Essay about Resistance to Stress
Caloric restriction extends longevity in yeast because the absence of Tor/Sch9 signaling causes a metabolic change that uses acetic acid, which is similar to the generation and use of ketone bodies, acetoacetic acid, and lower than that of glucose (Wei et al., 2009). High levels of acetic acid promotes apoptosis in yeast and is the primary factor promoting culture acidification, chronological aging, and apoptotic death (Burtner et al., 2009). Tor/Sch9 pathway blocks the utilization of acetate. Tor-Sch9 deficiency extends longevity by switching cells to an alternative metabolic mode, in which acetic acid can be utilized for the storage of stress resistance carbon sources.
According to Figure 1, they established the relationship between carbon source metabolites and CLS by measuring the levels of ethanol and acetic acid in chronologically aged yeast cultures. As previously stated (Fabrizio et al., 2005), ethanol remained relatively high in wild-type cultures until day 9, while it drops by day 3 in sch9D and ras2D mutants (Fig. 1B). These data rule out the possibility that wild-type cells die from carbon source starvation. Therefore, the removal of ethanol may partially contribute to the lifespan extension effects of Sch9 or Ras2 deficiency. Yeast cells were grown in SDC containing variant percentages of glucose supplemented with excess amounts of tryptophan, leucine, histidine, and uracil to avoid possible lifespan modification due to auxotrophic deficiencies of the strains. This is helpful to know to remove any other reasons for these yeast to live/die longer/faster.
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Stress resistance assay was used to examine whether the carbon source influences stress resistance. The cells were challenged with heat shock and oxidative stress (H2O2 treatment for 30 min) after switching them to various carbon sources for 24 hours. At physiological concentrations, all the carbon sources sensitized yeast cells only to oxidative stress (Fig. 2B). The effects found within this experiment on yeast are similar to those in mammals. This experiment of depleting extracellular glucose and other nutrients is similar to that of the ketone diet, where there is a metabolic change that utilizes acetic acid and induces more ketone bodies. In mammalian cells, ketone bodies, including acetone, acetoacetic acid, and b-hydroxybutyric acid, are generated from fatty acids and ketogenic amino acids catabolism. The usage of acetate shares similarities to ketone bodies via generation of leucine. However, the mechanisms underlying the aging process in mammals remain poorly understood.
The effect of energy intake on lifespan is well documented in organisms ranging from bacteria to mice and other mammals. In fact, a 20–40% restriction in calories intake extends lifespan and reduces the incidence of a variety of diseases (Wei et al., 2008; Fontana et al., 2010). Because high levels of acetic acid have been shown to cause apoptosis in yeast (Ludovico et al., 2001), the observation that acetic acid accumulates in cultures of nondividing yeast led to the hypothesis that acetic acid plays a key role in yeast chronological aging (Burtner et al., 2009; Kaeberlein, 2010).