In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Mably, Thomas A.; Moore, Robert W.; Peterson, Richard E.

doi:10.1016/0041-008x(92)90101-w

Cited by 310 publications

(69 citation statements)

References 25 publications

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“…This timing coincides with the peak of the neonatal testosterone surge, which is known to have important long-term effects on CNS function and behavior. The increase in neonatal testosterone due to birth hypoxia contrasts with the effects of many other manipulations, including neonatal cooling or anesthesia and maternal exposure to repeated hypoxia, stress, alcohol or toxins during pregnancy, which have been reported to decrease neonatal testosterone [9,10,11,12,13]. Birth hypoxia has been shown to be associated with alterations in levels of a wide variety of circulating hormones [15,16,17,18,19].…”

Section: Discussionmentioning

confidence: 99%

“…This increase in testosterone at a critical period of development has been implicated in the long-term modulation of a number of central nervous system (CNS) functions including play and sexual behavior, dopaminergic neurotransmission and responses to early CNS lesions [3,4,5,6,7,8]. The neonatal testosterone surge is relatively labile in that it has been shown to be altered by environmental manipulations such as cooling or anesthesia in the neonate and maternal exposure to repeated hypoxia, stress, alcohol or toxins during pregnancy [9,10,11,12,13]. In the current study we examined whether neonatal testosterone levels can be influenced by another environmental insult, namely birth hypoxia.…”

Section: Introductionmentioning

confidence: 99%

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Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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Background/Aims: Global birth hypoxia in rats has been shown to produce long-term changes in central nervous system functions, known to be influenced by neonatal testosterone secretion. Birth hypoxia alters levels of several circulating hormones, but it is unknown if it affects neonatal testosterone. Methods: Using a rat model of acute global hypoxia during cesarean section (C-section) birth, this study tested whether birth hypoxia affects neonatal testosterone. We then evaluated whether the observed hypoxia-induced changes in neonatal testosterone may be mediated via N-methyl-D-aspartate (NMDA) receptor activation and/or altered luteinizing hormone (LH), adrenocorticotropic hormone (ACTH) or corticosterone levels. Longer-term effects of birth hypoxia on testosterone-related function were also assessed. Results: Rats born by C-section + 15 min of anoxia had significantly higher plasma testosterone at 2 and 3 h after birth compared to controls born either vaginally or by C-section. Administration of an NMDA receptor antagonist at birth increased neonatal testosterone in both anoxic pups and controls. Pups exposed to birth anoxia under hypothermic conditions also showed increased neonatal testosterone. Circulating LH, follicle-stimulating hormone and corticosterone in neonates, and testosterone at adulthood were unaffected by birth hypoxia. However, plasma ACTH was significantly increased in anoxic neonates at 2 h after birth. Birth condition had no effect on anogenital distance or juvenile play behavior. Conclusion: It is concluded that birth hypoxia augments plasma testosterone during the critical period of the neonatal testosterone surge, by a mechanism that is independent of NMDA-mediated LH secretion, but may involve increased circulating ACTH.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Boksa

Zhang

2008

Neuroendocrinology

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“…Polychlorinated benzo-p-dioxins have been found to contaminate many commercial pentachlorophenol preparations [59]. The dioxins are known to have many effects on reproduction, especially in males [86][87][88]. The effects of dioxins in these processes are probably mediated through the Ah receptor [34], not directly through steroid receptors.…”

Section: Review Articlementioning

confidence: 99%

The effects of environmental hormones on reproduction

Danzo¹

1998

Cellular and Molecular Life Sciences (CMLS)

114

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Considerable attention has been given in the past few years to the possibility that man-made chemicals (xenobiotics) in the environment may pose a hazard to human reproductive health. The endocrine-disrupting effects of many xenobiotics can be interpreted as interference with the normal regulation of reproductive processes by steroid hormones. Evidence reviewed here indicates that xenobiotics bind to androgen and oestrogen receptors in target tissues, and to androgen-binding protein and to sex hormone-binding globulin. Although environmental chemicals have weak hormonal activity, their ability to interact with more than one steroid-sensitive pathway provides a mechanism by which their hazardous nature can be augmented. A given toxicant may be present in low concentration in the environment and, therefore, harmless. However, we are not exposed to one toxicant at a time, but, rather, to all of the xenobiotics present in the environment. Therefore, numerous potential agonists/antagonists working together through several steroid-dependent signalling pathways could prove to be hazardous to human reproductive health.

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“…In animal studies, dioxins, PCBs and, to some extent, PBDEs cause reproductive toxicity by delaying or disrupting the testicular descent and causing a decline in sperm output [31,32,33]. Therefore, it seems unlikely that we observed an exposure-outcome relationship due to chance alone.…”

Section: Effects Of the Exposure Variation And Genetic Variation On Ementioning

confidence: 52%

Exposure Variation and Endocrine Disruption of the Male Reproductive System

Toppari

Rodprasert²,

Koskenniemi³

2016

Horm Res Paediatr

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Exposure to endocrine disruptors varies geographically and temporally. Environmental levels of persistent organic pollutants have decreased after international regulation, whereas potential exposure to thousands of new chemicals has increased. The adverse effects of endocrine disruptors depend on susceptibility and timing of the exposure. Fetal and childhood exposures are often most harmful because of organizational and programming effects. In this review, we use the exposure to persistent organic pollutants such as polybrominated diphenyl ethers, dioxins and dioxin-like polychlorinated biphenyls and differences in the incidence of reproductive disorders between Denmark and Finland as an example to highlight how exposure variation and variation in genetic susceptibility may influence the strength of the association between the exposure to endocrine disruptors and adverse effects. Understanding the causes and implications of interindividual differences in susceptibility to endocrine disruptors is crucial for the protection of normal development.

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In utero and lactational exposure of male rats to 2,3,7,8-tetrachlorodibenzo-p-dioxin

Cited by 310 publications

References 25 publications

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

Global Birth Hypoxia Increases the Neonatal Testosterone Surge in the Rat

The effects of environmental hormones on reproduction

Exposure Variation and Endocrine Disruption of the Male Reproductive System

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