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Environ Toxicol Pharmacol. 2012 Nov;34(3):753-60. doi: 10.1016/j.etap.2012.09.012. Epub 2012 Sep 28.

Oxidative stress and cholinesterase inhibition in plasma, erythrocyte and brain of rats' pups following lactational exposure to malathion.

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  • 1Laboratory of Animal Ahysiology, Department of Biology, Faculty of Sciences, Tunis, Tunisia.


The organophosphorus (OP) pesticide malathion is a highly neurotoxic compound. Some studies have reported neurotoxicity signs after in utero exposure to OP pesticides. However there is no evidence of the exclusive contribution of the lactational exposure to malathion as a possible cause of neurotoxicity in rats' pups. In this respect, we investigated the exclusive contribution of malathion (200 mg/kg, b.w.) exposure through maternal milk in rat pups during lactation. We evaluated the activity of acetylcholinesterase (AChE) and butyrylcholinesterase (BChE), as well as on biochemical parameters related to the oxidative stress such lipoperoxidation and antioxidant enzyme activities as superoxide dismutase (SOD) and catalase (CAT) in the brain, plasma and erythrocytes of rats' pups at 21st postnatal day (Pnd). These parameters were also evaluated in the same tissues but at 51 Pnd. Our results showed that the malathion exposure during lactation induced a high inhibitory effect of the brain, plasma and erythrocyte AChE and BChE activities in rat pups. Many changes were observed in the biochemical parameters related to the oxidative stress for pups brain, plasma and erythrocyte. The present study shows, for the first time, that the exposure of postnatal pups to malathion via lactation inhibits the activity of brain, plasma and erythrocytes cholinesterase in the pups. These findings suggest that malathion exposure during lactation induced a cerebral alterations and oxidative stress in rat pups.

Copyright © 2012 Elsevier B.V. All rights reserved.

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