Role of antioxidant enzymatic defences against oxidative stress (H2O2) and the acquisition of oxidative tolerance in Candida albicans

In Candida albicans, trehalose plays an essential role as a protector of cell integrity against oxidative challenge. A double homozygous mutant, tps1/tps1, deficient in trehalose synthesis, displayed severe cell mortality when exposed to high H2O2 concentrations, compared with its congenic parental (CAI‐4) strain (Alvarez‐Peral et al., 2002 ). We have examined the putative role of a set of well‐known antioxidant enzymes as components of the defence mechanism against oxidative challenges. When exposed to mild non‐lethal oxidative treatment (0.5 mM H2O2), a significant induction of catalase, glutathione reductase (GR), and Cu,Zn‐superoxide dismutase (SOD) was recorded in tps1/tps1 exponential cultures. However, in CAI‐4 cells, subjected to the same conditions, there was only a clear activation of catalase, Mn‐SOD and Cu,Zn‐SOD activities. The degree of activation was always much more pronounced in the trehalose‐deficient mutant than in its wild‐type counterpart, except for Mn‐SOD activity. After exposure to severe oxidative stress (50 mM H2O2) only GR and catalase activities increased in tps1/tps1 cultures, whereas in CAI‐4 cells GR but not catalase was induced. In both cell strains, 50 mM H2O2 caused inhibition of the Mn‐ and Cu,Zn‐SOD isozymes, this inhibition being more pronounced in tps1/tps1 cells. C. albicans is able to acquire adaptive oxidative tolerance by pretreatment with a low non‐stressing concentration of H2O2 before exposure to a drastic oxidative challenge. When these antioxidant activities were measured during the adaptive response, a greater degree of enzymatic antioxidant induction was consistently observed in the tps1/tps1 mutant with respect to the CAI‐4 strain. Together with a higher intrinsic sensitivity of tps1/tps1 cells, we suggest that this unexpected increase might be explained in terms of a compensatory mechanism to overcome the lack of endogenous trehalose upon drastic oxidative exposure, although this induction was not sufficient to improve the percentage of cell viability. Copyright © 2003 John Wiley & Sons, Ltd.