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Effects of malathion subchronic exposure on rat skeletal muscle glucose metabolism

Regarding the widespread use of organophosphorous pesticides (OP) especially malathion in environment and reported cases of muscle disturbances in human and animal, the present work was undertaken to explore effects of malathion subchronic exposure on rat leg skeletal muscle glucose metabolism by me...

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Published in:Environmental toxicology and pharmacology 2005, Vol.19 (1), p.191-196
Main Authors: Pournourmohammadi, Shirin, Farzami, Bijan, Ostad, Seyed Nasser, Azizi, Ebrahim, Abdollahi, Mohammad
Format: Article
Language:English
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Summary:Regarding the widespread use of organophosphorous pesticides (OP) especially malathion in environment and reported cases of muscle disturbances in human and animal, the present work was undertaken to explore effects of malathion subchronic exposure on rat leg skeletal muscle glucose metabolism by measuring key enzymes of glycogenolysis and glycolysis. Malathion was administered through food for 4 weeks at concentrations of 100, 200, and 400 ppm to rats. Activities of enzymes including glycogen phosphorylase (GP), hexokinase (HK), and phosphofructokinase-1 (PFK) were measured in skeletal muscle homogenate of exposed rats. Levels of glucose and insulin were measured in blood. Four weeks administration of malathion at doses of 200 and 400 ppm increased blood glucose concentrations to 44.4 and 60.6% of control, respectively. Malathion at doses of 200 and 400 ppm increased blood insulin concentration to 36.6 and 143.2% of control, respectively. Malathion at doses of 100, 200, and 400 ppm increased muscle PFK activity to 40.4, 53.5, and 83.1% of control, respectively. Malathion at doses of 400 ppm increased skeletal muscle GP to 91.6% of control. Skeletal muscle HK was not influenced by malathion treatment. It is concluded that malathion influences muscle glycogenolysis and glycolysis as well as secretion of insulin from pancreas which all may explain diabetic potential of malathion.
ISSN:1382-6689
1872-7077
DOI:10.1016/j.etap.2004.07.002