Plasma Steroid Concentrations and Male Phallus Size in Juvenile Alligators from Seven Florida Lakes

Guillette, Louis J.; Woodward, Allan R.; Crain, D. Andrew; Pickford, Daniel B.; Rooney, A A; Percival, H. Franklin

doi:10.1006/gcen.1999.7375

Cited by 115 publications

(64 citation statements)

References 41 publications

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“…Many studies have demonstrated organizational reversal of secondary sexual characteristics, especially experiments on endocrine disrupting compounds. For example, female mosquitofish (Gambusia affinis holbrooki) exposed to metabolites of dichlorodiphenyltrichloroethane (DDT) express male characteristics, such as gonopodia and courtship behavior (Howell et al, 1980), and male alligators (Alligator mississippiensis) become feminized following exposure to the same compounds in the same area in Florida [Lake Apopka, FL, USA (Guillette et al, 1996;Guillette et al, 1999)]. Of particular interest are studies where the reversal of signal production is purely activational.…”

Section: Introductionmentioning

confidence: 99%

How to make a sexy snake: estrogen activation of female sex pheromone in male red-sided garter snakes

Parker

Mason

2012

Journal of Experimental Biology

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SUMMARYVertebrates indicate their genetic sex to conspecifics using secondary sexual signals, and signal expression is often activated by sex hormones. Among vertebrate signaling modalities, the least is known about how hormones influence chemical signaling. Our study species, the red-sided garter snake (Thamnophis sirtalis parietalis), is a model vertebrate for studying hormonal control of chemical signals because males completely rely on the female sex pheromone to identify potential mates among thousands of individuals. How sex hormones can influence the expression of this crucial sexual signal is largely unknown. We created two groups of experimental males for the first experiment: Sham (blank implants) and E2 (17-estradiol implants). E2 males were vigorously courted by wild males in outdoor bioassays, and in a Y-maze E2 pheromone trails were chosen by wild males over those of small females and were indistinguishable from large female trails. Biochemically, the E2 pheromone blend was similar to that of large females, and it differed significantly from Shams. For the second experiment, we implanted males with 17-estradiol in 2007 but removed the implants the following year (2008; Removal). That same year, we implanted a new group of males with estrogen implants (Implant). Removal males were courted by wild males in 2008 (implant intact) but not in 2009 (removed).Total pheromone quantity and quality increased following estrogen treatment, and estrogen removal re-established male-typical pheromone blends. Thus, we have shown that estrogen activates the production of female pheromone in adult red-sided garter snakes. This is the first known study to quantify both behavioral and biochemical responses in chemical signaling following sex steroid treatment of reptiles in the activation/organization context. We propose that the homogametic sex (ZZ, male) may possess the same targets for activation of sexual signal production, and the absence of the activator (17-estradiol in this case) underlies expression of the male phenotype.

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Section: Introductionmentioning

confidence: 99%

How to make a sexy snake: estrogen activation of female sex pheromone in male red-sided garter snakes

Parker

Mason

2012

Journal of Experimental Biology

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“…Recently, endocrine disruptors that cause a hormonal imbalance in animals have received a great deal of attention (Carson, 1962;Colborn et al, 1993Colborn et al, , 1996Cadbury, 1997), with reports of infertility in female sheep induced by a phytoestrogen (Obst et al, 1971), androgyny in conch caused by organic tin (Gibbs et al, 1987), and small penis in alligators exposed to polychlorinated biphenyls (Guillette et al, 1999), etc. Human health has also affected by endocrine disruptors; diethylstilbestrol which was used to prevent abortion in the 1960's induced abnormalities of the reproductive organs, such as vaginal cancer, prostatic hyperplasia, and testicular tumor (Herbst, 1981).…”

Section: Introductionmentioning

confidence: 99%

Vitamin A Insufficiency Accelerates the Decrease in the Number of Sperm Induced by an Environmental Disruptor, Bisphenol A, in Neonatal Mice

2001

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“…Organochlorines, such as the pesticide dichlorodiphenyltrichloroethane (DDT) and its metabolites, have been shown to mimic estrogen, binding to and activating the ERs, thereby often producing estrogen-like effects (2,(16)(17)(18)(19)(20)(21). DDT and its metabolites have displayed harmful feminizing effects on wildlife such as birds (22,23), fish (22,24), and reptiles (22,(25)(26)(27), altering endogenous hormone levels (25,26), elevating estrogen-regulated protein levels (24), and reducing male phallus size (25,26). These reports in wildlife have led to the suggestion that organochlorines may alter a number of harmful estrogen-regulated health effects in humans such as breast cancer (1,(28)(29)(30), endometriosis (1,(31)(32)(33), spontaneous abortion (34), reduced bone mineral density (35), and decreased sperm counts (36).…”

mentioning

confidence: 99%

DDT and its metabolites alter gene expression in human uterine cell lines through estrogen receptor-independent mechanisms.

Frigo

Burow

Mitchell

et al. 2002

Environ Health Perspect

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Endocrine-disrupting organochlorines, such as the pesticide dichlorodiphenyltrichloroethane (DDT), bind to and activate estrogen receptors (ERs), thereby eliciting estrogen-like effects. Although ERs function predominantly through activation of transcription via estrogen-responsive elements, both ERs, alpha and ss, can interact with various transcription factors such as activator protein-1 (AP-1). Additionally, estrogens may regulate early signaling events, suggesting that the biological effects of environmental estrogens may not be mediated through classic ER (alpha and ss) activity alone. We hypothesized that known environmental estrogens, such as DDT and its metabolites, activate AP-1-mediated gene transactivation through both ER-dependent and ER-independent means. Using two Ishikawa human endometrial adenocarcinoma cell line variants that we confirmed to be estrogen responsive [Ishikawa(+)] and estrogen unresponsive [Ishikawa(-)], we generated stably transfected AP-1 luciferase cell lines to identify the role of an estrogen-responsive mechanism in AP-1-mediated gene expression by various stimuli. Our results demonstrate that DDT and dichlorodiphenyldichloroethane (DDD) were the most potent activators of AP-1 activity; 2,2-bis(p-chlorophenyl) acetic acid failed to activate. Although stimulated in both Ishikawa(+) and Ishikawa(-) cells by DDT and its congeners, AP-1 activation was more pronounced in the estrogen-unresponsive Ishikawa(-) cells. In addition, DDT, DDD, and dichlorodiphenyldichloroethylene (DDE) could also stimulate AP-1 activity in the estrogen-unresponsive human embryonic kidney 293 cells using a different promoter context. Thus, our data demonstrate that DDT and its metabolites activate the AP-1 transcription factor independent of ER (alpha or ss) status.

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Plasma Steroid Concentrations and Male Phallus Size in Juvenile Alligators from Seven Florida Lakes

Cited by 115 publications

References 41 publications

How to make a sexy snake: estrogen activation of female sex pheromone in male red-sided garter snakes

How to make a sexy snake: estrogen activation of female sex pheromone in male red-sided garter snakes

Vitamin A Insufficiency Accelerates the Decrease in the Number of Sperm Induced by an Environmental Disruptor, Bisphenol A, in Neonatal Mice

DDT and its metabolites alter gene expression in human uterine cell lines through estrogen receptor-independent mechanisms.

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