxidant enzymes were significantly decreased and serious pathological findings were established in rats that received TCDD. Beside the rate of MNs in hepatocytes was increased after the treatment with dioxin. In rats treated with DHA alone, MNs were not changed and the activities of antioxidant enzymes were significantly increased. The presence of DHA with TCDD alleviated its pathological effects in hepatic tissue. DHA also prevented the suppression of antioxidant enzymes in the livers of animals exposed to TCDD and displayed a strong protective effect against MNs. It can be concluded that DHA has beneficial influences and could be able to antagonize TCDD toxicity in liver.
    Toxicology and Industrial Health 10/2011; 28(8):687-96. · 1.56 Impact Factor
  • Hasan Türkez, Mokhtar I Yousef, Fatime Geyikoglu
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    ABSTRACT: The present experiment was undertaken to determine the effectiveness of propolis in alleviating the toxicity of TCDD on cultured primary rat hepatocytes. Propolis (25, 50 and 100 μM) was added to plain culture or simultaneously with TCDD (5 and 10 μM). The hepatocytes were treated with TCDD and propolis for 48 h. Then cell viability was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD decreased cell viability. TCDD also increased TOS level and decreased TAC level in rat hepatocytes. On the basis of increasing doses, the TCDD caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG levels as compared to control culture. In cultures treated with propolis alone, cell viability and TOS level were not affected, while the level of TAC was significantly increased in dose-dependent fashion. The presence of propolis with TCDD modulated its toxic effects on primary hepatocytes cultures. Noteworthy, propolis has a protective effect against TCDD-mediated DNA damages.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 09/2011; 50(6):2142-8. · 2.99 Impact Factor
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    ABSTRACT: The present study was carried out to evaluate the potential protective role of quercetin and curcumin against paracetamol-induced oxidative injury, liver damage and impairment of kidney function, as well as haematotoxicity in rats. Also, N-acetylcysteine was used to evaluate the potency of quercetin and curcumin. Paracetamol caused an elevation in thiobarbituric acid-reactive substances (TBARS) paralleled with significant decline in glutathione peroxidase, glutathione S-transferase, superoxide dismutase and catalase activities (in plasma, brain, lung, heart, liver, kidney and testes) and glutathione content (in lung, liver and kidney). The apparent oxidative injury was associated with evident hepatic necrosis confirmed in histological examination, elevated plasma transmainases, alkaline phosphatase and lactate dehydrogenase. Paracetamol reduced plasma total protein, albumin and globulin, while increased bilirubin, urea and creatinine, and induced haematotoxicity. The presence of quercetin or curcumin with paracetamol successfully mitigated the rise in TBARS and restored the activities of antioxidant enzymes compared to the group treated with both paracetamol and N-acetylcysteine. They also protected liver histology, normalized liver and kidney functions, which was more pronounced with curcumin. Therefore, it can be concluded that concomitant administration of quercetin or curcumin with paracetamol may be useful in reversing the toxicity of the drug compared to N-acetylcysteine.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 11/2010; 48(11):3246-61. · 2.99 Impact Factor
  • Hasan Türkez, Mokhtar I Yousef, Fatime Geyikoglu
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    ABSTRACT: Aluminium is present in several manufactured foods and medicines and is also used in water purification. Therefore, the present experiment was undertaken to determine the effectiveness of propolis in modulating the aluminium chloride (AlCl(3)) induced genotoxicity and hepatotoxicity in liver of rats. Animals were assigned to 1 of 4 groups: control; 34 mg AlCl(3)/kg bw; 50mg propolis/kg bw; AlCl(3) (34 mg/kg bw) plus propolis (50mg/kg bw), respectively. Rats were orally administered their respective doses daily for 30 days. At the end of the experiment, rats were anesthetized and hepatocytes (HEP) were isolated for counting the number of micronucleated hepatocytes (MNHEPs). In addition, the levels of serum enzymes and histological alterations in liver were investigated. AlCl(3) caused a significant increase in MNHEPs, alkaline phosphatase, transaminases (AST and ALT) and lactate dehydrogenase (LDH). Furthermore, severe pathological damages such as: sinusoidal dilatation, congestion of central vein, lipid accumulation and lymphocyte infiltration were established in liver. On the contrary, treatment with propolis alone did not cause any adverse effect on above parameters. Moreover, simultaneous treatments with propolis significantly modulated the toxic effects of AlCl(3). It can be concluded that propolis has beneficial influences and could be able to antagonize AlCl(3) toxicity.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 10/2010; 48(10):2741-6. · 2.99 Impact Factor
  • Mokhtar I Yousef
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    ABSTRACT: The objective of the current study was to analyze the reproductive toxicity caused by lambda-cyhalothrin (LCT) in male rabbits, and to evaluate the possible protective effect of vitamin E (Vit. E) as antioxidant. Animals were orally administered their respective doses of LCT every other day and given drinking water supplemented with vitamin E for 16 weeks. Results showed that semen quality was deteriorated following treatment with LCT. Also, testosterone levels, body weight (BW), feed intake (FI), and relative testes (RTW) and epididymis (REW) weights were significantly decreased. Concentrations of thiobarbituric acid-reactive substances (TBARS) were significantly increased in seminal plasma of rabbits treated with LCT compared with control. While, activities of glutathione S-transferase (GST), transaminases and acid phosphatase (AcP) were significantly decreased. Vitamin E alone significantly increased testosterone levels, BW, FI, RTW, REW, semen characteristics and seminal plasma enzymes, and decreased the levels of TBARS. Also, the present study showed that vitamin E might be effective against LCT-induced reproductive toxicity. It was suggested that LCT exerted a significant adverse effect on reproductive performance of male rabbits. Furthermore, vitamin E antagonized the toxic effects of LCT and improved semen quality of male rabbit.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 02/2010; 48(5):1152-9. · 2.99 Impact Factor

Publication Stats

1k Citations
146.92 Total Impact Points

Institutions

  • 1995–2014
    • Alexandria University
      • • Department of Environmental Studies
      • • Department of Zoology
      • • Department of Biochemistry (Faculty of Science)
      Al Iskandarīyah, Alexandria, Egypt
  • 2009–2010
    • Mansoura University
      • Department of Zoology
      Ṭalkha, Muhafazat ad Daqahliyah, Egypt
    • Tanta University
      Ṭanṭa, Al Gharbīyah, Egypt