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Malondialdehyde–Superoxide Dismutase Redox Imbalance as an Early Biological Risk Indicator in Young Adult Smokers

Aug 2026 · Vascular Health and Risk Management · Vol 22, pp. 1-9 · 0 citations · 27 references
Medicine

TL;DR

Findings indicate a measurable oxidant–antioxidant imbalance associated with biochemical tobacco exposure in young adults and highlight the relevance of the MDA–SOD redox interplay as a biologically coherent marker pair for assessing early smoking-related redox disturbance in young adults.

Abstract

Purpose Young adult smokers represent a population in which smoking-related health risks may accumulate silently before the onset of clinically apparent disease. Although smoking-related changes in malondialdehyde (MDA) and superoxide dismutase (SOD) have been widely reported, less is known about their combined oxidant–antioxidant pattern in apparently healthy young adults during the early smoking trajectory. This study aimed to compare serum MDA and SOD levels between young adult smokers and non-smokers and to evaluate the MDA–SOD interplay as a marker of early redox imbalance. Patients and Methods A comparative cross-sectional study was conducted involving 190 participants aged 18–25 years, comprising 95 smokers and 95 non-smokers recruited from university communities. Smoking exposure was assessed using structured interviews and quantified by the Heaviness of Smoking Index and serum cotinine level. Serum MDA, SOD, and cotinine levels were measured using enzyme-linked immunosorbent assay methods. Group comparisons were performed using appropriate parametric or non-parametric tests, and associations between oxidative stress biomarkers were analysed using Spearman and Pearson correlation. Results Smokers exhibited significantly higher serum MDA concentrations than non-smokers [median 3.28 nmol/mL (range, 1.75–5.89) vs 2.27 nmol/mL (range, 0.99–5.83); p < 0.001] and significantly lower SOD activity (132.4 ± 26.7 vs 158.3 ± 29.1 U/L; p < 0.001). Across all participants, serum cotinine was positively associated with MDA (Spear man’s ρ = 0.576, p < 0.001) and inversely associated with SOD (Pearson’s r = −0.518, p < 0.001). MDA was also inversely associated with SOD (Spearman’s ρ = −0.318, p < 0.001). These findings indicate a measurable oxidant–antioxidant imbalance associated with biochemical tobacco exposure in young adults. Conclusion Young adult smokers exhibit early oxidant–antioxidant imbalance indicative of subclinical biological vulnerability associated with smoking exposure. These findings highlight the relevance of the MDA–SOD redox interplay as a biologically coherent marker pair for assessing early smoking-related redox disturbance in young adults.

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