Abstract
Acetic acid has long been considered a molecule of great interest in the yeast research field. It is mostly recognized as a by-product of alcoholic fermentation or as a product of the metabolism of acetic and lactic acid bacteria, as well as of lignocellulosic biomass pretreatment. High acetic acid levels are commonly associated with arrested fermentations or with utilization as vinegar in the food industry. Due to its obvious interest to industrial processes, research on the mechanisms underlying the impact of acetic acid in yeast cells has been increasing. In the past twenty years, a plethora of studies have addressed the intricate cascade of molecular events involved in cell death induced by acetic acid, which is now considered a model in the yeast regulated cell death field. As such, understanding how acetic acid modulates cellular functions brought about important knowledge on modulable targets not only in biotechnology but also in biomedicine. Here, we performed a comprehensive literature review to compile information from published studies performed with lethal concentrations of acetic acid, which shed light on regulated cell death mechanisms. We present an historical retrospective of research on this topic, first providing an overview of the cell death process induced by acetic acid, including functional and structural alterations, followed by an in-depth description of its pharmacological and genetic regulation. As the mechanistic understanding of regulated cell death is crucial both to design improved biomedical strategies and to develop more robust and resilient yeast strains for industrial applications, acetic acid-induced cell death remains a fruitful and open field of study.
Highlights
Acetic acid, or ethanoic acid (CH3COOH), is a weak organic acid best known as a frequent by-product of the alcoholic fermentation carried out by Saccharomyces cerevisiae and the main component of volatile acidity in wine
The present review aims to cover the current understanding of cell death induced by acetic acid and how this knowledge paves the way to its modulation in yeast-based bioprocesses
These data indicate that there is an intricate connection between the vacuole and mitochondria in AA-regulated cell death (RCD) involving the release of Pep4p, which mirrors the crosstalk between the lysosome and mitochondria in acetate-induced RCD in colorectal cancer (CRC) cells and the release of cathepsin D (CatD) (Pereira et al, 2010; Antonacci et al, 2012; Marques et al, 2013; Oliveira et al, 2015)
Summary
Ethanoic acid (CH3COOH), is a weak organic acid best known as a frequent by-product of the alcoholic fermentation carried out by Saccharomyces cerevisiae and the main component of volatile acidity in wine. It was first demonstrated that exposure of S. cerevisiae and of the non-conventional spoilage yeast Zygosaccharomyces parabailii ISA 1307 (formerly Z. bailii) to high concentrations of acetic acid (1–3% (v/v), 173–520 mM), pH 3.0, resulted in a late loss of plasma membrane integrity in both strains preceded by a deficit in vacuolar processing of the FUN-1 stain, reflecting a decrease in metabolic activity (Prudêncio et al, 1998) It was only in the beginning of the 21st century that biochemical markers of cell death induced by acetic acid were characterized for the first time. Acetic acid was shown to impact mitochondrial phospholipids, inducing a reduction of almost 50% in their relative phosphatidylinositol content (Martins et al, 2019)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
