ArticleBiology of reproduction2024
Trajectory of primordial follicle depletion is accelerated in obese mice in response to 7,12-dimethylbenz[a]anthracene exposure†.
Article in Biology of reproduction, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 2 citations in OpenAlex.
- Heat and chemical stressors: Independent and interactive impacts on the pig ovary.The Journal of reproduction and development · 2026Review
- Ovarian SUMO-2/3 targets and their differential response to genotoxic stress induced by 7,12-dimethylbenz(a) anthracene exposure in lean and obese female mice†.Biology of reproduction · 2025Article
- Association between urinary polycyclic aromatic hydrocarbon metabolites and premature menopause: a nationally representative cross-sectional study in the United States.Environmental health and preventive medicine · 2025Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Both obesity and exposure to environmental genotoxicants, such as 7,12-dimethylbenz[a]anthracene, negatively impair female reproductive health. Hyperphagic lean KK.Cg-a/a (n = 8) and obese KK.Cg-Ay/J (n = 10) mice were exposed to corn oil as vehicle control (CT) or 7,12-dimethylbenz[a]anthracene (1 mg/kg/day) for 7d intraperitoneally, followed by a recovery period. Obesity increased liver and spleen weight (P < 0.05), and 7,12-dimethylbenz[a]anthracene exposure decreased uterine weight (P < 0.05) in obese mice. Primordial follicle loss (P < 0.05) caused by 7,12-dimethylbenz[a]anthracene exposure was observed in obese mice only. Primary (lean P < 0.1; obese P < 0.05) and secondary (lean P < 0.05, obese P < 0.1) follicle loss initiated by 7,12-dimethylbenz[a]anthracene exposure continued across recovery. Reduced pre-antral follicle number in lean mice (P < 0.05), regardless of 7,12-dimethylbenz[a]anthracene exposure, was evident with no effect on antral follicles or corpora lutea number. Immunofluorescence staining of DNA damage marker, γH2AX, did not indicate ongoing DNA damage but TRP53 abundance was decreased in follicles (P < 0.05) of 7,12-dimethylbenz[a]anthracene-exposed obese mice. In contrast, increased (P < 0.05) superoxide dismutase was observed in the corpora lutea of 7,12-dimethylbenz[a]anthracene-exposed obese mice and reduced (P < 0.05) TRP53 abundance was noted in preantral and antral follicles of 7,12-dimethylbenz[a]anthracene-exposed obese mice. This study indicates that obesity influences ovotoxicity caused by a genotoxicant, potentially involving accelerated primordial follicle activation and hampering normal follicular dynamics.
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