Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 2018 Aug 2:9:945.
doi: 10.3389/fphys.2018.00945. eCollection 2018.

Is "Preparation for Oxidative Stress" a Case of Physiological Conditioning Hormesis?

Marcus F Oliveira  1 , Marcio A Geihs  2 , Thiago F A França  2 , Daniel C Moreira  3   4 , Marcelo Hermes-Lima  4
Affiliations

Is "Preparation for Oxidative Stress" a Case of Physiological Conditioning Hormesis?

Marcus F Oliveira et al. Front Physiol. .
No abstract available

Keywords: antioxidant; biochemical adaptation; estivation; hypoxia; oxidative stress; reactive oxygen species; redox.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Molecular oxygen is absolutely required for maintenance of cellular energy and redox homeostasis across different animal species. Although some organisms cannot tolerate slight hypoxia, others can adapt to and survive strong shortages in oxygen supply even for long periods of time. A common trend observed in some hypoxia-tolerant animals is their enhanced capacity to boost antioxidant defenses during a number of stresses, a phenomenon known as “preparation for oxidative stress” (POS). POS was identified in animals from 8 distinct phyla and despite the molecular mechanisms are not fully understood, we have recently proposed an explanation (Hermes-Lima et al., 2015), where the role of phosphatases and kinases in POS is highlighted herein, as well as the increased cellular oxidant production under hypoxia (A). During hypoxia, the redox state of ETS and mitochondrial dehydrogenases shifts toward a reduced state due to limited electron transfer from cytochrome c oxidase to oxygen. This leads to increased electron availability in many enzymes/complexes involved in redox reactions, consequently favoring superoxide production (Smith et al., 2017). Importantly, given that a very small percentage of molecular oxygen is converted to superoxide in isolated mammalian mitochondria (about 0.2%, Tahara et al., 2009) and that this figure is likely to be much lower in vivo (Murphy, 2009), it is suggestive that the electron availability, not oxygen concentration, would be the limiting factor in mitochondrial superoxide production (Campian et al., 2007). Therefore, even in hypoxia, increases in electron availability should boost mitochondrial superoxide production—at least until molecular oxygen concentration becomes so low that electron availability ceases to be the limiting factor. Thus, the overall pattern observed is an increase in oxidant formation during hypoxia. The pattern of transient activation of antioxidant defenses along hypoxic challenges, and the improved protection against stressful insults generated afterwards, follows the same trend observed in many cases of physiological conditioned hormesis. Limited time and magnitude exposure of animals to insults including hypoxia/anoxia, freezing and severe dehydration, as well as to conditions inducing estivation, activates a “physiological program” that reduces adaptive failure and/or mortality upon stronger challenges (the “hormetic zone”), as proposed in the hormesis concept. “Conditioned re-oxygenation” (or reoxygenation-like, during dehydration/rehydration and freezing/thawing), shown in (B), is a state where the protective POS-response range is maximum. However, longer and/or stronger exposure to these insults revert the protective hormetic effects (the “harmful zone”), increasing adaptive failure. Therefore, given their remarkable similarities in biological and biochemical outputs, we propose that POS should be included as a new example of physiological conditioning hormesis. Graphic elements adapted from Servier Medical Art.
See this image and copyright information in PMC

References

    1. Calabrese E. J. (2016). Preconditioning is hormesis part I: documentation, dose-response features and mechanistic foundations. Pharmacol. Res. 110, 242–264. 10.1016/j.phrs.2015.12.021 - DOI - PubMed
    1. Calabrese E. J., Bachmann K. A., Bailer A. J., Bolger P. M., Borak J., Cai L., et al. . (2007). Biological stress response terminology: integrating the concepts of adaptive response and preconditioning stress within a hormetic dose-response framework. Toxicol. Appl. Pharmacol. 222, 122–128. 10.1016/j.taap.2007.02.015 - DOI - PubMed
    1. Calabrese E. J., Blain R. (2005). The occurrence of hormetic dose responses in the toxicological literature, the hormesis database: an overview. Toxicol. Appl. Pharmacol. 202, 289–301. 10.1016/j.taap.2004.06.023 - DOI - PubMed
    1. Calabrese E. J., Blain R. B. (2011). The hormesis database: the occurrence of hormetic dose responses in the toxicological literature. Regul. Toxicol. Pharmacol. 61, 73–81. 10.1016/j.yrtph.2011.06.003 - DOI - PubMed
    1. Calabrese V., Cornelius C., Dinkova-Kostova A. T., Iavicoli I., Di Paola R., Koverech A., et al. . (2012). Cellular stress responses, hormetic phytochemicals and vitagenes in aging and longevity. Biochim. Biophys. Acta 1822, 753–783. 10.1016/j.bbadis.2011.11.002 - DOI - PubMed

LinkOut - more resources