Mechanisms of Reproductive Toxicity

Keating, Aileen F.; Hoyer, Patricia B.

doi:10.1002/9780470439265.ch24

Cited by 5 publications

(2 citation statements)

References 206 publications

(239 reference statements)

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“…The ovary is a dense structure in the pelvic cavity near the lateral walls [80], composed of somatic and germ cells [81]. The two primary functions of the ovary are (1) production and release of oocytes through the processes of oogenesis and folliculogenesis and (2) production and secretion of hormones (17β-estradiol (E2) and progesterone (P4)), which are essential for the proper functioning of the female reproductive system [79,82,83] and female general health [84].…”

Section: Female Reproductionmentioning

confidence: 99%

“…Environmental, occupational, medicinal, or xenoestrogenic chemicals can also cause adverse effects on the female reproductive system [83,[103][104][105][106][107][108][109][110][111]. Chemicals that affect ovarian function are known as ovotoxicants and can target different stages of follicular development [88,106,112], leading to harmful effects on follicle development, decreased oocyte quality and ovulation, disruption of the estrous cycle, and altered hormonal production [106,108,[113][114][115].…”

Section: Ovarian Toxicitymentioning

confidence: 99%

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Effects of Per- and Polyfluoroalkylated Substances on Female Reproduction

González-Alvarez,

Antwi-Boasiako,

Keating

2024

Toxics

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Per- and poly-fluoroalkylated substances (PFAS) are a large group of chemicals that persist both in the environment and in the body. Legacy PFAS, e.g., perfluorooctanoic acid and perfluorooctane sulfonic acid, are implicated as endocrine disruptors and reproductive and developmental toxicants in epidemiological and animal model studies. This review describes female reproductive outcomes of reported studies and includes where associative relationships between PFAS exposures and female reproductive outcomes have been observed as well as where those are absent. In animal models, studies in which PFAS are documented to cause toxicity and where effects are lacking are described. Discrepancies exist in both human and animal studies and are likely attributable to human geographical contamination, developmental status, duration of exposure, and PFAS chemical identity. Similarly, in animal investigations, the model used, exposure paradigm, and developmental status of the female are important and vary widely in documented studies. Taken together, support for PFAS as reproductive and developmental toxicants exists, although the disparity in study conditions and human exposures contribute to the variation in effects noted.

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Section: Female Reproductionmentioning

confidence: 99%

Section: Ovarian Toxicitymentioning

confidence: 99%

Effects of Per- and Polyfluoroalkylated Substances on Female Reproduction

González-Alvarez,

Antwi-Boasiako,

Keating

2024

Toxics

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Obesity alters the ovarian proteomic response to zearalenone exposure

González-Alvarez

McGuire

Keating

2021

Biology of Reproduction

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Zearalenone (ZEN), a non-steroidal estrogenic mycotoxin, is detrimental to female reproduction. Altered chemical biotransformation, depleted primordial follicles and a blunted genotoxicant response have been discovered in obese female ovaries, thus, this study investigated the hypothesis that obesity would enhance ovarian sensitivity to ZEN exposure. Seven week old female wild type non-agouti KK.Cg-a/a mice (lean) and agouti lethal yellow KK.Cg-Ay/J mice (obese) received food and water ad libitum, and either saline or ZEN (40 μg/Kg) per os for 15 days. Body and organ weights, and estrous cyclicity were recorded, and ovaries collected post-euthanasia for protein analysis. Body and liver weights were increased (P < 0.05) in the obese mice, but obesity did not affect (P > 0.05) heart, kidney, spleen, uterus, or ovary weight and there was no impact (P > 0.05) of ZEN exposure on body or organ weight in lean or obese mice. Obese mice had shorter proestrus (P < 0.05) and a tendency (P = 0.055) for longer metestrus/diestrus. ZEN exposure in obese mice increased estrus but shortened metestrus/diestrus length. Neither obesity or ZEN exposure impacted (P > 0.05) circulating 17β-estradiol or progesterone, or ovarian abundance of EPHX1, GSTP1, CYP2E1, ATM, BRCA1, DNMT1, HDAC1, H4K16ac, or H3K9me3. Lean mice exposed to ZEN had a minor increase in γH2AX abundance (P < 0.05). In lean and obese mice, LC–MS/MS identified alterations to proteins involved in chemical metabolism, DNA repair and reproduction. These data identify ZEN-induced adverse ovarian modes of action and suggest that obesity is additive to ZEN-induced ovotoxicity.

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