Pesticides: multiple mechanisms of demasculinization.
Many pesticides are known to produce reproductive and developmental effects in chronically exposed non-target organisms, including humans. Recent evidence suggests that demasculinization may be an important mechanism responsible for some of these effects. Some pesticides have been shown to interact with the androgen receptor and to act as antagonists, while others have been shown to interact with the estrogen receptor and function as estrogens in both in vitro and in vivo. Many pesticides can also lower serum androgen levels by altering rates of synthesis or metabolism. Given the ubiquity of pesticides in the environment and the multiple mechanisms whereby they can elicit demasculinizing effects, synergy between such compounds may produce clinical endocrine dysfunction at current human exposure levels.
LeBlanc
G A
GA
Department of Toxicology, North Carolina State University, Raleigh 27695-7633, USA.
Bain
L J
LJ
Wilson
V S
VS
D000726:Androgen Antagonists / Q000494:pharmacology*; D059002:Androgen Receptor Antagonists; D000818:Animals; D005260:Female; D005262:Feminization / Q000139:chemically induced; D005837:Genitalia, Male / Q000187:drug effects* / Q000254:growth & development; D006801:Humans; D008297:Male; D010575:Pesticides / Q000494:pharmacology*; D011960:Receptors, Estrogen / Q000187:drug effects
D000726:Androgen Antagonists; D059002:Androgen Receptor Antagonists; D010575:Pesticides; D011960:Receptors, Estrogen