The purpose of this study was to examine the effect of different levels of cigarette smoking on lipid peroxidation, glutathione enzymes and paraoxonase 1 (PON1) activity in a healthy population. The study included 130 subjects who were classified as mild (20 cigarettes daily, Group III, n=33) and never smokers (controls, Group IV, n=32). Malondialdehyde (MDA) levels, PON1 and erythrocyte glutathione enzyme activities were measured. MDA levels were significantly higher in smokers than never smokers (P<0.05 for Group I, P<0.001 for Group II and III). PON1 activity was significantly lower in heavy smokers (P<0.001). Glutathione peroxidase (GSH-Px) activity was significantly lower in the smokers (P<0.0001). Glutathione reductase (GR) activity was significantly higher in smokers (P<0.0001). MDA levels negatively correlated with PON1 and GSH-PX activities (P<0.01), whereas they positively correlated with GR activities (P<0.001). At every level, cigarette smoking is associated with increased lipid peroxidation and causes an impairment in antioxidant systems.

Increased Cys C and beta2-microglobulin in diabetics may be early indicators of incipient DN. The diagnostic accuracies of Cys C and beta2-microglobulin are superior to that of serum creatinine in distinguishing between mild and moderately reduced GFR.

Results of this study indicate that lower serum PON1 activity is associated with oxidative stress and the activity of PON1 is not related to HDL-cholesterol.

Oxidative stress contributes to the pathogenesis of H/R-induced intestinal injury. The glutathione redox cycle may have a crucial role in the H/R-induced intestinal injury. L-arginine and L-carnitine supplementations ameliorate the histological evidence of H/R-induced intestinal injury and decrease lipid peroxidation but do not alter the glutathione-related antioxidant enzyme activities.

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