The aryl hydrocarbon receptor pathway and sexual differentiation of neuroendocrine functions.
Historically, much of the research on health effects of environmental pollutants focused on ascertaining whether compounds were carcinogenic. More recent findings show that environmental contaminants also exert insidious effects by disrupting hormone action. Of particular concern are findings that developmental exposure to dioxins, chemicals that act through the aryl hydrocarbon receptor pathway, permanently alters sexually differentiated neural functions in animal models. In this review, we focus on mechanisms through which dioxins disrupt neuroendocrine development as exemplified by effects on a brain region critical for ovulation in rodents. We also provide evidence that dysregulation of GABAergic neural development may be a general mechanism underlying a broad spectrum of effects seen after perinatal dioxin exposure.
Petersen
Sandra L
SL
Department of Biology, University of Massachusetts-Amherst, Amherst, Massachusetts 01003 USA. sandyp@bio.umass.edu
Krishnan
Sudha
S
Hudgens
Edward D
ED
D000818:Animals; D004147:Dioxins / Q000633:toxicity*; D004781:Environmental Exposure; D004958:Estradiol / Q000502:physiology; D005260:Female; D018698:Glutamic Acid / Q000502:physiology; D006801:Humans; D008024:Ligands; D009474:Neurons / Q000187:drug effects; D009490:Neurosecretory Systems / Q000187:drug effects* / Q000196:embryology*; D000072317:Polychlorinated Dibenzodioxins / Q000633:toxicity; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D018336:Receptors, Aryl Hydrocarbon / Q000502:physiology*; D012098:Reproduction / Q000187:drug effects; D012733:Sex Differentiation; D005680:gamma-Aminobutyric Acid / Q000502:physiology
D004147:Dioxins; D008024:Ligands; D000072317:Polychlorinated Dibenzodioxins; D018336:Receptors, Aryl Hydrocarbon; D018698:Glutamic Acid; D004958:Estradiol; D005680:gamma-Aminobutyric Acid