Fatma M. El-Demerdash

The present study was designed to evaluate the toxic effects induced by different time intervals of methomyl exposure on liver antioxidant defense system, oxidative stress, liver function biomarkers and histopathology in CD-1 mice. Ten male mice per group were assigned to one of four treatment groups. Group one served as control while group 2, 3 and 4 were orally treated with one mg methomyl/kg BW for 10, 20 and 30 days, respectively. Results obtained showed that methomyl significantly induced TBARS and decreased the activity of antioxidant enzymes, glutathione S-transferase, superoxide dismutase and catalase and the levels of reduced glutathione in mice liver. Aminotransferases and alkaline phosphatase activities were significantly decreased in liver due to methomyl administration, while the activities of these enzymes were significantly increased in serum. In addition, liver lactate dehydrogenase activity was significantly increased. On the contrary, methomyl treatment caused a significant decrease in liver acid phosphatase. The histology of mice liver treated with methomyl for 10, 20 and 30 days of duration showed dilation of central vein, sinusoids between hypertrophied hepatocytes and nuclear degeneration with mononuclear cell infiltration. In conclusion, exposure to methomyl induced toxicity and oxidative stress in mice liver via free radicals mechanism. Also, methomyl might have affected cell metabolism, cell membrane permeability and the detoxification system in liver.

A mixture of pyrethroids plus organophosphates was assessed for their potential effects on lipid peroxidation, the antioxidant defense system and lactate dehydrogenase (LDH) in rat kidney in vitro. Various insecticide concentrations were incubated with kidney homogenate at 37°C for different incubation times. Treatment with fenitothion (FNT) plus lambda-cyhalothrin (LC) caused a significant induction (P < 0.05) in thiobarbituric acid reactive substances (TBARS), which might be associated to decreased levels of reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), glutathione S-transferase (GST) activities and protein content in rat kidney. However, a significant induction of lactate dehydrogenase (LDH) activity was observed. The effect was concentration and time dependent. It can be concluded that depletion of GSH might indicate that reactive oxygen species (ROS) could be involved in the toxic effects of FNT plus LC which lead to marked perturbations in antioxidant defense system.

The effects of organophosphorus [fenitrothion (FNT)] and pyrethroid (lambda-cyhalothrin (LC)] pesticides mixture on the antioxidant defense system and liver function enzymes in rat liver were assessed. Various concentrations of FNT + LC were incubated with liver homogenate at 37°C for various incubation times. Results showed that FNT plus LC caused a significant concentration-dependent and time-related inhibition of glutathione S-transferase (GST), superoxide dismutase (SOD) and catalase (CAT) activities, and reduction of glutathione (GSH) content. The depletion of GSH might indicate that reactive oxygen species could be involved in the toxic effects of FNT plus LC. In addition, a significant inhibition in transaminases (AST, ALT) and phosphatases (AcP, AlP) activities was observed. On the other hand, FNT + LC increased the activity of lactate dehydrogenase (LDH) and thiobarbituric acid reactive substances (TBARS) levels. It can be concluded that such biomarkers may be used in assessing adverse/toxic effects of pesticides as environmental stressors.

Deleterious effects of chromium (VI) compounds are diversified affecting almost all the organ systems in a wide variety of animals. Therefore, the present study was carried out to determine the effectiveness of folic acid (FA) in alleviating the toxicity of chromium (VI) on certain biochemical parameters, lipid peroxidation, and enzyme activities of male New Zealand white rabbits. Six rabbits per group were assigned to one of four treatment groups: 0 mg FA and 0 mg Cr(VI)/kg BW (control); 8.3 μg FA/kg BW; 5 mg Cr(VI)/kg BW; 5 mg Cr(VI) plus 8.3 μg FA/kg BW, respectively. Rabbits were orally administered their respective doses every day for 10 weeks. Results obtained showed that Cr(VI) significantly (P < 0.05) increased the levels of free radicals and the activity of glutathione S-transferase (GST), and decreased the content of sulfhydryl groups (SH groups) in liver, testes, brain, kidney, and lung. The activities of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AlP), acid phosphatase (AcP), and lactate dehydrogenase (LDH) were significantly decreased in liver and testes due to Cr(VI) administration. Also, AlP and AcP activities were significantly decreased in kidney and lung. The activity of acetylcholinesterase (AChE) was significantly decreased in brain and plasma. Contrariwise, the activities of AST and ALT were significantly increased in plasma, while AlP and AcP decreased. Chromium (VI) treatment caused a significant decrease in plasma total protein (TP) and globulin, and increased total lipids (TL), cholesterol, glucose, urea, creatinine, and bilirubin concentrations. Folic acid alone significantly decreased the levels of free radicals in liver, brain, and kidney, and increased the content of SH-group. The activities of AST, ALT, and LDH in liver; AST, ALT, AlP, AcP, and LDH in testes; AcP in kidney; AlP and AcP in lung, and LDH in brain were significantly increased. Plasma TP and albumin were increased, while urea and creatinine were decreased. The presence of FA with Cr(VI) restored the changes in enzyme activities and biochemical parameters. In conclusion, folic acid could be effective in the protection of chromium-induced toxicity.

Role of alpha-tocopherol (vitamin E), beta-carotene and/or their combination as antioxidants against the toxicity of fenvalerate on blood hematology, free radicals, biochemical parameters, and semen quality were studied in male rats. Fenvalerate (20 mg/kg BW), vitamin E (100 mg/kg BW), beta-carotene (10 mg/kg BW), and vitamin E plus beta-carotene (100 + 10 mg/kg BW, respectively) were given alone or in combination with fenvalerate. The tested doses were given to rats every other day for 30 days. Results obtained showed that fenvalerate significantly (P < 0.05) induced free radicals in plasma and brain and insignificantly in liver and testes. While, vitamin E, beta-carotene alone and/or in combination decreased the levels of free radicals in plasma, liver, testes, and brain. The activities of glutathione S-transferase (liver), alkaline phosphatase (plasma and liver), aspartate aminotransferase (plasma, liver, and testes) and alanine aminotransferase (plasma and liver) were significantly (P < 0.05) increased due to fenvalerate administration. The activity of acetylcholinesterase was significantly (P < 0.05) decreased in brain and plasma, while plasma glucose, urea, creatinine, and bilirubin concentrations were significantly (P < 0.05) increased in rats treated with fenvalerate. Also, results showed a significant (P < 0.05) alterations in plasma proteins, hematological parameters, body weight, and relative weights of organs. Sperm concentration and motility (%) were significantly (P < 0.05) decreased, while dead and abnormal sperm increased in rats exposed to fenvalerate. Vitamin E, beta-carotene alone and/or in combination did not cause any changes in the investigated parameters, but improved semen quality and minimized the toxic effect of fenvalerate. The obtained results demonstrated the beneficial influences of vitamin E, beta-carotene alone and/or in combination in reducing the harmful effects of fenvalerate.