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Mutagenous effects of hormones

作者
Ninoslav Djelić,Dijana Đelić
出处
期刊:University of Belgrade, Faculty of Veterinary Medicine - Veterinar – Repository of the Faculty of Veterinary Medicine, University of Belgrade 卷期号:40 (4): 53-67
摘要

There is a widely accepted view that the endogenous substances, including hormones, do not have any mutagenous effect when present in the usual physiological concentrations. However, beside relative stability and permanence of the genetic material, its changeability is also needed to provide for the biological evolution. Thus, it is possible to expect that certain reactions, due to the complexity of the mechanism of the signal transduction under the effect of hormones, still lead to the creation of reactive derivatives able to inter-react with the DNA molecules thus encouraging the emergence of mutations. This paper gives a survey of the exploration of the hormones' genotoxic effects in various test-systems, namely, from the bacteric through the cell cultures and experiments in vivo upon laboratory guinea-pigs, up to the determination of the mutagenous effects in the people that were treated by hormones. The steroid hormones' effects are described in detail in the literature while, on the other hand, there is not sufficient knowledge yet about possible changes of the genetic material under the influence of the non-steroid hormones. The examinations of the steroid hormones geonotoxicity in the bacterial systems have mainly given negative results. In more complex eukaryotic systems in vitro and in vivo most of the steroid hormones manifest mutagenous effects, though the result may vary depending one the type of cell or the biological species used in the experiment. As for the non-steroid hormones, though they have been studied less, it seems that they do not mostly express mutagenous effects. Today it is clear that the steroid hormones (especially estrogen) are completely cancerigenic and that they are capable of encouraging the process of cancerogenesis both by inducing covalent simulating the cell division (tumor promoters).

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