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For decades, conventional thinking has championed the idea that oxidative stress — the internal and external factors that give rise to oxidative damage to cellular proteins, membranes, and DNA — was “bad”, serving as the rationale for using dietary supplementation with antioxidants as a strategy to promote health and fight disease. Yet, even today, the precise role of reactive oxygen species (ROS) in most human diseases remains mostly unknown [1,2]. In some instances, elevated markers of oxidative damage may merely correlate with pathology, rather than be causative. Antioxidant interventions may lower oxidative damage, but still have no significant impact on disease outcomes. Methodological shortcomings encountered in the measurement of ROS production and oxidative damages need to be meticulously addressed so that sound conclusions can be drawn from the burgeoning number of clinical and mechanistic studies [1].

acta scientific nutritional health

A Matter of Context: How an Understanding of Redox Homeostasis Informs the Consideration of Pro-oxidant Strategies to Target Tuberculosis, HIV, and Cancer Metastasis