Filiz Demir

Malathion-induced testicular toxicity in male rats and the protective effect of vitamins C and E

Sexually mature male Wistar rats (weighing 300-320 g and each group 6 animals) were given malathion (27 mg/kg; 1/50 of the LD(50) for an oral dose) and/or vitamin C (200mg/kg)+vitamin E (200mg/kg) daily via gavage for 4 weeks. The sperm counts, sperm motility, sperm morphology, FSH, LH, and testosterone levels, and histopathological changes in the testes of these rats, were investigated at the end of the 4th week. By the end of 4th week, rats given malathion alone, or in combination with vitamins C and E, had significantly lower sperm counts and sperm motility, and significantly higher abnormal sperm numbers, than the untreated control rats. The rats given malathion alone or in combination with vitamins also had significantly lower plasma FSH, LH and testosterone levels than the control rats. Co-treatment of malathion-exposed rats with vitamins E and C had a protective effect on sperm counts, sperm motility and abnormal sperm numbers, but not on plasma FSH, LH and testosterone levels. Light microscopic investigations revealed that 4 weeks of malathion exposure was associated with necrosis and edema in the seminiferous tubules and interstitial tissues. Degenerative changes in the seminiferous tubules were also observed in the rats which received malathion and supplemented with vitamins C and E, but milder histopathological changes were observed in the interstitial tissues. Thus, it appears that vitamins C and E ameliorate malathion testicular toxicity but are not completely protective.

Malathion-induced hepatotoxicity in rats: the effects of vitamins C and E.

Mature male Wistar rats (weighing 300-320 g and each group six animals) were given malathion (27 mg/kg; 1/50 of the LD50 for an oral dose), vitamin C (200 mg/kg)+vitamin E (200 mg/kg), or both daily via gavage for 4 weeks. At the end of the fourth week, the malathion-treated group and the malathion plus vitamin-treated group both had significantly higher white blood cell (WBC) and thrombocyte counts than the control group. Compared to the control group, the two groups also had significantly higher serum total cholesterol, alkaline phosphatase (ALP), alanine aminotransferase (ALT), aspartate aminotransferase (AST), and lactate dehydrogenase (LDH) levels, and significantly lower triglyceride and very low density lipoprotein (VLDL) levels. The malathion-treated rats also had significantly lower serum total protein and albumin levels, but the malathion plus vitamin-treated group did not differ from the control group in terms of these parameters. Moreover, concomitant vitamin treatment significantly normalized, at least partially, all of the other hematological and biochemical parameters that were altered by malathion. Light microscopic analyses revealed that both the malathion-treated and malathion plus vitamin-treated groups exhibited histopathological changes in liver tissues, although some pathological features were only observed in the malathion-treated group. Thus, vitamins C and E can reduce malathion hepatotoxicity, although the degree of protection they provide is limited.

Protective effects of catechin and quercetin on antioxidant status, lipid peroxidation and testis-histoarchitecture induced by chlorpyrifos in male rats

Mature male Wistar rats were given chlorpyrifos (5.4 mg/kg, 1/25 of the oral LD(50)), catechin (20 mg/kg),quercetin (20 mg/kg), catechin plus chlorpyrifos, and quercetin plus chlorpyrifos daily via gavage for four weeks. No statistical differences were found in the catechin-only and quercetin-only groups compared with the control group. By the end of the fourth week, chlorpyrifos alone increased the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), while decreased glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities compared with the control group in rat testis tissues. In the catechin-plus-chlorpyrifos and quercetin-plus-chlorpyrifos groups, there were statistically significantly decreased MDA levels, SOD and CAT activities, while increased GPx and GST activities compared with the chlorpyrifos-only group. Light microscopic analyses revealed that chlorpyrifos-only induced numerous histopathological changes in the testis tissues. Milder pathological alterations were observed in rats catechin-plus-chlorpyrifos, and quercetin-plus-chlorpyrifos. Thus, it appears that catechin and quercetin ameliorate chlorpyrifos induced toxicity except histopathological changes in rat testis tissues.

Protective effect of catechin and quercetin on chlorpyrifos-induced lung toxicity in male rats.

The mature male Wistar rats (n=36, 300-320 g) were divided into six groups having six animals, i.e., Group I (control), Group II (catechin, 20 mg/kg bw), Group III (quercetin, 20 mg/kg bw), Group IV (chlorpyrifos 5.4 mg/kg, 1/25 LD50), Group V (catechin+chlorpyrifos) and Group VI (quercetin+chlorpyrifos). Rats were given chlorpyrifos, catechin and quercetin daily via gavage for 4 weeks. Chlorpyrifos increased the levels of malondialdehyde (MDA), superoxide dismutase (SOD), and catalase (CAT), and decreased glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in lung tissues compared to the control group. In the catechin plus chlorpyrifos- and quercetin plus chlorpyrifos-treated groups, there were statistically significant increases in CAT and SOD activities, while no statistically significant changes were observed in MDA, GST and GPx activities relative to the control. Compared to the chlorpyrifos-treated group, however, the catechin plus chlorpyrifos- and quercetin plus chlorpyrifos-treated groups showed significantly increased GST and GPx activity, while the activity of MDA, SOD and CAT was significantly decreased. Light microscopic investigations revealed that 4 weeks of chlorpyrifos exposure induced numerous histopathological alterations in the lung. Milder histopathological changes were observed in animals co-treated with catechin plus chlorpyrifos or quercetin plus chlorpyrifos. Thus, it appears that catechin and quercetin ameliorate chlorpyrifos-induced lung toxicity but are not completely protective.

Mercuric chloride-induced testicular toxicity in rats and the protective role of sodium selenite and vitamin E

Mercury has been recognized as an environmental pollutant that adversely affects male reproductive systems of animals. This study examined the effects of mercuric chloride on the antioxidant system and histopathological changes and also evaluated the ameliorating effects of sodium selenite and/or vitamin E in the rat testis tissues. Sexually mature male Wistar rats (weighing 300-320g and each group six animals) were given mercuric chloride (1mg/kg bw) and/or sodium selenite (0.25mg/kg bw)+vitamin E (100mg/kg) daily via gavage for 4weeks. In the present study, mercuric chloride exposure resulted in an increase in the TBARS level and a decrease in the SOD, CAT, GPx activities, with respect to the control. Further, light microscopic investigation revealed that mercury exposure induced histopathological alterations in the testis tissues. Supplementation of sodium selenite and/or vitamin E to mercury-induced groups declined lipid peroxidation, increased SOD, CAT, GPx activities. While some histopathological changes were detected in mercuric chloride treated group, milder histopathological changes were observed in animal co-treated with sodium selenite and/or vitamin E supplementation to mercuric chloride-treated rats. As a result, mercuric chloride induced testicular toxicity is reduced by sodium selenite and/or vitamin E, but not ameliorate completely.

Sodium selenite and vitamin E in preventing mercuric chloride induced renal toxicity in rats

This study aims to investigate improving effects of sodium selenite and/or vitamin E on mercuric chloride-induced kidney impairments in rats. Wistar male rats were exposed either to sodium selenite (0.25mg/kgday), vitamin E (100mg/kgday), sodium selenite+vitamin E, mercuric chloride (1mg/kgday), sodium selenite+mercuric chloride, vitamin E+mercuric chloride and sodium selenite+vitamin E+mercuric chloride for 4weeks. Mercuric chloride exposure resulted in an increase in the uric acid, creatinine, blood urea nitrogen and malondialdehyde (MDA) levels and a decrease in the superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities. Histopathological changes were detected in kidney tissues in mercuric chloride-treated groups. A significant decrease in the uric acid, creatinine, blood urea nitrogen and MDA levels and a significant increase in the SOD, CAT and GPx activities were observed in the supplementation of sodium selenite and/or vitamin E to mercuric chloride-treated groups. Conclusively, sodium selenite, vitamin E and vitamin E+sodium selenite significantly reduce mercuric chloride induced nephrotoxicity in rats, but not protect completely.

Lead Nitrate Induced Testicular Toxicity in Diabetic and Non-Diabetic Rats: Protective Role of Sodium Selenite

Among heavy met als, lead is one of the common pollutants found in the environment and biological system. In the present study, streptozotocin-induced diabetic and normal non-diabetic male Wistar rats were given sodium selenite (1.0 mg/kg bw), lead nitrate (22.5 mg/kg bw) and sodium selenite plus lead nitrate (1.0 mg/kg+22.5 mg/kg bw, respectively) through gavage. At the end of 4th week, malondialdehyde (MDA) levels, antioxidant enzyme activities [superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione-S-transferase (GST)], and histopathological changes of testes were investigated compared to the control group. No significant differences were observed between the control and sodium selenite treated groups. However, lead nitrate increased the levels of MDA, SOD, CAT, GPx and GST activities compared with the control group in diabetic and non-diabetic rats. Light microscopic analyses revealed that lead nitrate induced numerous histopathological changes in testis tissues of diabetic and non-diabetic rats. In the diabetic and non-diabetic sodium selenite plus lead nitrate treated groups, there were statistically significantly decreased MDA levels and antioxidant enzymes activities and mild pathological changes. As a result, sodium selenite significantly reduced lead nitrate induced testicular toxicity for both diabetic and non-diabetic rats.