title: Protective effect of N-acetylcysteine against arsenic-induced depletion in vivo of carbohydrate.
abstract: N-acetylcysteine (NAC), a synthetic aminothiol, possesses antioxidative and cytoprotective properties. The present study evaluates the effect of NAC supplementation on arsenic-induced depletion in vivo of carbohydrates. Arsenic (as sodium arsenite) treatment (i.p.) of male Wistar rats (120-140 g b.w.) at a dose of 5.55 mg/kg body weight (35% of LD50) per day for a period of 30 days produced a significant decrease in blood glucose level (hypoglycemia) and a fall in liver glycogen and pyruvic acid contents. The free amino acid nitrogen content of liver increased while that of kidney decreased after arsenic treatment. Arsenic also enhanced the liver lactate dehydrogenase activity whereas glucose 6-phosphatase activity in both liver and kidney decreased significantly following arsenic treatment. Transaminase activities in liver and kidney were not significantly altered except the glutamate-pyruvate transaminase activity that was reduced in kidney after arsenic treatment. Oral administration of NAC (163.2 mg/kg/day) for last 7 days of treatment prevented the arsenic-induced hypoglycemia and glycogenolytic effects to an appreciable extent. There was also recovery of liver pyruvic acid as well as liver and kidney free amino acid nitrogen content after NAC supplementation. Arsenic-induced alteration of glucose 6-phosphatase activity in both liver and kidney was also counteracted by NAC. It is suggested that carbohydrate depletion in vivo due to exposure to arsenic can be counteracted by NAC supplementation.
authors.affiliation: Biochemistry and Nutrition Laboratory, Department of Physiology, University of Calcutta, 92, Acharya Prafulla Chandra Road, Kolkata 700 009, India.
authors.forename: Sudipta
authors.initials: S
authors.lastname: Pal
authors.forename: Ajay Kumar
authors.initials: AK
authors.lastname: Chatterjee
mesh_terms: D000111:Acetylcysteine / Q000627:therapeutic use*; D000818:Animals; D018053:Arsenites / Q000037:antagonists & inhibitors* / Q000633:toxicity; D001786:Blood Glucose / Q000187:drug effects; D056486:Chemical and Drug Induced Liver Injury / Q000201:enzymology / Q000378:metabolism / Q000517:prevention & control*; D004791:Enzyme Inhibitors / Q000633:toxicity*; D005952:Glucose-6-Phosphatase / Q000378:metabolism; D007003:Hypoglycemia / Q000139:chemically induced / Q000517:prevention & control; D007668:Kidney / Q000187:drug effects / Q000201:enzymology; D008297:Male; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism; D017670:Sodium Compounds / Q000037:antagonists & inhibitors* / Q000633:toxicity
chemical_list: D018053:Arsenites; D001786:Blood Glucose; D004791:Enzyme Inhibitors; D017382:Reactive Oxygen Species; D017670:Sodium Compounds; C017947:sodium arsenite; D005952:Glucose-6-Phosphatase; D000111:Acetylcysteine