Reproductive dysgenesis in wildlife: a comparative view.
Abnormal reproductive development in males has been linked to environmental contaminant exposure in a wide variety of vertebrates. These include humans, rodent models, and a large number of comparative wildlife species. In human males, abnormal reproductive development can manifest as a suite of symptoms, described collectively as testicular dysgenesis syndrome (TDS). TDS is also described as demasculinization or feminization of the male phenotype. The suite includes cryptorchidism, in situ germ cell carcinoma of the testis and overt testicular cancer, reduced semen quality, and hypospadias. In this paper, we review examples of TDS among comparative species. Wildlife exposed to environmental contaminants are susceptible to some of the same developmental abnormalities and subsequent symptoms as those seen in human males with TDS. There are additional end points, which are also discussed. In some cases, the symptoms are more severe than those normally seen in humans with TDS (i.e. oocytes developing within the testis) because some non-mammalian species exhibit greater innate reproductive plasticity, and are thus more easily feminized. Based on our review, we present an approach regarding the ontogeny of TDS. Namely, we suggest that male susceptibility to the androgynizing influences of environmental contaminants originates in the sexually undifferentiated embryo, which, in almost all species, including humans, consists of bipotential reproductive tissues. These tissues can develop as either male or female and their ultimate direction depends on the environment in which they develop.
Edwards
Thea M
TM
Department of Zoology, University of Florida, Gainesville, 32611, USA. tedwards@zoo.ufl.edu
Moore
Brandon C
BC
Guillette
Louis J
LJ
D000818:Animals; D000835:Animals, Wild; D003456:Cryptorchidism / Q000473:pathology; D052244:Endocrine Disruptors / Q000633:toxicity*; D004781:Environmental Exposure / Q000009:adverse effects; D005260:Female; D005262:Feminization / Q000139:chemically induced; D006059:Gonadal Dysgenesis / Q000139:chemically induced* / Q000473:pathology; D006801:Humans; D007021:Hypospadias / Q000139:chemically induced / Q000473:pathology; D008297:Male; D009373:Neoplasms, Germ Cell and Embryonal / Q000139:chemically induced / Q000473:pathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects; D013736:Testicular Neoplasms / Q000139:chemically induced / Q000473:pathology; D013737:Testis / Q000187:drug effects* / Q000196:embryology
D052244:Endocrine Disruptors