There is a considerable body of evidence indicating that oxidative stress is a causal factor both in lipofuscinogenesis as well as in aging. Studies on the effects of pro-oxidants and antioxidants on lipofuscin accumulation in cultured rat cardiac myocytes and human glial cells indicated that pro-oxidants accelerate while antioxidants retard the rate of lipofuscin accumulation. Lipofuscin was measured by microspectrofluorometry; the reliability of this method was independently validated by comparison with electron microscopical morphometry. In vivo studies on hibernating mammals and on insects indicate that rate of lipofuscin is enhanced while life span is shortened by elevation in metabolite rate. The increase in metabolic rate has been shown to enhance the rate of lipid peroxidation, measured as n-pentane exhalation in vivo. Overall, it seems that there is enough evidence at hand to reasonably infer that lipofuscin can be used as a marker of oxidative stress and aging.