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Background: Numerous recent studies have suggested that oxidative damage may be important in the ageing process, and lipid peroxidation is an important biological consequence of oxidative cellular damage. Objective: The aim of this work was to analyze the activities of the two protective enzymes, superoxide dismutase (SOD) and catalase (CAT), and the levels of malondialdehyde (MDA) to examine the relationship between the ageing process and defence antioxidant and lipid peroxidation. Method: SOD activity was measured in red blood cells using the Minami and Yoshikawa method; CAT activity was measured in hemolysates by the Aebi method, and MDA levels were measured in erythrocytes by high-performance liquid chromatography. Results: SOD activity shows statistically significant differences between newborns and the rest of the sample (ANOVA p < 0.001; Student-Newman-Keuls test p < 0.001). CAT activity did not show significant differences between the age groups. We observed statistically significant differences in MDA levels between the different groups (ANOVA p < 0.001; Student-Newman-Keuls test p < 0.05). In the regression analysis and rectilinear/curvilinear adjustment compared to age, SOD and CAT showed coefficients close to zero (SOD linear = 0.16; SOD exponential = 0.15; CAT linear = 0.056; CAT exponential = 0.068), indicating in that way their independence from age. Only MDA obtained a regression coefficient superior to 0.75 (p < 0.05). The best adjustment was reached through an exponential expression, giving the following parametric relation: MDA = 103.117e^0.0021.AGE. No statistically significant variation in SOD and CAT activity and MDA levels, related to sex could be demonstrated. Conclusions: Our data show that old age is associated with an increase in systemic oxidative stress.

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Urinary 8-OHdG, 15-F(2t)-IsoP and AGEs may represent a non-invasive quantitative index of oxidant stress in healthy smokers, being AGEs a possible indicator of tobacco toxin exposure. The increased oxidative stress in healthy smokers observed may be generated because of an excessive production of reactive oxygen species and not by exhaustion of antioxidant defenses.