Ovarian Toxicology, Second Edition (Target Organ Toxicology)
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Today, we are exposed to an increasing number of chemicals in the environment and there is a growing awareness of the effects of these chemicals on the ovaries. Infertility resulting from environmental exposures may not be obvious until the reproductive life span is waning. As such, the potential for xenobiotic-induced infertility needs to be better understood.
In recent years, research into chemicals that have the potential to cause early menopause by destroying pre-antral ovarian follicles is gaining greater appreciation. Ovarian Toxicology, Second Edition represents a compilation of chapters prepared by researchers who have substantially contributed to our understanding of the impact of xenobiotics and environmental factors on ovarian function. The second edition substantially updates newly investigated ovotoxicants as well as improved mechanistic insights that have emerged since the first edition.
- Ovarian physiology and the metabolism of xenobiotics
- The effect of pesticides, heavy metals, phthalates, BPA, and cigarette smoking on the ovaries
- Ovarian cancer, including endocrine effects and new perspectives on chemoresistance
- Epidemiology and human health risk assessment for environmental chemicals and pharmaceuticals
The first book to focus specifically on ovarian toxicology, this resource is ideal for scientists in academia, regulatory agencies, and industry who would benefit from a survey of the impact of xenobiotic chemicals on ovarian function.
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(Peretz et al., 2012). As in the previous study, follicles treated with BPA exhibited reduced growth in both wild-type and ESR1 overexpressing follicles and reduced follicle growth was associated with atresia. ESR1 overexpressing follicles were not more sensitive to the effects of BPA when compared to wild-type follicles and replacement of estradiol to the cultures did not affect the BPA-induced follicle growth inhibition. To begin to determine potential BPA-initiated mechanisms of growth
females were administered atrazine for 14 days and monitored for an additional 14 days. Treated rats exhibited disrupted estrous cycles and reduced ovary weight, and ovaries had reduced numbers of old corpora lutea and completely lacked new corpora lutea; serum estradiol was increased. Analysis of specific mRNAs revealed that AR, ERα, LHR, and sulfatase mRNA were reduced in ovaries from treated rats, while aromatase mRNA levels and aromatase activity were increased (Quignot et al., 2012a).
Keating AF. 2011. Ovarian metabolism of xenobiotics. Exp Biol Med 236:765–771. Bhattacharya P, Keating AF. 2012a. Impact of environmental exposures on ovarian function and role of xenobiotic metabolism during ovotoxicity. Toxicol Appl Pharmacol 261:227–235. Bhattacharya P, Keating AF. 2012b. Protective role for ovarian glutathione S-transferase isoform pi during 7,12-dimethylbenz[a]anthracene-induced ovotoxicity. Toxicol Appl Pharmacol 260:201–208. Bhattacharya P, Sen N, Hoyer PB et al. 2012c.
begins during the development of the fetus at which time the female produces all of the oocytes that she will use during her entire life. In this way, oogenesis is very different from spermatogenesis in which males continually produce sperm. Oogenesis occurs through the process of mitosis and meiosis. Initially, oogonia undergo mitosis to produce oocytes. The oocyte then undergoes the initial stages of meiosis, but that process is arrested at the diplotene stage of prophase 1. The cell stays at
Role of diepoxides. Chemical Research in Toxicology 8:963–969. El-Nemir, A., Al-Shawaf, T., Sabatini, L., Wilson, C., Lower, A.M., and Grudzinskas, J.G. 1998. Effect of smoking on ovarian reserve and ovarian stimulation in in vitro fertilization and embryo transfer. Human Reproduction 13:2192–2198. Everson, R.B., Sandler, D.P., Wilcox, A.J., Schreinemachhers, D., Shore, D.L., and Weinberg, C. 1986. Effect of passive exposure to smoking on age at natural menopause. British Medical Journal 293:792.