Protective effect of acetic acid against ethanol-induced cell death in Saccharomyces cerevisiae

Abstract

Ethanol is a well-known end product of alcoholic fermentation carried out by Saccharomyces cerevisiae. At high concentrations it is responsible for the reduction of cell viability and inhibition of fermentation. Furthermore, during fermentation some weak acids such as acetic, butyric and pyruvic acids, produced by yeast metabolism may accumulate in the growth medium, and enhance ethanol toxicity resulting in a higher inhibition of growth and fermentation. However, previous data obtained in our lab showed that S. cerevisiae cells treated simultaneously with toxic concentrations of ethanol and low concentrations of acetic acid displayed higher survival (measured either by CFU or by propidium iodide staining) when compared to cells treated only with ethanol. These results indicated that acetic acid induces a cellular response that provides protection against the cytotoxic effect of ethanol (Vieira et al unplublished results). Subsequently we showed that mitogen-activated protein kinase (MAPK) Hog1p and the aquoglyceroporin Fps1p, involved in acetic acid resistance, did not mediate this protective effect of the acid1. The aim of the present work was to study the role of other signaling pathways and the mechanisms conferring protection of acetic acid against death induced by ethanol (13% v/v, pH 3.5). We found that this effect is dose-dependent being optimal for 0.1% (v/v) of acetic acid, Propionic, but not lactic or formic acids, also confer protection. Deficiency in the MAPK Slt2/Mpk1, known to be activated in the presence of acetic acid2, partially revert the protective effect, especially regarding the preservation of plasma membrane integrity. The presence of trehalose in the culture medium promoted the protective effect of acetic acid. Threalose transport and accumulation seem to be necessary for protection by acetic acid of the plasma membrane integrity but not of cell viability. A Rho o mutant of the wild type strain did not display higher cell viability in the presence of acetic acid, when compares ethanol treatment alone, suggesting that mitochondria may be involved in the protective effect.

1. Trindade, D. A. M. (2009). Tese de Mestrado em Genética Molecular, Escola de Ciências, Universidade do Minho, Braga. 2. Mollapour, M. & Piper, P. W. (2006). FEMS Yeast Res 6,1274–1280.