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In this study, we investigated the role played by cytoplasmic catalase (Ctt1) in resistance against water loss using the yeast Saccharomyces cerevisiae as eukaryotic cell model. Comparing a mutant possessing a specific lesion in CTT1 with its parental strain, it was observed that both control and ctt1 strains exhibited increased levels of lipid peroxidation after dehydration, suggesting that catalase does not protect membranes during drying. Although the ctt1 strain has only 1 catalase isoform (peroxisomal catalase), the mutant showed the same levels of total catalase activity as the control strain. Furthermore, in cells deficient in Ctt1, the reduced glutathione:oxidized glutathione ratio (GSH:GSSG) of dry cells was higher than that of the control strain, indicating a compensatory mechanism of defense in response to dehydration. Even so, desiccation tolerance of the ctt1 strain was significantly lower than in the control strain. Using a fluorescent probe sensitive to oxidation, we observed that cells of the ctt1 strain showed levels of intracellular oxidation 70% higher than those of control strain, suggesting that Ctt1 plays a role in the maintenance of the intracellular redox balance during dehydration and, therefore, in tolerance against a water stress.

No abstract

Alzheimer's disease is the most common neurodegenerative disorder. One of the factors that promotes neurodegeneration is the accumulation of senile plaques formed by Aβ peptide. In this paper, it was analyzed that if oxidative stress is cause or consequence of amyloid cascade and the role of antioxidant defense system in this process, using S. cerevisiae (with a multicopy plasmid containing the Aβ1-42 sequence) as experimental model. Cells grown on glycerol were more tolerant than when grown on glucose, strengthening the role of the antioxidant defense system against Aβ accumulation. Antioxidant defense deficiency did not change the pattern of amyloid aggregation. On the other hand, the presence of Aβ increased the level of intracellular oxidation and induced the activity of catalase, superoxide dismutase, and aconitase. Peroxissomal catalase deficient cells (Δcta1), were more sensitive to Aβ toxicity than the wild type strain, while mitochondrial superoxide dismutase (Sod2) deficient cells displayed the highest frequency of petites. Besides, Aβ alters the oxygen consumption and the activity of complex III and IV. Taken together, our results point out that the Aβ toxicity mechanism involves an oxidative stress induction by increasing ROS production into the mitochondria, where Cta1 and Sod2 play a crucial role in the regulation of the redox balance. J. Cell. Biochem. 118: 1442-1452, 2017. © 2016 Wiley Periodicals, Inc.