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Tobacco smoking is a practice of burning tobacco and inhaling the smoke (consisting of gaseous phases and particles). A more broad definition may include taking tobacco smoke into the mouth, and then releasing it, as is done by some with tobacco pipes and cigars. The practice may have begun as early as 5000-3000 BC (Nagaraj et al., 2014). Cigarette smoking is probably the most addictive and dependence producing form of object-specific, self-administered gratification known to man. According to present estimates, tobacco is responsible for causing more than 5 million deaths every year (World Health Organization, 2008).

The harmful effects of cigarette smoking on human health have been well documented. It has been known that cigarette smoke carries around 4000 chemicals including toxic metals, poisonous gases and free radicals (Schumacher et al., 2009). Amongst these constituents, free radicals are considered to be more dangerous as these owing to their unpaired electron

are highly reactive and can cause oxidative damage to biomolecules and biomembranes (Sen et al., 2010).

Smoking plays an important role in disturbing the antioxidant balance. Normally blood contains a healthy complement of antioxidants that keep oxidative damage to a minimum. Tobacco smoke contains abundant reactive oxygen species and also activated neutrophils released due to smoking also add to the pool of reactive oxygen species which deplete these antioxidant mechanisms leading to tissue damage (Kumar et al., 2010).

Malondialdehyde is a organic compound with the formula CH2 (CHO). This reactive species occurs naturally and is a marker for oxidative stress. Reactive oxygen species degrade polyunsaturated lipids present on cell membrane forming malondialdehyde. This aldehyde product is used as a biomarker to measure the level of oxidative stress in an organism (Nagaraj et al., 2014).

Antioxidants depletion or deficiency may contribute to oxidative stress. Antioxidants not only protect against the direct injurious effects of oxidants, but also alter the inflammatory events that play an important role in the pathogenesis of oxidative stress related diseases (MacNee, 2010). Vitamin C is a water soluble free radical scavenger, can directly scavenge O2 and OH- radicals and help to neutralize physiological oxidant burden created by both exogenous and endogenous sources (Rai and Phadke, 2006).

Vitamin E, a well-known chain-breaking antioxidant in cell membrane protects the membrane against lipid peroxidation either directly by scavenging the free radicals or indirectly by controlling the reduced glutathione levels. Vitamin E itself is kept in reduced state by vitamin C, another antioxidant vitamin (Shah et al., 2015).



The act of smoking has been a contributing effect to so many physiologic disorder; with enormous release of free radicals and important biochemical intermediates, they have been implicated in a very large number of human diseases including ischaemic heart disease, cancer, diabetes mellitus, cataract, respiratory diseases and ageing. Some studies have been done to compare the level of lipid peroxidation products and antioxidant vitamin among smokers and non-smokers but there is scarcity of such study in Africa.  Therefore, the present study was undertaken to assess the levels of lipid peroxidation product, Malondialdehyde and antioxidants (vitamin C and vitamin E) in smokers and non-smokers.









To evaluate the level of vitamin C, Vitamin E and Malondialdehyde in male smokers and non smokers.


  1. To determine the levels of malondialdehyde in adult smokers;
  2. To determine the levels of vitamin C in adult smokers;
  3. To determine the levels of vitamin E in adult smokers.


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