%0 Journal Article
%T Carbofuran Induced Oxidative Stress in Rat Heart: Ameliorative Effect of Vitamin C
%A Sunil Kumar Jaiswal
%A Nikhat J. Siddiqi
%A B. Sharma
%J ISRN Oxidative Medicine
%D 2013
%R 10.1155/2013/824102
%X The aim of this study was to evaluate the effect of carbofuran on the levels of certain biomarkers in heart of rat exposed to sublethal concentrations of pesticide for 30 days after each interval of 24£¿h. The ameliorative effect of vitamin C by pretreatment of rats was also monitored. The results indicated that the activities of acetylcholinesterase and lactate dehydrogenase (LDH) decreased significantly in rat heart tissues, the extent of inhibition being concentration dependent. In contrast, the level of LDH increased in serum. The levels of malondialdehyde, total thiols, and glutathione were significantly elevated whereas the activities of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione-S-transferase were remarkably decreased in rat heart tissues. The serum concentrations of cholesterol increased by 47 and 77% and high density lipids decreased by 35 and 64%, respectively, due to exposure to 5 and 10% LD50 of carbofuran. The prior treatment of rats with vitamin C (100£¿mg£¿kg£¿1 body weight) exerted significant ameliorative effect. The recovery was higher at low carbofuran concentration (5%) tested. The results indicated that carbofuran induced oxidative stress and caused damage to cardiac tissues, which could be recovered by prior application of vitamin C. 1. Introduction The pesticides have been widely used since past few decades to improve the yield of agricultural and forestry plant products. It is also used to protect the industry and household items. The use of pesticide is not specific which may lead to number of toxicological consequences to the environmental components [1]. The lower toxicity and lesser environmental persistence of organocarbamates have led their application more frequent than any other pesticide such as organophosphate (OP), organochlorines (OCl). The OP pesticides inactivate acetylcholinesterase (AChE) via irreversible ester bond formation with hydroxyl group of serine residue present at the active site of enzyme. AChE is responsible for hydrolyzing the neurotransmitter, acetylcholine (ACh), in central as well as in peripheral nervous systems [2]. The mechanism of action of organochlorine pesticides such as lindane ( -hexachlorocyclohexane) is hyperexcitability [3] by both stimulating the synaptic transmission and suppressing the GABA-activated chloride current by interacting with the receptor GABA-chloride channel complex [4]. The organocarbamate pesticides cause reversible inhibition of AChE by carbamylation of serine residue of AChE. The inhibition is therefore short lived. Thus, it causes
%U http://www.hindawi.com/journals/isrn.oxidative.medicine/2013/824102/