Ameliorative Role of Dietary Supplemented Conjugated Linolenic Acid against Nicotine-Induced Toxicity in Rats

Krishna Chattopadhyay,

doi:10.4172/2153-2435.1000182

Abstract

Increasing consumption of tobacco in different forms harms almost every organs of our body. Nicotine is the culprit for various physiological repercussions arouse due to the uptake of tobacco. As nutritional status alters the actions, potencies and detoxification of toxicants, the present study was undertaken to evaluate the natural antioxidant efficacy of conjugated linolenic acid present in Karalla seed against nicotine-induced toxicity. Experiments were conducted on male albino rats (120–130 g body weight) by injecting nicotine tartarate (3.5 mg/kg body wt. /day for 15 days) subcutaneously and thereby simultaneously supplementing conjugated linolenic acid (0.5 and 1.0%) to their diets. Nicotine significantly altered serum and liver lipid profiles, lipid peroxidation and activities of antioxidant enzymes. It caused significant decrease of DNA contents (P<0.01) and DNA damage (P<0.001) of liver tissue. Conjugated linolenic acid has the ability to bind with DNA and protein similar to nicotine and thereby ameliorates nicotine-induced toxicity in rats. Thus intake of Karalla that contains conjugated linolenic in its seeds, in our daily diet can effectively attenuate nicotine-induced cellular and genetic damages.

Highlights

IntroductionNicotine the culprit component of tobacco causes oxidative damage in the tissues and nucleic acids leading to several diseases
Increasing uses of tobacco products is an alarming danger for health worldwide [1]
It was noted that conjugated linolenic acid supplementation significantly ameliorated the nicotine-induced oxidative damage in rats and the effect was more prominent when used at lower concentration of conjugated linolenic acids (CLnA) in the diet

Summary

Introduction

Nicotine the culprit component of tobacco causes oxidative damage in the tissues and nucleic acids leading to several diseases. During the smoking of cigarette and/or chewing of tobacco, nicotine is at first being converted into highly mutagenic nitrosamine and later metabolized into cotinine [3]. Experiments have shown that chronic administration of nicotine causes increased lipid peroxidation products in serum and various tissues of rats, which is dose dependent [4]. The increase of lipid peroxidative products is associated with decreased activity of endogenous antioxidants, catalase and superoxide dismutase [5]. Kleinsasser et al [7] have shown that nicotine expresses significant direct genotoxic effects in human target cells in vitro. Nicotine exerts genotoxic effect on hepatic cells [8] and blood cells [9] of rat

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Conclusion