There is a growing body of evidence demonstrating that exposure of cells to reactive oxygen species (ROS) leads to oxidative modification of nucleic acids, proteins, and lipids, and that such modifications can contribute to the development of a number of diseases and aging. This raises the question: If ROS are so damaging to cells, why have cells selected ROS to trigger activation of so many cell signaling pathways?
We examined the distribution of nonspecific esterase (NSE) activity in the brain of the goldfish, Carawius auracus, and found that the enzyme is expressed at high levels in cells that appeared to be radial astrocytes. Several instances in which neurons expressed NSE activity were also seen. To confirm the identity of the radial profiles as astrocgtes, similar sections were labeled with antiserum against goldfiih glial fibrillary acidic protein (GFAP). The concordance between the NSE and the anti-GFAP data in both the visual system and the telencephalon was essentially complete, confirming that the NSE reaction was labeling astrocytes in these structures. The two methods also gave similar results in both the cerebellum and the vagal lobes, although the concordance between them in these instances was somewhat less complete.
The hypothesis that oxidative damage arising from heat shock might significantly contribute to cell death and in particular to apoptosis has been tested in human peripheral blood lymphocytes. Cellular glutathione content and protein carbonyl groups were measured as indicators of oxidative injury. Cell viability and proliferative capacity were evaluated as measures of irreversible damage. Heat shock caused dose-dependent decreases in cell viability, and apoptotic cell death was found to be a major component of heat-shock-mediated mortality. However, only the more severe heat treatment (1 h, 45°C) caused an immediate decrease in glutathione content. The content in carbonyl groups was not significantly affected by heat shock. N-acetyl-cysteine, when added before the hyperthermic treatment, did increase the glutathione content of the cells, but this did not favourably affect the survival of heat-shocked lymphocytes. It is suggested that oxidative damage is not a significant component of heat shock-mediated cell injury, and that, at least in this experimental model, apoptosis is triggered by stimuli other than an altered redox state of the cell.
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