4.2 Article

Bisphenol A-Induced Endocrine Toxicity and Male Reprotoxicopathy are Modulated by the Dietary Iron Deficiency

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出版社

BENTHAM SCIENCE PUBL LTD
DOI: 10.2174/1871530318666180521095443

关键词

Endocrine disrupting chemicals; hormonal imbalance; iron deficiency anemia; confounding factor; histological injury; bisphenol A

资金

  1. Council for Scientific and Industrial Research (CSIR), Government of India
  2. Basic Scientific Research (BSR) scheme of University Grants Commission (UGC), Government of India

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Introduction: Bisphenol A (BPA) is suspected to cause hormonal imbalance in humans. Dietary factors are known to bring changes in hormonal profile. In order to study chemico-biological interaction of iron deficiency on toxicity outcome of BPA exposure, we studied the modulatory effects of iron deficiency on the hormone levels in rats chronically-exposed to BPA. Methods: Weanling rats maintained on normal and iron-deficient diets were exposed to low level of BPA at 0, 1, 5 and 10 ppm for six months through drinking water. The serum levels of thyroid-stimulating hormone (TSH), testosterone, progesterone and estradiol were measured in the animals by enzyme-linked immunosorbent assay kit. Histopathology was performed to check the pathological changes in gonads. Results: No significant change was observed in TSH, progesterone and estradiol levels at 1 and 5 ppm BPA. However, at 10 ppm BPA a significant increase in TSH level was observed in the animals maintained on an iron-deficient diet of either sex. BPA caused a significant change in testosterone level even at 5 and 10 ppm doses in animals of either sex. However, in male rats 1 ppm dose also showed a significant effect in the animals maintained on iron deficient diet. Changes in the histoarchitecture of the testes at high dose of BPA (10 ppm) were more remarkable in anemic rats. Conclusion: These results suggest that iron deficiency has no generalized effect on hormonal levels in BPA-treated animals and trends indicate a more remarkable effect in male animals at hormonal and tissue levels.

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