Unbalance between Pyridine Nucleotide Cofactors in The SOD1 Deficient Yeast <i>Saccharomyces cerevisiae</i> Causes Hypersensitivity to Alcohols and Aldehydes

Alcohol and aldehyde dehydrogenases are especially relevant enzymes involved in metabolic and detoxification reactions that occur in living cells. The comparison between the gene expression, protein content, and enzymatic activities of cytosolic alcohol and aldehyde dehydrogenases of the wild-type s...

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Bibliographic Details
Main Authors: Magdalena Kwolek-Mirek, Sabina Bednarska, Aleksandra Dubicka-Lisowska, Roman Maslanka, Renata Zadrag-Tecza, Pawel Kaszycki
Format: Article
Language:English
Published: MDPI AG 2022-12-01
Series:International Journal of Molecular Sciences
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Online Access:https://www.mdpi.com/1422-0067/24/1/659
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Summary:Alcohol and aldehyde dehydrogenases are especially relevant enzymes involved in metabolic and detoxification reactions that occur in living cells. The comparison between the gene expression, protein content, and enzymatic activities of cytosolic alcohol and aldehyde dehydrogenases of the wild-type strain and the Δ<i>sod1</i> mutant lacking superoxide dismutase 1, which is hypersensitive to alcohols and aldehydes, shows that the activity of these enzymes is significantly higher in the Δ<i>sod1</i> mutant, but this is not a mere consequence of differences in the enzymatic protein content nor in the expression levels of genes. The analysis of the NAD(H) and NADP(H) content showed that the higher activity of alcohol and aldehyde dehydrogenases in the Δ<i>sod1</i> mutant could be a result of the increased availability of pyridine nucleotide cofactors. The higher level of NAD<sup>+</sup> in the Δ<i>sod1</i> mutant is not related to the higher level of tryptophan; in turn, a higher generation of NADPH is associated with the upregulation of the pentose phosphate pathway. It is concluded that the increased sensitivity of the Δ<i>sod1</i> mutant to alcohols and aldehydes is not only a result of the disorder of redox homeostasis caused by the induction of oxidative stress but also a consequence of the unbalance between pyridine nucleotide cofactors.
ISSN:1661-6596
1422-0067