Exploring Antioxidants

Abstract

The antioxidant, reactive species, oxidative stress nexus The term 'antioxidant' is used with ever-increasing frequency in both the popular media and biomedical literature. Notwithstanding its common usage, it can be a difficult term to define precisely. According to one current and useful definition from an authoritative source, antioxidant refers to "any substance that delays, prevents, or removes oxidative damage to a target molecule" (1). In the human body, antioxidants help to prevent, protect, or reduce damage to biological molecules from exposure to specific chemical substances, known as reactive species and which are often generated by endogenous metabolic processes. These reactive species comprise free radicals, such as the hydroxyl radical and superoxide radical, and non-radicals, which include hydrogen peroxide, peroxynitrite ions and hypochlorous acid (2). Notably, the range of biologically important reactive species is believed to be counteracted in vivo by an impressive array of antioxidant biomolecules. These include the antioxidant enzymes: catalase, superoxide dismutase and glutathione Stransferase; endogenously synthesized molecules such as glutathione and thioredoxin; and nutritionally derived antioxidants, such as vitamin C and vitamin E (3, 4). A severe imbalance between the generation of reactive species and their removal by antioxidants can result in a phenomenon typically referred to as oxidative stress (1). Oxidative stress, in turn, has been implicated in the pathogenesis of a wide variety of diseases, such as stroke, diabetes, breast cancer and severe acute malnutrition (5).

A cross‐sectional clinic‐based study exploring whether variants within the glutathione S‐transferase, haptoglobin and uridine 5′‐diphospho‐glucuronosyltransferase 1A1 genes are associated with interindividual phenotypic variation in sickle cell anaemia in Jamaica

“…Free haem, a potent pro-oxidant, can generate reactive oxygen species (such as the superoxide anion and hydroxyl radical) at accelerated rates, which could, in turn, result in oxidative stress, a pathophysiological state that can be defined as a severe imbalance between the generation of reactive species and their safe disposal. 9,10 Our hypothesis is that functional polymorphisms within genes coding for molecules that perform these protective roles might be causally related to deficits in the capacity to respond to the heightened demands imposed by accelerated rates of haemolysis and so might underlie phenotypic variability among HbSS patients. Accordingly, in this study, we report findings from a cross-sectional study involving participants from an internationally recognised sickle cell clinic that explores whether specific, well-defined functional variants within the GST, UGT1A1 and HP genes are associated with interindividual variation in HbSS.…”

“…Protective processes mediated through these functional variants might be of pivotal importance in HbSS, where elevated rates of intravascular haemolysis will typically increase free haem concentrations. Free haem, a potent pro‐oxidant, can generate reactive oxygen species (such as the superoxide anion and hydroxyl radical) at accelerated rates, which could, in turn, result in oxidative stress, a pathophysiological state that can be defined as a severe imbalance between the generation of reactive species and their safe disposal …”