Dietary exposure of largemouth bass to OCPs changes expression of genes important for reproduction.
Dieldrin and p,p'-DDE are ubiquitous contaminants known to act as endocrine disruptors, causing impaired development and reproduction in fish and wildlife. In order to elucidate the mechanisms by which dieldrin and p,p'-DDE cause endocrine disruption in largemouth bass (Micropterus salmoides), fish were exposed subchronically through the diet to both contaminants. Following 120 days of exposure, p,p'-DDE decreased estradiol in females, but increased 11-ketotestosterone in both sexes. Dieldrin on the other hand, decreased estradiol and 11-ketotestosterone in both sexes. Both pesticides also altered steady state mRNA expression levels of a set of genes chosen to represent three possible mechanisms of endocrine disruption: (1) direct interaction with soluble sex steroid receptors, (2) biosynthesis of endogenous sex hormones, and (3) metabolism of endogenous hormones. p,p'-DDE acted as a weak estrogen, increasing the expression of vitellogenin and estrogen receptor alpha in the liver. p,p'-DDE also altered the expression of genes involved in the synthesis of endogenous hormones as well as their metabolism. Dieldrin, on the other hand, only altered expression of vitellogenin and not estrogen receptor alpha. Dieldrin also altered the expression of genes involved in hormone synthesis and metabolism, and it dramatically lowered plasma hormone levels. Both pesticides targeted expression of genes involved in all three modes of action, suggesting that they each have multiple modes of action.
Garcia-Reyero
Natàlia
N
Department of Physiological Sciences and Center for Environmental and Human Toxicology, University of Florida, Gainesville, FL, USA.
Barber
David S
DS
Gross
Timothy S
TS
Johnson
Kevin G
KG
Sepúlveda
María S
MS
Szabo
Nancy J
NJ
Denslow
Nancy D
ND
D000818:Animals; D001492:Bass / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D003577:Cytochrome P-450 Enzyme System / Q000096:biosynthesis / Q000235:genetics; D003633:Dichlorodiphenyl Dichloroethylene / Q000493:pharmacokinetics / Q000633:toxicity*; D004026:Dieldrin / Q000493:pharmacokinetics / Q000633:toxicity*; D015536:Down-Regulation / Q000187:drug effects; D052244:Endocrine Disruptors / Q000493:pharmacokinetics / Q000633:toxicity*; D004958:Estradiol / Q000097:blood; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D008297:Male; D010575:Pesticides / Q000493:pharmacokinetics / Q000633:toxicity*; D010750:Phosphoproteins / Q000096:biosynthesis / Q000235:genetics; D012333:RNA, Messenger / Q000096:biosynthesis / Q000235:genetics; D011960:Receptors, Estrogen / Q000096:biosynthesis / Q000235:genetics / Q000378:metabolism; D012098:Reproduction / Q000187:drug effects / Q000235:genetics; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000662:veterinary; D013739:Testosterone / Q000031:analogs & derivatives / Q000097:blood; D014819:Vitellogenins / Q000235:genetics / Q000378:metabolism; D000098682:Steroidogenic Acute Regulatory Protein
D052244:Endocrine Disruptors; D010575:Pesticides; D010750:Phosphoproteins; D012333:RNA, Messenger; D011960:Receptors, Estrogen; D014819:Vitellogenins; D000098682:Steroidogenic Acute Regulatory Protein; D013739:Testosterone; D003633:Dichlorodiphenyl Dichloroethylene; D004958:Estradiol; D003577:Cytochrome P-450 Enzyme System; D004026:Dieldrin; C003600:11-ketotestosterone