Cellular injury oxidative stress

Whilst experimentally it is relatively easy to investigate the eflFect of the exogenous application of GSH and GSSG on cardiac Na/K ATPase activity, one further approach that has been exploited in many aspects of oxidant-induced cell injury has been the depletion of cellular glutathione levels. The hypothesized importance of GSH in the cell s antioxidant armoury would be expected to be reflected in an increased susceptibility to oxidant stress-... 

Exposure of cells to elevated temperatures, or heat shock, induces the transcription and translation of a set of proteins known as the heat-shock proteins (HSPs) or the stress proteins. This event usually occurs with the concomitant inhibition of biosynthesis of other cellular components. The response is believed to be an attempt by the cells to protect themselves from injury, and there is some evidence to indicate that it may also be linked to oxidative stress. Evidence in favour of this idea comes from observations such as the following ... 

All aerobic organisms contain substances that help prevent injury mediated by free radicals, and these include antioxidants such as a-tocopherol and the enzymes superoxide dismutase and glutathione peroxidase. When the protective effect of the antioxidants is overwhelmed by the production of reactive oxygen species, the intracellular milieu becomes oxidative, leading to a state known as oxidative stress (Halliwell and Gutteridge, 1999). Thus the balance between the generated free radicals and the efficiency of the protective antioxidant system determines the extent of cellular damage. 

The loss of control of endogenous oxidative events in the use of molecular oxygen by the cell is the major factor in oxidative stress injury. Such a process, which is known as chemical-induced oxidative stress, may occur to an extent that ranges from a minor to a major contribution to overall toxicity. For example, chemicals that are known to undergo redox cycling cause exogenous oxidative stress to such a degree that they play a major role in chemically induced cell injury. In addition, some of these chemicals are known to form adducts with cellular constituents, particularly... 

The model of carbon monoxide toxicity proposed by Kao and Nanagas (2006) combines the cascade of changes resulting from three primary events - binding to HB, direct cellular injury, and increased NO activity. CO is not a radical but many of the injuries produced by it are those that are caused by oxidative stress, which is secondary to hypoxia. In the model of Kao and Nanagas (2006), the oxidant is NO, which contributes to oxidative damage to the brain and produces the clinical syndrome of delayed neurologic sequelae (Thom et al, 1997). 

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