1887

Abstract

The cellular response to the oxidative stress caused by hydrogen peroxide and its putative correlation with the stress protector trehalose was investigated in CAI.4 and the / double mutant, which is deficient in trehalose synthesis. When exponential wild-type blastoconidia were exposed to high concentrations of hydrogen peroxide, they displayed a high cell survival, accompanied by a marked rise of intracellular trehalose. The latter is due to a moderate activation of trehalose synthase and the concomitant inactivation of neutral trehalase. Identical challenge in the / double mutant severely reduced cell viability, a phenotype which was suppressed by overexpression of the gene. Pretreatment of growing cultures from both strains with either a low, non-lethal concentration of HO (05 mM) or a preincubation at 37 °C, induced an adaptive response that protected cells from being killed by a subsequent exposure to oxidative stress. During these mild oxidative preincubations, trehalose was not induced in CAI.4 cells and remained undetectable in their / counterpart. Blastoconidia from the two strains exhibited a similar degree of cell protection during the adaptive response. The induction of trehalose accumulation by HO was not due to an increased expression of mRNA. These results are consistent with a mainly protective role of trehalose in during direct oxidative stress but not during acquired oxidative tolerance.

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2002-08-01
2020-08-10
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