engleski

Potential of metals to act as endocrine-disrupting chemicals in human reproduction

Synthetic endocrine disrupting (ED) chemicals can mimic, enhance, or inhibit the action of endogenous hormones that are responsible for maintaining homeostasis and controlling normal development. They have been a focus of major concern since the early 1990s in mammals including humans. Reproductive and developmental toxicology studies have yielded increasing evidence that metals and metalloids (cadmium, lead, mercury, arsenic, uranium, and other) have the insidious ED potential and may act as metalloestrogens in reproductive tissues and during foetal development (Henson MC, Piasek M et al., In: Endocrine Toxicology 3rd Ed. 2010, pp. 256-79). As for cadmium, within the last two decades human and animal studies have demonstrated its potential to affect gonadotropins, steroidogenesis, and placental leptin that may adversely impact male and female reproductive functions. Our own research work in experimental animals under in vivo and in vitro exposure conditions and in cadmium-exposed tobacco smoking postpartum women has added considerably to the evidence identifying cadmium as an ED chemical in the female reproductive system (Piasek M, Laskey JW et al., IAOEH 2002, 75, S36-44). This is scientifically still a rather controversial issue. A better understanding of ED effects of metals and metalloids bears great clinical relevance as they constitute an important part of our ecosystem and lifestyle and their production and use is unlikely to be discontinued in the foreseeable future. Complementary results attained from different experimental paradigms should all be carefully evaluated. Future research should assess critical exposure levels, reliable endpoints, and underlying mechanisms of endocrine disrupting action in humans.

cadmium exposure; endocrine disruption; metalloestrogens; reproductive and developmental toxicity

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