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1. Introduction
Cigarette smokers continuously inhale thousands of carcinogens and free radicals. It is estimated that about 1017 oxidant molecules are present in each puff of cigarette smoke [1]. Free radicals are known to cause oxidative damage by increasing polymorphonuclear leukocytes and by inducing lipid peroxidation [2, 3]. Additionally, several markers of oxidative stress are elevated in cigarette smokers. These include increased release of reactive oxygen species from phagocytes, such as superoxide from peripheral blood neutrophils, oxidized low density lipoprotein cholesterol (LDL), increased lipid hydroperoxides and malondialdehyde, and decreased plasma antioxidant capacity [4–11].
Among the many adverse health effects from cigarette smoke are dyslipidemia and systemic inflammation. The fact that cigarette smoke increases total cholesterol and triglycerides, as well as decreases high density lipoprotein cholesterol (HDL), has long been established. A meta-analysis of 54 studies revealed that smokers have about 3% higher serum cholesterol and 9% greater serum triglyceride concentrations than nonsmokers. Smokers were also found to have 5.7% lower HDL than nonsmokers [12]. The increases in total cholesterol and triglycerides, with the corresponding decreases in HDL, were found to be dose-dependent when the data were analyzed by smoking frequency. Population-based studies have also revealed that markers of systemic inflammation, such as C-reactive protein (CRP), are also elevated in smokers as well as those exposed to second-hand smoke [13, 14]. Smoking-related elevations in CRP are also accompanied with a rise in serum homocysteine levels [15].
While the molecular mechanisms of tobacco smoke toxicity are still not fully understood, free radical-mediated oxidative stress is believed to play a central role [16, 17]. Oxidative stress, as measured by serum malondialdehyde concentration, is positively correlated to elevated triglyceride and cholesterol levels in smokers [18]. Not only does cigarette smoke increase oxidative stress by increasing free radicals but also by weakening of antioxidant defenses, such as decreasing paraoxonase enzyme activity [19]. These conditions lead to the damage of mitochondria [20], and cigarette smoke may even induce liver injury via lipid peroxidation and corresponding inflammation [21, 22]. Such alterations are likely to lead to imbalances in lipid metabolism.
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