Salmonid sexual development is not consistently altered by embryonic exposure to endocrine-active chemicals.
Fish sexual development is sensitive to exogenous hormone manipulation, and salmonids have been used extensively as environmental sentinels and models for biomedical research. We simulated maternal transfer of contaminants by microinjecting rainbow trout (Oncorhynchus mykiss) and chinook salmon (Oncorhynchus tshawytscha) embryos. Fish were reared for 6 months and sexed, and gonads were removed for histology and measurement of in vitro steroid production. Analysis of fat samples showed that dichlorodiphenylethylene (DDE) levels, o, p'M-DDE and p,o, p'-DDE isomers, were elevated 6 months after treatment. A preliminary study showed an increased ratio of males to females after treatment with 80 mg/kg and 160 mg/kg of the xenoestrogen o,o, p'-DDE. One fish treated with 160 mg/kg o,o, p'-DDE had gonads with cells typical of both males and females. A follow-up study, using more fish and excluding the highly toxic 160 mg/kg o,o, p'-DDE dose, showed no effect on sex ratio or gonadal histology. Embryonic exposure of monosex male trout, monosex female trout, and mixed sex salmon to o, o, p'-DDE, p,o, p'-DDE, mixtures of DDE isomers, and octylphenol failed to alter sexual development. We observed no treatment-dependent changes in in vitro gonadal steroid production in any experiments. Trout exposed in ovo and reared to maturity spawned successfully. These results suggest that mortality attributable to the xenoestrogens o,o, p'-DDE, chlordecone, and octylphenol, and the antiandrogen p,o, p'-DDE, is likely to occur before the appearance of subtle changes in sexual development. Because trout appeared to be sensitive to endocrine disruption, we cannot dismiss the threat of heavily contaminated sites or complex mixtures to normal sexual development of salmonids or other aquatic organisms.
Carlson
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DB
Department of Environmental and Molecular Toxicology and Marine Freshwater Biomedical Sciences Center, Oregon State University, Corvallis, Oregon 97331, USA.
Curtis
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LR
Williams
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DE
D000818:Animals; D007631:Chlordecone / Q000009:adverse effects*; D003633:Dichlorodiphenyl Dichloroethylene / Q000009:adverse effects*; D012734:Disorders of Sex Development; D004353:Drug Evaluation, Preclinical; D004625:Embryo, Nonmammalian / Q000187:drug effects*; D004784:Environmental Monitoring / Q000379:methods; D004967:Estrogens / Q000009:adverse effects*; D005260:Female; D006066:Gonads / Q000187:drug effects / Q000648:ultrastructure; D007306:Insecticides / Q000009:adverse effects*; D008297:Male; D018811:Maternal Exposure / Q000009:adverse effects*; D008845:Microinjections; D008939:Mitotane / Q000009:adverse effects / Q000031:analogs & derivatives*; D017686:Oncorhynchus mykiss; D010573:Pesticide Residues / Q000009:adverse effects / Q000032:analysis; D010636:Phenols / Q000009:adverse effects*; D012474:Salmon; D012733:Sex Differentiation / Q000187:drug effects*
D004967:Estrogens; D007306:Insecticides; D010573:Pesticide Residues; D010636:Phenols; D003633:Dichlorodiphenyl Dichloroethylene; D008939:Mitotane; C054919:2,2-(2-chlorophenyl-4'-chlorophenyl)-1,1-dichloroethene; C105260:4-tert-octylphenol; D007631:Chlordecone