Academic journal article Journal of Health Population and Nutrition

Protective Effect of Fish Oil Supplementation on DNA Damage Induced by Cigarette Smoking

Academic journal article Journal of Health Population and Nutrition

Protective Effect of Fish Oil Supplementation on DNA Damage Induced by Cigarette Smoking

Article excerpt

INTRODUCTION

8-hydroxy-2'-deoxyguanosine (8-OHdG) is a product of oxidative DNA damage induced by the action of hydroxyl radicals on the DNA base deoxyguanosine (dG) (1,2) and DNA single-strand breakage (3,4). Damage to DNA may lead to the initiation of carcinogenesis. Evidence suggests that 8-OHdG is reflective of the potentially-precancerous disease processes. However, the precise predictive value of 8-OHdG for the development of cancer remains obscure (5). A decrease in 8-OHdG would show a decrease in oxidative damage to DNA (6).

Several studies have examined the effects of dietary intake of antioxidant nutrients, such as vitamin E, vitamin C, and [beta]-carotene on biomarkers of oxidative stress (7). As dietary supplementation with n-3 fatty acids may diminish the release of free radicals from stimulated human monocytes and polymorphonuclear cells, changes in the cellular free radical production due to omega-3 fatty acids may, in turn, influence cell-mediated oxidative modifications of DNA in vivo (8).

Some studies, with contradictory results, have evaluated the effect of omega-3 fatty acids on oxidative DNA damage in animal and human models (9). Manna S et al. (10) reported in an in vivo study that n-3 polyunsaturated fatty acids (PUFAs) protect against the generation of DNA-strand breaks in rat mammary carcinogenesis. However, some reports have indicated that lipid peroxides that arise from both spontaneous and enzymatic oxidation of polyunsaturated fatty acids are the major source of endogenous DNA damage linked to various age-related pathologies and initiating carcinogenesis (11).

Cigarette smoke contains approximately 1 x [10.sup.15] free radicals per puff (12) and is believed to induce oxidative stress in the body through several mechanisms, including direct damage by free radicals and inflammatory responses. Peroxyl radicals and reactive nitrogen species (13), including NO, ONO[O.sup.-], and ROONO (1), directly damage (13) biological systems by stimulating lipid peroxidation (6,13) and oxidizing and nitrating proteins, lipids, and DNA bases (13). Relatively high amounts of these free radicals and other oxygen-derived species in cigarette smoke can deplete antioxidants, modify proteins and amino acids, promote atherosclerotic disease, and oxidize lipoproteins, particularly lowdensity lipoprotein (LDL) which is more atherogenic than native LDL (7,14). The hydroquinone/quinine complexes of tar-phase cigarette smoke diffuse across cell membranes and produce semiquinones, superoxide radicals ([O.sub.2.sup.-]), and hydrogen peroxide ([H.sub.2][O.sub.2]) (3). Smoking causes inflammatory reactions in the lungs, which may lead to elevated oxidative stress and pulmonary diseases (15).

Epidemiological studies have shown that cigarette smoking is a main contributory factor for biomolecular damage, tissue injuries, and long-term associations with cigarette smoke-related diseases. Nearly 50% of the deaths in the industrialized world result from coronary artery disease. There is increasing evidence that cigarette smoking contributes considerably to this mortality (3,12). The available evidence also demonstrates that cigarette smoke induces the formation of 8-OHdG (1-4). It has been demonstrated that smokers are exposed to high concentrations of oxidants and free radicals from both gas-phase cigarette smoke and particulate matter (14,16). These free radicals are a major cause of oxidative damage to macromolecules, such as lipids, proteins, and DNA, and deplete some plasma antioxidants in vitro (17). Additionally, as polyunsaturated fatty acids (PUFAs) are highly susceptible to free radical oxidation, current smoking may reduce the amount of PUFAs in plasma and red blood cells (18). Therefore, smoking cigarettes may lead to an enhanced requirement for PUFAs. Long-chain polyunsaturated omega-3 fatty acids, such as docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA), that are mainly found in fish oil have been shown to reduce the risk of age-related macular degeneration (19) and chronic obstructive pulmonary disease (20) in cigarette smokers. …

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