Impairment in protein expression profile of testicular steroid receptor coregulators in male rat offspring perinatally exposed to Bisphenol A

Salian, Smita; Doshi, Tanvi; Vanage, Geeta

doi:10.1016/j.lfs.2009.04.005

Cited by 107 publications

(68 citation statements)

References 33 publications

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“…Four of these miRNAs (hsa-miR-146b-5p, hsamiR-509-5p, hsa-miR-519d and hsa-miR-652) have already been shown to be altered in the testes, seminal plasma and/or semen environmental toxins and factors) can induce harmful phenotypes in the descendants of exposed individuals. [6][7][8][9][10][11][12][13][14] Although the mechanisms underlying transmission of environmentallyinduced phenotypes through generations are not well understood, epigenetic changes within the germ line appear to play a central role. The association of DNA methylation with environmental exposures and heritable phenotypes has been widely established.…”

Section: Discussionmentioning

confidence: 99%

“…6,7 Such multigenerational toxicity has been observed following exposure to other environmental chemicals and environmental factors such as nutrition and stress. [8][9][10][11][12][13][14] Epidemiological studies suggest that this phenomenon may also occur in human populations. [15][16][17][18][19] recent work has suggested that environmental chemicals, including those contained in cigarette smoke, can have adverse effects on the exposed individuals as well as their future progeny.…”

Section: Introductionmentioning

confidence: 99%

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Smoking induces differential miRNA expression in human spermatozoa: A potential transgenerational epigenetic concern?

et al. 2012

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Smoking induces differential miRNA expression in human spermatozoa: A potential transgenerational epigenetic concern?

et al. 2012

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“…However, abnormal spermatogenesis, reduced fertility, changes to the expression of ER alpha and Steroid Receptor Coactivator-1 in the brain have been reported to persist in male F 2 and in completely unexposed male F 3 animals after perinatal exposure to a low environmental dose of BPA [13,52]. Changes were observed even after exposure to the parent chemical had ceased.…”

Section: Discussionmentioning

confidence: 99%

Environmental levels of oestrogenic and antiandrogenic compounds feminize digit ratios in male rats and their unexposed male progeny

Auger¹,

Denmat

Berges

et al. 2013

Proc. R. Soc. B.

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Digit length ratios, especially the second-to-fourth digit ratio (2D : 4D), are associated with various pathological and behavioural conditions in many species including humans and are dependent upon prenatal androgen to oestrogen balance. It is unknown whether digit ratios are modified by environmental exposure to ubiquitous endocrine disruptors. We studied the effect on adult male Wistar rat digit ratios of a gestational exposure to the oestrogenic and antiandrogenic compounds bisphenol A (BPA), genistein and vinclozolin, in low doses, and in combination with investigating in parallel a possible sexual dimorphism of this trait. We also investigated the effects on the male progeny not exposed during gestation. X-rays were taken of the left and right forepaws, and 2D-5D proximal to distal phalanx distances were measured by a standardized procedure based on semi-automatic image analysis. We provide evidence that there is a sexual dimorphism of digit ratios in the Wistar rat, and we found that BPA alone or in combination with genistein and vinclozolin significantly feminized digit ratios in male rats. Intriguingly, significant feminization of digit ratios was also found in the unexposed male progeny of males that had been exposed to compound mixtures. In conclusion, prenatal environmental levels of endocrine-active substances permanently disrupt digit ratios. Digit ratio measurement in adults is thus a promising biomarker of prenatal exposure to low-dose endocrine disruptors in rodents, with potential implications for future studies in humans.

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“…Transgenerational effects in response to exposure to environmental toxicants during pregnancy have also been observed for other substances such as the synthetic estrogen diethylstilbestrol (DES), the environmental estrogen bis-phenol A (BPA) (Salian et al, 2009), the contaminant dioxin (TCDD) (Bruner-Tran and Osteen, 2011), or the pesticide methoxychlor (MXC) . Several studies have demonstrated that DES can increase the incidence of tumors in the offspring and grandoffspring (Walker, 1984;Walker and Haven, 1997;Newbold et al, 2006).…”

Section: Environmental Toxicantsmentioning

confidence: 98%

Epigenetic Inheritance of Disease and Disease Risk

Bohacek

Mansuy

2012

Neuropsychopharmacol

151

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Epigenetic marks in an organism can be altered by environmental factors throughout life. Although changes in the epigenetic code can be positive, some are associated with severe diseases, in particular, cancer and neuropsychiatric disorders. Recent evidence has indicated that certain epigenetic marks can be inherited, and reshape developmental and cellular features over generations. This review examines the challenging possibility that epigenetic changes induced by environmental factors can contribute to some of the inheritance of disease and disease risk. This concept has immense implications for the understanding of biological functions and disease etiology, and provides potential novel strategies for diagnosis and treatment. Examples of epigenetic inheritance relevant to human disease, such as the detrimental effects of traumatic stress or drug/toxic exposure on brain functions, are reviewed. Different possible routes of transmission of epigenetic information involving the germline or germline-independent transfer are discussed, and different mechanisms for the maintenance and transmission of epigenetic information like chromatin remodeling and small noncoding RNAs are considered. Future research directions and remaining major challenges in this field are also outlined. Finally, the adaptive value of epigenetic inheritance, and the cost and benefit of allowing acquired epigenetic marks to persist across generations is critically evaluated.

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Impairment in protein expression profile of testicular steroid receptor coregulators in male rat offspring perinatally exposed to Bisphenol A

Cited by 107 publications

References 33 publications

Smoking induces differential miRNA expression in human spermatozoa: A potential transgenerational epigenetic concern?

Smoking induces differential miRNA expression in human spermatozoa: A potential transgenerational epigenetic concern?

Environmental levels of oestrogenic and antiandrogenic compounds feminize digit ratios in male rats and their unexposed male progeny

Epigenetic Inheritance of Disease and Disease Risk

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