Ascorbate prevents prooxidant effects of vanadium pentoxide on wildtype Saccharomyces cerevisiae UEME3

Abstract

Vanadiumpentoxide,V2O5, (V5+) themosttoxiccompoundof vanadium behaves as an amphoteric oxide and a powerful oxidizing agent which may be an oxidative stress inducer. The vanadium (V5+) is generally reduced by living cells to vanadium (V4+), less toxic, using enzymes which mobilize the reducing equivalents of NADPH, or nonenzymatically using ascorbate. Nevertheless, species generated by vanadium (V4+) from H2O2 and lipid peroxidation, via Fenton reaction can have a significant role in the metabolism of vanadium and induce cell damage in physiological conditions. Although vanadium is an element with ubiquitous environmental distribution, combustion of fossil fuels represents an important source of vanadium in the environment. Biological studies to evaluate the influence of vanadium on living organisms has shown that is mutagenic and genotoxic. Having in account that toxicity mechanisms of vanadium on eukaryotic cells are not entirely clear, the main objectives of this work was to evaluate the synergistic effects of 0.025mMascorbate vs 2mMV2O5 on cell survival, alkaline phosphatase (ALP), catalases A and T (CAT A, T) and glutathione reductase (GR) activities of Saccharomyces cerevisiae UEME3. Cells at midexponential phase were inoculated in YEPD medium with 2% (w/v) glucose and incubated during 72 h in a water bath with orbital stirring, at 28 ◦C, in the absence or in presence of 2mM V2O5, or 0.025mM ascorbate plus 2mM V2O5. Samples from each treatment were used to obtain growth curves and to prepare post12,000 g supernatant, used for enzymatic activities determination. The results shown that ascorbate counteracted growth inhibition, the decrease of ALP and CAT activities, as well as the increase of GR antioxidants activities, caused by 2mMV2O5, to values similar of control cells.