ABSTRACT
ABSTRACT This study was done to evaluate the effects of lead nitrate and mercury chloride in testis tissues of Wistar rats. Lead nitrate and mercury chloride are widely used heavy metals in industry. Oral lead and mercury administrations to adult male rats at doses 45 mg/kg bw and 0.02 mg/kg bw, respectively for 4 weeks caused a significant increasing in MDA levels and antioxidant enzyme activities (SOD, CAT, GPx and GST). The MDA levels and acivities of antioxidant enzymes was lower in rats that were administrated by lead nitrate than mercury chloride treated group. Light microscopic analyses revealed that lead nitrate and mercury chloride induced numerous histopathological changes in testis tissues of rats. Histopathological observations of the testis tissues showed that mercury chloride caused more harmful effects than lead nitrate, too. The results indicate that lead nitrate and mercury chloride have reproductive toxicity, in male rats at the tested doses. The effect which we observed applying the lead nitrate and mercury chloride together, was more greater than when we used them alone.
ABSTRACT
Furan is a food and environmental contaminant and a potent carcinogen in animals. Lycopene is one dietary carotenoid found in fruits such as tomato, watermelon and grapefruit. The present study was designed to explore the protective effect of lycopene against furan-induced oxidative damage in streptozotocin (STZ)-induced diabetic rat kidney. At the end of the experimental period (28 days), we found that lycopene markedly decreased the malondialdehide (MDA) levels in the kidney, urea, uric acid and creatinine levels in the serum of furan-treated rats. The increase of histopathology in the kidney of furan-treated rats were effectively suppressed by lycopene. Furthermore, lycopene markedly restored superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione-S-transferase (GST) activities in the kidney of furan-treated rats. In conclusion, these results suggested that lycopene could protect the rat kidney against furan-induced injury by improving renal function, attenuating histopathologic changes, reducing MDA production and renewing the activities of antioxidant enzymes.
ABSTRACT
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.
ABSTRACT
Organophosphate (OP) pesticides such as dichlorvos (DDVP) intoxication has been shown to produce oxidative stress due to the generation of free radicals, which alter the antioxidant defense system in erythrocytes. In this study, the effects of DDVP (1, 10, 100 µM) or DDVP + vitamin C (VC; 10 µM) or vitamin E (VE; 30 µM), on the levels of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) activities in human erythrocytes were examined in vitro. There were no statistical differences between all groups for 1 µM concentration of DDVP. Treatment with DDVP alone produced an increase in the level of MDA and decreased activities of antioxidant enzymes (P < 0.05). Groups treated with vitamins and DDVP showed protective effects of vitamins against DDVP-induced changes in antioxidant enzyme activity and lipid peroxidation (LPO) (10 µM). At 100 µM concentration of DDVP vitamins had no effect on DDVP-induced toxicity. The results show that administration of DDVP resulted in the induction of erythrocyte LPO and alterations in antioxidant enzyme activities, suggesting that reactive oxygen species (ROS) may be involved in the toxic effects of DDVP. Also the data show that the plasma level of VC and VE may ameliorate OP-induced oxidative stress by decreasing LPO in erythrocytes at certain doses of OP pesicides.