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Stimulatory effects of malathion on the key enzymes activities of insulin secretion in langerhans islets, glutamate dehydrogenase and glucokinase.

Authors
Type
Published Article
Journal
Toxicology Mechanisms and Methods
1537-6524
Publisher
Informa UK (Taylor & Francis)
Publication Date
Volume
16
Issue
4
Pages
161–167
Identifiers
DOI: 10.1080/15376520500191623
PMID: 20021041
Source
Medline
License
Unknown

Abstract

Previous studies showed that malathion induces hyperglycemia mainly through influence on glucose metabolism in liver and skeletal muscles. The main objective of the present study was to determine what will happen on pancreatic key enzymes of insulin secretion, including glucokinase (GK) and glutamate dehydrogenase (GDH), if animals would be in acute or subchronic exposure to various doses of malathion, an organophosphorous insecticide in rats. In the subchronic study, malathion was administered orally at doses of 100 to 400 ppm for 4 weeks. In the acute experiment, animals received various doses of 3 to 75 mg/kg of malathion intraperitoneally. In each experiment, islets were isolated from the pancreas of rats by a standard collagenase digestion, separation by centrifugation, and hand-picking technique. The activities of the mitochondrial GDH and the nonmitochondrial GK enzymes were determined in islets homogenates spectrophotometrically. Blood sample was taken by cardiac puncture for glucose and insulin assays. In the acute experiment, malathion (3, 15, 75 mg/kg) increased blood glucose and insulin (15 and 75 mg/kg). In the subchronic experiment, malathion (100, 200, 400 ppm) increased blood glucose and insulin (200 and 400 ppm). All doses in both acute and subchronic experiments increased the mitochondrial GDH activity. Acute (15 and 75 ppm) and subchronic (200 and 400 ppm) increased the islets GK activity. It was concluded that pancreatic islet key enzymes are stimulated following acute and subchronic exposure to malathion though not enough to overcome to hyperglycemia. Activation of islets muscarinic receptors by malathion in favor of hyperinsulinemia, overproduction of glutamate/glutathione by GDH, and overproduction of glucose via increased glycogenolysis in counteracting with malathion-induced oxidative stress are possible mechanisms for observed effects. A new NOAEL acceptable daily intake must be established for malathion.

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