Dioxin exposure and porcine reproductive hormonal activity

Gregoraszczuk, Ewa Ł.

doi:10.1590/s0102-311x2002000200010

Cited by 43 publications

(31 citation statements)

References 32 publications

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“…Dioxin-like contaminants are regarded as an endocrinedisrupters with the ability to disrupt reproductive systems (Baba et al, 2005;Heiden et al, 2008;Kakeyama et al, 2008;Li et al,1995), and reproductive hormone changes were frequently mentioned as a reason for this (Gregoraszczuk et al, 2002;Morán et al, 2003;Myllymäki et al, 2005;Matsumoto et al, 2010). In the current study, the serum estrogen levels were significantly decreased in female mice drinking TCDD or canal waters.…”

Section: Discussionmentioning

confidence: 99%

“…This result also showed uterine AhR and cyp1A2 expression increased, which may account for partial alteration of the uterine function. The combinational effects of uterine malfuction, higher TCDD concentration and reproductive hormonal changes (Myllymäki et al, 2005;Matsumoto et al, 2010;Morán et al, 2003;Gregoraszczuk et al, 2002) could lead to morphologic abnormality and function failure leading to high mortality in the first few days after birth.…”

Section: Discussionmentioning

confidence: 99%

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Three-generation experiment showed female C57BL/6J mice drink drainage canal water containing low level of TCDD-like activity causing high pup mortality

et al. 2011

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Three-generation experiment showed female C57BL/6J mice drink drainage canal water containing low level of TCDD-like activity causing high pup mortality

et al. 2011

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“…In porcine follicular cells, recent studies indicate a TCDD-induced decrease in estrogen synthesis and that the exposure to the action of AhR or ER blockers (alpha naphthoflavone and 4-OH-tamoxifen respectively) is able to completely reverse the inhibitory effect (Gregoraszczuk 2002). A further report indicates a potentiation of TCDD activity through contemporary exposure to estradiol in mouse ovarian cells, and that this effect can be reversed through exposure to specific ER blockers (Son et al 2002).…”

Section: Ahr Cross-talk With Steroid Hormone Receptorsmentioning

confidence: 97%

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Pocar

Fischer²,

Klonisch³

et al. 2005

Reproduction

168

126

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The dioxin/aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor responsive to both natural and man-made environmental compounds. AhR and its nuclear partner ARNT are expressed in the female reproductive tract in a variety of species and several indications suggest that the AhR might play a pivotal role in the physiology of reproduction. Furthermore, it appears to be the mediator of most, if not all, the adverse effects on reproduction of a group of highly potent environmental pollutants collectively called aryl hydrocarbons (AHs), including the highly toxic compound 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). Although a large body of recent literature has implicated AhR in multiple signal transduction pathways, the mechanisms of action resulting in a wide spectrum of effects on female reproduction are largely unknown. Here we summarize the major types of molecular cross-talks that have been identified for the AhR and linked cell signaling pathways and that are relevant for the understanding of the role of this transcription factor in female reproduction.

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“…The effects of TCDD on porcine steroidogenesis have been described by others and the subject has been reviewed previously (Gregoraszczuk 2002). Therefore, this section will focus on providing an updated and brief overview of the subject including data obtained using other species.…”

Section: Polyhalogenated Arylhydrocarbonsmentioning

confidence: 99%

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

Craig¹,

Wang²,

Flaws³

2011

Reproduction

230

123

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Endocrine-disrupting chemicals (EDCs) are exogenous agents with the ability to interfere with processes regulated by endogenous hormones. One such process is female reproductive function. The major reproductive organ in the female is the ovary. Disruptions in ovarian processes by EDCs can lead to adverse outcomes such as anovulation, infertility, estrogen deficiency, and premature ovarian failure among others. This review summarizes the effects of EDCs on ovarian function by describing how they interfere with hormone signaling via two mechanisms: altering the availability of ovarian hormones, and altering binding and activity of the hormone at the receptor level. Among the chemicals covered are pesticides (e.g. dichlorodiphenyltrichloroethane and methoxychlor), plasticizers (e.g. bisphenol A and phthalates), dioxins, polychlorinated biphenyls, and polycyclic aromatic hydrocarbons (e.g. benzo[a]pyrene).

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Dioxin exposure and porcine reproductive hormonal activity

Abstract: To characterize the action of 2,3,7,

Cited by 43 publications

References 32 publications

Three-generation experiment showed female C57BL/6J mice drink drainage canal water containing low level of TCDD-like activity causing high pup mortality

Three-generation experiment showed female C57BL/6J mice drink drainage canal water containing low level of TCDD-like activity causing high pup mortality

Molecular interactions of the aryl hydrocarbon receptor and its biological and toxicological relevance for reproduction

Endocrine-disrupting chemicals in ovarian function: effects on steroidogenesis, metabolism and nuclear receptor signaling

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