Editorial: Understanding the impact of loneliness and social isolation on the health of older adults with cancer.

Cigarette smoking is a well-established exogenous source of reactive oxygen species (ROS) and reactive nitrogen species (RNS), generating a substantial oxidative burden that disrupts cellular and systemic redox homeostasis. Each puff of cigarette smoke introduces a complex mixture of free radicals and pro-oxidant compounds capable of overwhelming endogenous antioxidant defences, particularly under habitual exposure. When oxidant generation exceeds antioxidant capacity, oxidative stress ensues, triggering early molecular disturbances implicated in endothelial dysfunction, mitochondrial impairment, redox-sensitive signalling dysregulation, and increased tissue vulnerability. Importantly, these biochemical alterations often precede overt clinical manifestations, positioning oxidative stress as an early biological signal of future health risk rather than an immediate disease outcome. One of the most prominent consequences of excessive ROS exposure is lipid peroxidation, a chain reaction that damages polyunsaturated fatty acids within cellular membranes. Malondialdehyde (MDA), a stable terminal product of lipid peroxidation, is widely recognised as a reliable biomarker of oxidative lipid injury and systemic oxidative stress. Elevated MDA concentrations reflect enhanced membrane damage and are closely linked to inflammatory activation and altered cellular function., In contrast, superoxide dismutase (SOD) represents a primary enzymatic antioxidant defence, catalysing the dismutation of superoxide radicals into hydrogen peroxide and molecular oxygen. Alterations in SOD activity therefore serve as sensitive indicators of compromised antioxidant capacity. Rather than interpreting MDA or SOD in isolation, their combined evaluation provides a biologically coherent representation of redox imbalance: MDA reflects downstream oxidative lipid injury, whereas SOD reflects the enzymatic antioxidant response to superoxide burden. The reciprocal behaviour of these two biomarkers, conceptualised as the MDA–SOD redox interplay, offers a mechanistically informative framework for evaluating oxidant–antioxidant balance and early biological vulnerability in vivo. Although smoking-related oxidative stress has been extensively documented, important knowledge gaps remain regarding how these markers behave together during the early stages of smoking exposure, particularly among apparently healthy young adults. Existing evidence has predominantly focused on older individuals or populations with established cardiometabolic or pulmonary comorbidities. In contrast, young adult smokers remain comparatively underrepresented in redox biology and health risk research, despite young adulthood representing a critical window during which chronic oxidative exposure may initiate subtle biochemical perturbations that predispose individuals to long-term disease trajectories. Emerging evidence indicates that markers of oxidative stress and impaired antioxidant capacity can already be detected in young smokers at a subclinical stage, even in the absence of symptoms or diagnosed disease, suggesting that biological risk accumulation begins early in the smoking trajectory., Therefore, the novelty of the present study lies not in assessing MDA or SOD as standalone biomarkers, but in examining their oxidant–antioxidant relationship in young adult smokers before clinically apparent disease is present.