ascorbic-acid and cyhalothrin

The photodegradation processes of fenpropathrin and λ-cyhalothrin were studied in hexane, methanol/water (1:1, v/v), and acetone in both ultraviolet light and simulated sunlight. Intermediates in the photodegradation process were identified using gas chromatography/mass spectrometry (GC/MS), and the analysis of intermediates was used to speculate on possible photodegradation pathways. The photodegradation processes of fenpropathrin and λ-cyhalothrin followed pseudo first-order kinetics. The photodegradation rates varied according to the solvent in decreasing order: hexane>methanol/water (1:1, v/v)>acetone. The effects of substances coexisting in the environment on the photodegradation of pyrethroids were also investigated in the research. Acetone, humic acid, and riboflavin increased photodegradation rates while L-ascorbic acid slowed the process. This study provides a theoretical basis for the removal of pyrethroid pollution from the natural environment.

Topics: Ascorbic Acid; Gas Chromatography-Mass Spectrometry; Humic Substances; Kinetics; Nitriles; Photochemical Processes; Photochemistry; Photolysis; Pyrethrins; Sunlight; Water Pollutants, Chemical

The wide use and wide-spectrum toxicity of synthetic pyrethroid (SP) insecticides make them an emerging ecotoxicological concern. The objective of the current study was aimed to investigate the involvement of oxidative stress in lambda-cyhalothrin (LTC)-induced cerebellum damages in adult rats and to evaluate the possible protective effect of vitamin C (vit C) as antioxidant. Exposure of rats to LTC during 3 weeks caused a significant (p < 0.05) increase in the levels of lipid peroxidation (LPO), nitric oxide (NO) and protein carbonyls (PCO) along with a significant (p < 0.05) decrease in the levels of reduced glutathione (GSH) and the activities of acetylcholinesterase, superoxide dismutase, catalase, glutathione peroxidase and gluthione-S-transferase (p < 0.05) when compared with the control group. The oral administration of vit C (200 mg/kg per d) to LTC-treated rats significantly (p < 0.05) diminished the levels of LPO, NO and PCO and significantly (p < 0.05) increased the activities of GSH and antioxidant enzymes. Our results showed that the administration of vit C could ameliorate some of the oxidative damage in the cerebellum induced by SPs exposure, suggesting that the ascorbic acid could exhibit a potential antioxidant activity against neurotoxicity induced by pesticides exposure.

Topics: Acetylcholinesterase; Animals; Antioxidants; Ascorbic Acid; Cerebellum; Glutathione; Insecticides; Lipid Peroxidation; Male; Nitric Oxide; Nitriles; Oxidation-Reduction; Oxidative Stress; Protein Carbonylation; Pyrethrins; Rats; Rats, Wistar; Sodium-Potassium-Exchanging ATPase

Lambda-cyhalothrin is a synthetic pyrethroid insecticide used worldwide in agriculture, home pest control, protection of foodstuff and disease vector control. The objective of this study was to investigate the propensity of lambda-cyhalothrin (LTC) to induce oxidative stress, changes in biochemical parameters and enzyme activities in the kidney of male rats and its possible attenuation by Vitamin C (vit C). Renal function, histopathology, tissue malondialdehyde (MDA), protein carbonyl (PCO) levels, antioxidant enzyme activities and reduced glutathione (GSH) levels were evaluated. Exposure of rats to lambda-cyhalothrin, during 3 weeks, caused a significant increase in kidney MDA and protein carbonyl levels (p<0.01) as compared to controls. Co-administration of vitamin C was effective in reducing MDA and PCO levels. The kidney of LTC-treated rats exhibited severe vacuolations, cells infiltration and widened tubular lumen. The activities of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST) were significantly decreased due to lambda-cyhalothrin exposure. Co-administration of vitamin C ameliorated the increase in enzymatic activities of aminotransferases (AST and ALT), lactate dehydrogenase (LDH), creatinine and urea levels and improved the antioxidant status. These data indicated the protective role of ascorbic acid against lambda-cyhalothrin-induced nephrotoxicity and suggested a significant contribution of its antioxidant property to these beneficial effects.

Topics: Animals; Antioxidants; Ascorbic Acid; Catalase; Glutathione; Insecticides; Kidney; Lipid Peroxidation; Male; Malondialdehyde; Nitriles; Oxidative Stress; Protein Carbonylation; Pyrethrins; Rats; Rats, Wistar; Superoxide Dismutase

Pyrethroid pesticides were used preferably over organochlorines and organophosphates due to their high effectiveness, low toxicity to non-target organisms and easy biodegrability. It has widespread applications in agriculture through the world and in Tunisia. The present study investigates lambda-cyhalothrin (LTC) effects on biochemical parameters, hepatotoxicity and their attenuation by vitamin C. Male Wistar rats were randomly divided into three groups of seven each: a control group (C) and two treated groups during 3 weeks with LTC administrated either alone in drinking water for LTC group or coadministred with vitamin C for LTC+vit C group. Lactate deshydrogenase (LDH) activity was significantly increased in liver (+51%, p<0.001) and in plasma (+40%, p<0.001) compared to those of control group. A significant increase of malondialdehyde (MDA) levels in liver (+53%; p<0.001) associated with a decrease in antioxidants enzyme activities and reduced glutathione (GSH) content was observed in LTC group compared to controls. The administration of vitamin C to LTC+vit C group improved all parameters studied. We conclude that LTC induces oxidative stress and modifies biochemical parameters and histological aspects of liver. Administration of vitamin C alleviates the toxicity induced by this synthetic pyrethroid insecticide.

Topics: Alanine Transaminase; Animals; Ascorbic Acid; Aspartate Aminotransferases; Catalase; Chemical and Drug Induced Liver Injury; Glutathione; Insecticides; L-Lactate Dehydrogenase; Liver Diseases; Male; Malondialdehyde; Nitriles; Pyrethrins; Rats; Rats, Wistar; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Vitamins

Erythrocytes are a convenient model to understand the membrane oxidative damage induced by various xenobiotic-prooxidants. This study was designed to investigate (1) the possibility of lambda-cyhalothrin (LC), a type II pyrethroid, to induce oxidative stress response in rabbit erythrocytes in vitro and its effect on selected antioxidant enzymes and (2) the role of vitamin C (VC; 20mM) and vitamin E (VE; 2mM) in alleviating the cytotoxic effects of LC. Erythrocytes were divided into three groups. The first group, previously prepared erythrocytes was incubated for 4h at 37 degrees C with different concentrations (0, 0.1, 0.5, 1, 2.5, 5mM) of LC. The second and third groups were preincubated with VC or VE, respectively for 20 min and followed by LC incubation for 4h. Following in vitro exposure, LC caused a significant induction of oxidative damage in erythrocytes at different concentrations as evidenced by increased thiobarbituric acid reactive substances (TBARS) levels. However, a significant decrease in the content of sulfhydryl groups (SH-groups), and the activities of acetylcholinesterase (AChE), superoxide dismutase (SOD), catalase (CAT) and glutathione S-transferase (GST) were observed. The response was concentration dependent. VC or VE pretreated erythrocytes showed a significant protection against the cytotoxic effects induced by LC on the studied parameters. In conclusion, antioxidant vitamins especially VE could be able to ameliorate LC-induced oxidative stress by decreasing lipid peroxidation and altering antioxidant defense system in erythrocytes.

Topics: Acetylcholinesterase; Animals; Antioxidants; Ascorbic Acid; Biomarkers; Catalase; Dose-Response Relationship, Drug; Drug Antagonism; Erythrocytes; Free Radical Scavengers; Glutathione Transferase; Insecticides; Male; Nitriles; Oxidative Stress; Pyrethrins; Rabbits; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Vitamin E