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. 1998 Feb;106(Suppl 1):357–362. doi: 10.1289/ehp.98106s1357

Hormesis as a biological hypothesis.

E J Calabrese 1, L A Baldwin 1
PMCID: PMC1533282  PMID: 9539030

Abstract

A comprehensive effort was undertaken to identify articles demonstrating chemical hormesis. Nearly 4000 potentially relevant articles were retrieved from preliminary computer database searches by using various key word descriptors and extensive cross-referencing. A priori evaluation criteria were established including study design features (e.g., number of doses, dose range), statistical analysis, and reproducibility of results. Evidence of chemical hormesis was judged to have occurred in approximately 350 of the 4000 studies evaluated. Chemical hormesis was observed in a wide range of taxonomic groups and involved agents representing highly diverse chemical classes, many of potential environmental relevance. Numerous biological end points were assessed; growth responses were the most prevalent, followed by metabolic effects, longevity, reproductive responses, and survival. Hormetic responses were generally observed to be of limited magnitude. The average low-dose maximum stimulation was approximately 50% greater than controls. The hormetic dose-response range was generally limited to about one order of magnitude, with the upper end of the hormetic curve approaching the estimated no observable effect level for the particular end point. Based on the evaluation criteria, high to moderate evidence of hormesis was observed in studies comprised of > 6 doses; with > 3 doses in the hormetic zone. The present analysis suggests that chemical hormesis is a reproducible and relatively common biological phenomenon. A quantitative scheme is presented for future application to the database.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

  1. Calabrese E. J., Baldwin L. A., Mehendale H. M. G2 subpopulation in rat liver induced into mitosis by low-level exposure to carbon tetrachloride: an adaptive response. Toxicol Appl Pharmacol. 1993 Jul;121(1):1–7. doi: 10.1006/taap.1993.1121. [DOI] [PubMed] [Google Scholar]
  2. Calabrese E. J., McCarthy M. E., Kenyon E. The occurrence of chemically induced hormesis. Health Phys. 1987 May;52(5):531–541. doi: 10.1097/00004032-198705000-00002. [DOI] [PubMed] [Google Scholar]
  3. Calabrese E. J., Mehendale H. M. A review of the role of tissue repair as an adaptive strategy: why low doses are often non-toxic and why high doses can be fatal. Food Chem Toxicol. 1996 Mar;34(3):301–311. doi: 10.1016/0278-6915(95)00101-8. [DOI] [PubMed] [Google Scholar]
  4. Davis J. M., Svendsgaard D. J. U-shaped dose-response curves: their occurrence and implications for risk assessment. J Toxicol Environ Health. 1990 Jun;30(2):71–83. doi: 10.1080/15287399009531412. [DOI] [PubMed] [Google Scholar]
  5. Stebbing A. R. Hormesis--the stimulation of growth by low levels of inhibitors. Sci Total Environ. 1982 Feb;22(3):213–234. doi: 10.1016/0048-9697(82)90066-3. [DOI] [PubMed] [Google Scholar]
  6. TOWNSEND J. F., LUCKEY T. D. Hormoligosis in pharmacology. J Am Med Assoc. 1960 May 7;173:44–48. doi: 10.1001/jama.1960.73020190007010. [DOI] [PubMed] [Google Scholar]
  7. Vichi P., Tritton T. R. Stimulation of growth in human and murine cells by adriamycin. Cancer Res. 1989 May 15;49(10):2679–2682. [PubMed] [Google Scholar]

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