Asymmetric Redox Status and Cardiovascular Risk Factors in Smoker Women and Men

Abstract

Profuse epidemiological evidence supports a higher risk for coronary heart disease and stroke in smoker women than in men with the same habit. Although it is already known that cigarette smoking alters the redox state, is unknown if the imbalance in the normal equilibrium between oxidants and antioxidants is responsible for the elevated female susceptibility. Therefore, the aim of this work was to estimate the effect of smoking on serum redox status in women compared with men, accounting for divergences in other major risk factors for cardiovascular disease. Lipid profile, antioxidant capacity, and serum carbonyls were assessed in 116 healthy Uruguayans, composed by 50 females and 66 males. The smoking habit was declared by 17 females (34 %) and 36 males (54 %). The lipid profile was modified by cigarette smoking, affecting in a different way males and females. In particular, HDL-C that was higher in non-smoker females (59 (28) mg/dL) than in non-smoker males (46 (14) mg/dL) significantly decreased in smoker females (51 (13) mg/dL), remaining unchanged in the smoker male population (42 (12) mg/dL). Conversely LDL-C, which gave similar values for non-smoker females (110.1 ± 35.2 mg/dL) and males (98.5 ± 36.0 mg/dL), increased exclusively in smoker males (122.2 ± 36.4 mg/dL, p<0.05). In turn, the level of serum antioxidants that was higher in non-smoker males (1.9  0.3 mM FRAP) than females (1.5  0.4 mM /FRAP), remained unchanged in smokers. Similar results were obtained for carbonyls, which showed higher levels in non-smoker males (0.90 ± 0.32 nmol/mg of protein) than females (0.74 ± 0.32 nmol/mg of protein), and while the level remained unmodified in smokers males (0.86  0.28 nmol/mg of protein) increased non-significantly in smoker females (0.79  0.31 nmol/mg of protein). Whereas the oxidation index correlated positively with LDL-C (r = 0.45) in smoker males, and with triglycerides in both non-smoker and smoker females(r = 0.42 and 0.79, respectively), a negative and intense correlation with HDL-C (r = -0.79), and a positive one with the LDL-C/HDL-C index (r = 0.87) was observed exclusively in smoker females. Our results point to an association at the molecular level between oxidative stress footprints and plasma lipoprotein/cholesterol concentration predominantly in smoker females, and support the concept that the higher sensitivity of women to smoking related cardiovascular pathology is associated with oxidants-mediated biomolecular insults.