Hormesis

Hormesis is a biological phenomenon where a low dose of a potentially harmful stressor, such as a toxin or environmental factor, stimulates a beneficial adaptive response in an organism. In other words, small doses of stressors that would be damaging in larger amounts can actually enhance resilience, stimulate growth, or improve health at lower levels. [1]

Hormesis is a two-phased dose-response relationship to an environmental agent whereby low-dose amounts have a beneficial effect and high-dose amounts are either inhibitory to function or toxic.[1][2][3][4] Within the hormetic zone, the biological response to low-dose amounts of some stressors is generally favorable. An example is the breathing of oxygen, which is required in low amounts (in air) via respiration in living animals, but can be toxic in high amounts, even in a managed clinical setting.[5]

In toxicology, hormesis is a dose-response phenomenon to xenobiotics or other stressors. In physiology and nutrition, hormesis has regions extending from low-dose deficiencies to homeostasis, and potential toxicity at high levels.[6] Physiological concentrations of an agent above or below homeostasis may adversely affect an organism, where the hormetic zone is a region of homeostasis of balanced nutrition.[7] In pharmacology, the hormetic zone is similar to the therapeutic window.

In the context of toxicology, the hormesis model of dose response is vigorously debated.[8] The biochemical mechanisms by which hormesis works (particularly in applied cases pertaining to behavior and toxins) remain under early laboratory research and are not well understood.[6]

  1. ^ a b Bhakta-Guha, Dipita; Efferth, Thomas (2015-12-16). "Hormesis: Decoding Two Sides of the Same Coin". Pharmaceuticals (Basel, Switzerland). 8 (4): 865–883. doi:10.3390/ph8040865. ISSN 1424-8247. PMC 4695814. PMID 26694419.
  2. ^ Mahalakshmi, R.; Priyanga, J.; Bhakta-Guha, Dipita; Guha, Gunjan (2022-01-01). "Hormetic effect of low doses of rapamycin triggers anti-aging cascades in WRL-68 cells by modulating an mTOR-mitochondria cross-talk". Molecular Biology Reports. 49 (1): 463–476. doi:10.1007/s11033-021-06898-6. ISSN 1573-4978. PMID 34739690.
  3. ^ Mahalakshmi, R.; Priyanga, J.; Bhakta-Guha, Dipita; Guha, Gunjan (2022-10-01). "Hormetic alteration of mTOR–mitochondria association: An approach to mitigate cellular aging". Current Opinion in Environmental Science & Health. 29: 100387. doi:10.1016/j.coesh.2022.100387. ISSN 2468-5844.
  4. ^ Calabrese EJ (2014). "Hormesis: a fundamental concept in biology". Microbial Cell. 1 (5): 145–9. doi:10.15698/mic2014.05.145. PMC 5354598. PMID 28357236.
  5. ^ Hochberg CH, Semler MW, Brower RG (September 2021). "Oxygen toxicity in critically ill adults". American Journal of Respiratory and Critical Care Medicine. 204 (6): 632–641. doi:10.1164/rccm.202102-0417CI. PMC 8521700. PMID 34086536.
  6. ^ a b Mattson, M. P (2007). "Hormesis defined". Ageing Research Reviews. 7 (1): 1–7. doi:10.1016/j.arr.2007.08.007. PMC 2248601. PMID 18162444.
  7. ^ Hayes, D. P. (2007). "Nutritional hormesis". European Journal of Clinical Nutrition. 61 (2): 147–159. doi:10.1038/sj.ejcn.1602507. ISSN 1476-5640. PMID 16885926.
  8. ^ Cite error: The named reference Kaiser was invoked but never defined (see the help page).