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The reproductive development of alligators from a contaminated and a control lake in central Florida was examined. Lake Apopka is adjacent to an EPA Superfund site, listed due to an extensive spill of dicofol and DDT or its metabolites. These compounds can act as estrogens. Contaminants in the lake also have been derived from extensive agricultural activities around the lake that continue today and a sewage treatment facility associated with the city of Winter Garden, Florida. We examined the hypothesis that an estrogenic contaminant has caused the current failure in recruitment of alligators on Lake Apopka. Supporting data include the following: At 6 months of age, female alligators from Lake Apopka had plasma estradiol-17 beta concentrations almost two times greater than normal females from the control lake, Lake Woodruff. The Apopka females exhibited abnormal ovarian morphology with large numbers of polyovular follicles and polynuclear oocytes. Male juvenile alligators had significantly depressed plasma testosterone concentrations comparable to levels observed in normal Lake Woodruff females but more than three times lower than normal Lake Woodruff males. Additionally, males from Lake Apopka had poorly organized testes and abnormally small phalli. The differences between lakes and sexes in plasma hormone concentrations of juvenile alligators remain even after stimulation with luteinizing hormone. Our data suggest that the gonads of juveniles from Lake Apopka have been permanently modified in ovo, so that normal steroidogenesis is not possible, and thus normal sexual maturation is unlikely. Images p680-a Figure 1. Figure 2. Figure 3. A Figure 3. B Figure 3. C Figure 4. A Figure 4. B Figure 4. C Figure 4. D Figure 5. A Figure 5. B Figure 5. C

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.

Lactating pregnant and nonpregnant dairy cows were used to determine if summer heat stress alters responsiveness of the uterus to an oxytocin-induced secretion of prostaglandin F 2α . Cows were assigned to thermoneutral (evaporatively-cooled barn), or heat stress (exposure to summer environment) treatments for 7.5 h on Day 17 post-estrus. Blood samples were collected during the first 6 h. Oxytocin (100 IU) was then administered and blood collected for a further 1.5 h. Conceptuses were recovered nonsurgically to determine pregnancy status. Prior to oxytocin treatment, plasma concentrations of 13,14-dihydro-15-keto PGFM 2α (PGFM) were similar among cows, regardless of treatment or pregnancy status. Oxytocin increased mean PGFM concentrations, but the increase was higher for nonpregnant and pregnant cows with embryos retarded in development than for pregnant cows with normal embryos. Heat stress increased oxytocin-induced PGFM concentrations in nonpregnant cows, but had no effect on PGFM in pregnant cows. Endometrial explants from cyclic and pregnant cows were used to determine if heat-induced endometrial secretion of prostaglandin (PG, PGF and PGE 2 ) is regulated by an intracellular inhibitor of PG synthesis. Endometrial explants were incubated at 39 or 42°C, and conditioned medium analyzed for PGF and PGE 2 . Cotyledonary microsomes from parturient cows were utilized as a PG generating system for detection of endometrial inhibitors of PG synthesis. Endometrial synthesis of PGE at 39°C was greater for cyclic than pregnant cows, while PGE 2 synthesis was similar between statuses. Heat stress increased PGF and PGE 2 synthesis by endometrium from cyclic and pregnant cows. Synthesis of PGF by the generating system was decreased 44% when incubated with endometrium of pregnant cows cultured at 39°C and this decrease was 35.3% less with cytosol from endometrium of pregnant cows incubated at 42°C. Decreased uterine PGF production by pregnant cows, carrying viable embryos, in response to oxytocin in vivo and by endometrial explants from pregnant cows, indicates that the conceptus attenuates release of uterine PGF. Heat stress amplified PG synthesis by nonpregnant cows and in endometrial explants from cyclic and pregnant cows. Decreased responsiveness of the pregnant uterus to oxytocin and heat stress suggests a conceptus-induced factor attenuates responsiveness of the uterine PG generating system to stimulation by heat stress.