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This study was conducted to shed light on the effect of exposure of lactating rat to chlorpyrifos (CPF). CPF was orally administered to lactating rats at 0.01 mg kg(-1) b.wt. (acceptable daily intake, ADI), 1.00 mg kg(-1) b.wt. (no observed adverse effects level, NOAEL) and 1.35 mg kg(-1) b.wt. (1/100 LD( 50)) from postnatal day 1 (PN1) until day 20 (PN20) after delivery. Results indicated decreases in body weight and increases in relative liver and kidney weights of exposed dams. Significant damage to liver was observed via increased plasma levels of aminotransferases (aspartate aminotransferase (AST) and alanine aminotransferase (ALT)) lactate dehydrogenase (LDH) and γ-glutamyle transferase (γ-GT) in a dose-dependent manner. At two high doses of CPF (1.00 and 1.35 mg kg(-1) b.wt.), the lactating mothers showed significant decrease in the activity of cholinesterase (ChE). Lipid peroxidation was significantly increased, while glutathione s-transferase (GST) and superoxide dismutase (SOD) were significantly decreased compared to control. At high dose of CPF (1.35 mg kg(-1) b.wt.), total protein and uric acid levels were significantly increased. CPF caused dose-related histopathological changes in liver and kidney of the CPF-treated dams.

Erythrocytes are a convenient model to understand the membrane oxidative damage induced by various xenobiotic pro-oxidants. This study was designed to investigate the possibility of methomyl (Lannate 90% SP), S-methyl N-(methylcarbamoyloxy) thioacetimidate, to induce oxidative stress response in rat erythrocytes in vitro. Erythrocytes were incubated for 4 hours at 37 degrees C with different concentrations (0.0, 0.1, 0.5, 1.0, 1.5 and 2.0 mM) of methomyl. The results showed that methomyl decreased acetylcholinesterase (AChE), superoxide dismutase (SOD) and glutathione S-transferase (GST) activities and increased level of lipid peroxidation (LPO) as well as the percentage of haemolysis. The response occurred in a concentration-dependent manner. The study suggested that methomyl has the capability to induce oxidative damage as evidenced by increasing LPO and perturbations in various antioxidant enzymes.

The present study was undertaken to evaluate the oxidative damage, biochemical and histopathological alterations in sucking rats whose mothers were exposed to the insecticide chlorpyrifos (CPF). Dams were administered CPF, via oral route. Doses equalled 0.01 mg kg—1 body weight (b.wt.; acceptable daily intake, ADI), 1.00 mg kg—1 b.wt. (no observed adverse effects level, NOAEL) and 1.35 mg kg—1 b.wt. (1/100 lethal dose [LD50]) from postnatal day 1 until day 20 after delivery. At two high doses of CPF, the body weight gain and relative liver and kidney weight of suckling pups were significantly decreased. Exposure of the mothers to CPF caused increase in lipid peroxidation (LPO) and decrease in superoxide dismutase (SOD) and glutathione-s-transferase (GST) in lactating pups. CPF altered the level of the marker parameters related to the liver and kidneys. Consistent histological changes were found in the liver and kidneys of the subjected pups, especially at the higher doses. The results suggested that the transfer of CPF intoxication through the mother’s milk has resulted in oxidative stress and biochemical and histopathological alterations in the suckling pups. The data of this study may be considered as a contribution to the problem of lactational transfer of the relatively less persistent OP pesticides, such as CPF.

Pesticides are omnipresent in environment, water, fruits, and vegetables and are considered as risk factors for human health. Consumers are mainly exposed to pesticides through diet, and the main question to be answered concerns the impact of such exposure on health. In this study, we developed a mouse model to mimic consumer exposure. During gestation and lactation periods, the experimental mouse dams (M) received one of the following treatments: (a) diet-free of pesticides; (b) diet enriched with chlorpyrifos (CPF; 44.0 μg kg(-1)); c) diet + oral vitamin E (vit. E; α-tocopherol; 200 mg/kg/mouse); and (d) diet enriched with CPF (44.0 μg/kg + oral vit. E (200 mg/kg/mouse). At weaning, pups (P) and dams were killed, and organs as well as blood samples were collected. Compared with control results, CPF induced alteration of measured parameters (e.g. organ weight, alkaline phosphatase, urea, malondialdehyde, superoxide dismutase, and cholinesterase) either in mouse dams or in their offspring. Also, CPF induced histological impairment in kidney, liver, and ovary. Administration of vit. E in conjunction with CPF clearly alleviated deviation of these parameters than those of control ones. In conclusion, a dietary exposure of mice during gestation and lactation to low dose of CPF led to significant changes in the mother but also in the weaned animals that have not been directly exposed to this pesticide. These biological and histological modifications could be reversed by an oral supplementation of vit. E.

Exposure to mixtures of toxicants (e.g., pesticides) is common in real life and a subject of current concern. The present investigation was undertaken to assess some toxicological effects in male rats following exposure to methomyl (MET), abamectin (ABM), and their combination (MET+ABM), and to evaluate the ameliorative effect of zinc co-administration. Three groups of rats were designated for MET, ABM, and the mixture treatments. Three other groups were designated for zinc in conjunction with the pesticides. Additionally, one group received water only (control), and the other represented a positive zinc treatment. The obtained results revealed that MET was acutely more toxic than ABM. The tested pesticides induced significant elevation in lipid peroxidation and catalase levels, while declined the levels of the other tested parameters e.g., Superoxide dismutase (SOD), Glutathione-S-transferase (GST), Glutathione peroxidase (GPx), Glutathione reductase (GR), Cytochrome P450 (CYP450), testosterone, and thyroxine). Biochemical alterations induced by the mixture were greater than those recorded for each of the individual insecticides. The joint action analysis, based on the obtained biochemical data, revealed the dominance of antagonistic action among MET and ABM. Zinc supplementation achieved noticeable ameliorative effects. It was concluded that zinc may act as a powerful antioxidant, especially in individuals who are occupationally exposed daily to low doses of such pesticides.

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