Effects of bisphenol A and nonylphenol on mammary carcinogenesis, uterine adenomyosis and bone mineral density of tibia in mice

Tohru Nakayama; Shuji Sassa; Hiroyuki Kikuchi

Effects of bisphenol A and nonylphenol on mammary carcinogenesis, uterine adenomyosis and bone mineral density of tibia in mice

Tohru Nakayama, Shuji Sassa, Hiroyuki Kikuchi

In: 関東学院大学人間環境研究所所報 · 2012 · vol. 11(11) , pp. 23–28 · W356246534

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⚙ AI-generated summary by gemini-2.5-flash-lite, 2026-07-14 ⓘ

Bisphenol A and nonylphenol did not affect mammary tumors or uterine adenomyosis in mice, but both reduced tibial bone mineral density, with BPA suppressing body growth.

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⚙ AI-generated deep summary by claude@2026-07, 2026-07-14 · read from full text ⓘ

The paper investigated whether endocrine-disrupting compounds bisphenol A and nonylphenol affect mammary carcinogenesis, uterine adenomyosis, and tibia bone mineral density in steroid-stable, virgin Crl:CD1(ICR) mice, using dietary dosing for either 21 days (bisphenol A and nonylphenol at 60 mg/kg and 60 mg/kg respectively) or 210 days for nonylphenol, followed by assessment of tumor and reproductive organ outcomes and dual-energy X-ray absorptiometry–derived bone mineral density, with plasma and enyzme marker measurements. It reports that bisphenol A reduced body weight gain and, despite not changing mammary tumor incidence or number, reduced uterine adenomyosis incidence/grade at 40 weeks and reduced bone mineral density, alongside modest effects on bone markers (notably increased bone-mineral-density–related changes not fully aligning with uterine outcomes). Nonylphenol did not change uterine adenomyosis incidence or mammary tumor-related metrics, did not reduce tibia bone mineral density as much as bisphenol A, and showed compound-specific, organ-specific dissociation between reproductive pathology and bone outcomes, with the authors noting that uterine histopathology depended on age and tissue metrics and that hormone-related mechanisms were inferred rather than directly proven. This paper includes uterine adenomyosis as a primary measured endpoint and evaluates how bisphenol A and nonylphenol alter uterine adenomyosis in mice, so it directly relates to adenomyosis research.

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Abstract

Bisphenol A and nonylphenol are estrogenic compounds and endocrine disruptors.These environmental chemicals have given adverse effects on the developing reproductive system as an endocrine disruptor, and the tissue injuries on many organs leading to formation of reactive oxygen species.The SHN mice have been known as a strain with a high potential for the incidence of mammary tumors and uterine adenomyosis.Both endocrine disruptors did not affect in the incidence and numbers of mammary tumors, the latent periods of tumorigenesis and the survival rate in the mice, and in the incidence of the uterine adenomyosis.However, Bisphenol A markedly suppressed the body-growth in mice.Both endocrine disruptors reduced the tibial bone mineral density.It may be suggested that these agents act via the estrogen receptors in mice with estrous cycle, followed by the steroidal dysfunction, decreases in the circulating levels of endogenous estrogens and the bone absorption in tibia.These findings may be able to suggest that Bisphenol A and nonylphenol predominantly have a cytotoxic characteristic and an endocrine disrupting characteristic, respectively.

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