Abstract
Cadmium is a heavy metal that has no known beneficial biological role. Although naturally occurring, it owes its presence in todays environment mainly to contamination from consumer goods (electric batteries, paints, etc.), industrial wastes, and soil fertilizers. Cadmium is a constituent of foods (seafood, grains, vegetables) and tobacco smoke, which are its main sources of exposure to the general population. Human exposure has been linked to a vast array of ill effects ranging from those affecting lung, kidney and bone, to those affecting reproductive organs and specific cell functions. By virtue of its demonstrated capacity to alter the rates of ovarian and placental steroidogenesis, thereby adversely impacting normal reproduction in both humans and animals, cadmium has been added to the list of acknowledged endocrine disrupting chemicals (EDCs). Extensive evidence suggests direct effects on specific components of the steroidogenic pathway, including the low density lipoprotein (LDL)-cholesterol receptor and P450 side chain cleavage enzyme. In addition to exerting its effects via both transcriptional and post-transcriptional mechanisms, cadmium may also regulate hormone binding and intracellular second messenger pathways. Women may be at increased risk for the reproductive anomalies associated with exposure and, as demonstrated in numerous studies, the metal may also function as a potent nonsteroidal agent; a xenoestrogen, that can mimic or block the effects of endogenous estrogens. The effects of cadmium on reproduction, combined with its abundance in the human environment, continue to call for more detailed studies dedicated to elucidating the mechanisms that control the metals influence as an EDC.
Keywords: Cadmium, Endocrine Disruption, Environmental Exposure, Toxic Metals, Ovary, Placenta, Reproduction, Steroidogenesis
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