Background Lipid peroxidation (LPO) is one of the most important effects of ROS-induced cell damage that, along with the formation of reactive and mutagenic aldehyde products such as malondialdehyde (MDA), leads to defective functions in spermatozoa. Total antioxidant capacity (TAC) in the seminal plasma neutralizes ROS so they could be a defense system against LPO. We evaluated the effect of seminal LPO and TAC on the motility and morphology of spermatozoa. We also determined the relationship between cigarette smoking as an exogenous source of ROS in increased levels of MDA and decreased TAC to estimate the intensity of oxidative stress. Methods MDA concentration and the TAC levels of seminal plasma were measured in asthenoteratospermic cigarette smokers (n = 15), asthenoteratospermic non-smokers (n = 17) and healthy non-smokers (n = 13) using the TBARs and FRAP methods, respectively. Results The mean TAC in the seminal plasma of healthy men was significantly higher than that in asthenoteratospermic smokers (P = 0.007) and non-smokers (P = 0.012). In contrast, MDA levels in the control group were significantly lower than in smoking (P = 0.005) and non-smoking (P = 0.031) patients. Conclusions It is suggested that antioxidant deficiency and LPO may contribute to low motility and morphology in the spermatozoa of asthenoteratospermic patients, and that cigarette smoking is a risk factor for increased oxidative damage of seminal plasma in infertile men.
