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Neonatal and juvenile alligators from contaminated Lake Apopka in central Florida exhibit abnormal plasma sex steroid concentrations as well as morphological abnormalities of the gonad and phallus. This study addresses whether similar abnormalities occur in juvenile alligators inhabiting six other lakes in Florida. For analysis, animals were partitioned into two subsets, animals 40-79 cm total length (1-3 years old) and juveniles 80-130 cm total length (3-7 years old). Plasma testosterone (T) concentrations were lower in small males from lakes Apopka, Griffin, and Jessup than from Lake Woodruff National Wildlife Refuge (NWR). Similar differences were observed in the larger juveniles, with males from lakes Jessup, Apopka, and Okeechobee having lower plasma T concentrations than Lake Woodruff males. Plasma estradiol-17beta (E(2)) concentrations were significantly elevated in larger juvenile males from Lake Apopka compared to Lake Woodruff NWR. When compared to small juvenile females from Lake Woodruff NWR, females from lakes Griffin, Apopka, Orange, and Okeechobee had elevated plasma E(2) concentrations. Phallus size was significantly smaller in males from lakes Griffin and Apopka when compared to males from Lake Woodruff NWR. An association existed between body size and phallus size on all lakes except Lake Apopka and between phallus size and plasma T concentration on all lakes except lakes Apopka and Orange. Multiple regression analysis, with body size and plasma T concentration as independent covariables, explained the majority of the variation in phallus size on all lakes. These data suggest that the differences in sex steroids and phallus size observed in alligators from Lake Apopka are not limited to that lake, nor to one with a history of a major pesticide spill. Further work examining the relationship of sex steroids and phallus size with specific biotic and abiotic factors, such as antiandrogenic or estrogenic contaminants, is needed.

The relationships between testicular and plasma hormone levels and the decline in fertility in aging roosters were examined. Body mass, testicular mass, and fertility were measured in roosters from 20 to 72 weeks of age. Plasma was assayed for LH and testosterone, and estradiol and testicular extracts were assayed for testosterone and estradiol contents. Fertility increased rapidly in young roosters to a peak of 96.2 +/- 3.9% at 37 weeks of age. Thereafter, fertility declined and by 72 weeks of age was significantly lower than at 37 weeks. Plasma LH reached 16.8 +/- 2.5 ng/ml at 27 weeks and remained high until 60 weeks of age, when it decreased significantly. Plasma and testicular testosterone levels increased from low levels in young birds to a peak that coincided with highest fertility and declined thereafter. Plasma and testicular estradiol showed a striking inverse relationship with testosterone. Plasma estradiol was 29.4 +/- 4.0 pg/ml in 20-week-old birds, decreased rapidly as testosterone increased, and increased again in older birds as testosterone decreased. Thus, the decline in fertility in aging roosters was associated with a decrease in plasma LH and testosterone and an increase in plasma and testicular estradiol. It is suggested that plasma levels of LH and testosterone in roosters are regulated by a negative feedback mechanism involving estradiol that is produced not only by the aromatization of testosterone in the brain but also by peripheral estradiol originating in the testes and that estradiol has a major role in the decline in fertility in aging roosters.

To determine effects of progesterone (P4) treatment on luteinizing hormone (LH) secretion in turkey hens, two trials were conducted. Trial 1 was to determine changes in LH, P4, and testosterone (T) during photostimulation. Photosensitive turkey hens were maintained under short days (SD) of 6 h light and 18 h dark. At the beginning of Trial 1, blood samples were taken daily for 4 days, then one-half of the hens were switched to long days (LD) of 14 h light and 10 h dark, and daily blood samples were continued until 5 days after eggs were laid by all the hens switched to LD. Concentrations of LH, P4, and T increased significantly 1 day after switching hens from SD to LD, but the increase in P4 was initially low with a further increase occurring by 3 days prior to first eggs. In Trial 2, turkey hens were injected with exogenous P4 to determine if P4 is an initiator of the preovulatory surge of LH. P4 or vehicle were injected im in hens at three different reproductive states: (1) while hens were maintained under SD, (2) on the 5th day after hens were switched from SD to LD, and (3) after hens were laying for 1 week. The hens were serially bled at 10-min intervals for 8 h to monitor changes in LH and P4. After 2 h of serial bleeding, P4 or vehicle was injected and bleeding was continued for an additional 6 h. After P4 injection, its concentration increased rapidly from a base level of 0.25-1.20 ng/ml to a postinjection high level of 4.42-6.10 ng/ml within 20 min. The high level of P4 was then maintained throughout the remaining 6 h. No increases of LH secretion were observed after P4 or vehicle injection in hens at either State 1 or State 2. Small increases of LH secretion were detected about 2 h after P4 injection in hens at State 3, but these increases were not significantly above vehicle-injected controls. Thus, there was no positive feedback effect of P4 injection on LH secretion in this trial. These results suggest that P4 might not induce LH secretion in immature or mature turkey hens and might not be the factor which induces the preovulatory surge of LH in laying turkey hens. Nonsteroidal factors of ovarian origin might be involved in regulating the preovulatory surge of LH in turkey hens.

Male Japanese quail were reared on short days (6L:18D) and at 15-20 weeks of age those which had become sexually mature (i.e., scotorefractory) were transferred to long days (18L:6D) for between 2 and 29 weeks. The birds were then returned to 6L:18D for 3 weeks to test for the dissipation of scotorefractoriness. This was assessed by a decrease in at least 3 of 4 indices of reproductive function: testicular weight, area of the cloacal gland, and levels of plasma LH and testosterone. There was great individual variation in the photoperiodic requirement for the dissipation of scotorefractoriness, ranging between 6 and 29 weeks of exposure to long days. Scotorefractoriness was dissipated in about 50% of the birds after exposure to long days for between 6 and 12 weeks. It is concluded that the photoperiodic requirement for the dissipation of scotorefractoriness in quail cannot be defined precisely.

Hormone profiles during the ovulatory cycle were studied in goldfish. Blood samples were taken from female goldfish every 4 days between 1400 and 1700 hr during the course of repeated ovulations for a duration of 3 months, and plasma hormone levels of 3 days before and after ovulation were compared. Plasma gonadotropin (GtH) levels did not show significant changes except a surge for ovulation, but tended to show higher levels before the surge than those after the surge. Plasma testosterone before ovulation showed significantly higher levels compared with those after ovulation. Plasma estradiol-17 beta (E2) levels remained low for 3 days prior to ovulation. Postovulation E2 levels that were significantly higher than the preovulation levels were kept elevated and declined on the third day after ovulation. These results indicate that E2 is mainly produced in the first part of the ovulatory cycle and testosterone in the latter part followed by the GtH surge and ovulation at the end of the cycle. This shift in steroid pattern from E2 to testosterone seems to be similar to those observed in salmonid fishes except for the time scale. The synchrony of ovulation in goldfish is also discussed in relation to physiological and external factors which influence the occurrence of ovulation.

When ring doves are transferred to short days in autumn, their gonads will regress in size, but the change is only transitory, the gonads recover their original size after 2–3 months. In the present study blood samples were collected from male doves repeatedly every 3 hr from 6:00 am to 9:00 pm , 2, 4, and 13 weeks after transfer to short days when the testes were either regressed (Weeks 2 and 4) or had recovered their original size (Week 13). Plasma testosterone, LH, and to some extent FSH were lower in birds which had been exposed to short days for 2 or 4 weeks, but the levels of these three hormones were similar in birds exposed to short or long days after 13 weeks of experiment. The gonadal regression and recovery is thus controlled by changes in the plasma gonadotrophins. Although these changes in the plasma gonadotrophins are apparently not a result of phase shift of peak gonadotrophins, as the mean LH level of short-day birds reached that of long-day birds by Week 13, the tendency of LH to peak at 3:00 pm in short-day birds also disappeared by that time. Daily variations in the concentration of these hormones were also detected. Plasma testosterone decreased between the morning and the afternoon while gonadotrophins tended to change in the opposite direction (highest levels in the late afternoon or early evening). The possible mechanisms underlying these daily changes in plasma hormones are discussed.

The plasma concentrations of all the major steroids thus far isolated from sockeye salmon were determined on fish captured at various stages of sexual maturity. The same steroids were determined in the plasma of spawned Atlantic salmon of both sexes. The data are discussed in relation to previous studies on liver glycogen levels and the source of energy expended by migrating salmon. There is a quantitative change in certain plasma steroids which coincides with the beginning of the river phase of the spawning migration. The results give some support to a “hormone trigger theory” for spawning migration. 11-Ketotestosterone was shown to have no significant effect on the deposition of liver glycogen in the adrenalectomized rat. This observation is discussed in relation to an apparent discrepancy in a previous determination of plasma steroids in Atlantic salmon by chemical and biological assay.