Gene Expression Changes Induced in the Testis by Transplacental Exposure to High and Low Doses of 17α-Ethynyl Estradiol, Genistein, or Bisphenol A

Naciff, Jorge M.; Hess, Karla A.; Overmann, Gary J.; Torontali, Suzanne M.; Carr, Gregory J.; Tiesman, Jay P.; Foertsch, Leslie M.; Richardson, Brian; Martínez, Joel E.; Daston, George P.

doi:10.1093/toxsci/kfi198

Cited by 90 publications

(71 citation statements)

References 88 publications

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“…Importantly, the adverse effects were persistent in the sexually mature pups at postnatal day (PND) 42, and were consistent with signifi cant reductions of epididymal sperm counts (Xi et al 2012 ). Analysis of RNA samples from the hypothalamus, testes, and epididymides of rat fetuses, exposed to BPA in utero from GD 11-20, or GD 6-21, revealed modifi cation of the gene expression profi le, including hypothalamic estrogen receptors (ERs), testicular luteinizing hormone receptor (LHR), cholesterol side chain cleavage enzyme (Cyp11a1), and StAR (Naciff et al 2005 ;Cao et al 2013 ). BPA exposure affects hypothalamic development in the embryo.…”

Section: Effects Of In Utero Exposure To Bisphenol a On Male Reproducmentioning

confidence: 64%

Adverse Effects of Bisphenol A on Male Reproductive Function

Manfo

Jubendradass

Nantia

et al. 2013

Reviews of Environmental Contamination and Toxicology

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BPA is a ubiquitous environmental contaminant, resulting mainly from manufacturing,use or disposal of plastics of which it is a component, and the degradation of industrial plastic-related wastes. Growing evidence from research on laboratory animals, wildlife, and humans supports the view that BPA produces an endocrine disrupting effect and adversely affects male reproductive function. To better understand the adverse effects caused by exposure to BPA, we performed an up-to-date literature review on the topic, with particular emphasis on in utero exposure, and associated effects on spermatogenesis, steroidogenesis, and accessory organs.BPA studies on experimental animals show that effects are generally more detrimental during in utero exposure, a critical developmental stage for the embryo. BPA has been found to produce several defects in the embryo, such as feminization of male fetuses, atrophy of the testes and epididymides, increased prostate size, shortening of AGD, disruption of BTB, and alteration of adult sperm parameters (e.g.,sperm count, motility, and density). BPA also affects embryo thyroid development.During the postnatal and pubertal periods and adulthood, BPA affects the hypothalamic-pituitary-testicular axis by modulating hormone (e.g., LH and FSH,androgen and estrogen) synthesis, expression and function of respective receptors(ER, AR). These effects alter sperm parameters. BPA also induces oxidative stress in the testis and epididymis, by inhibiting antioxidant enzymes and stimulating lipid peroxidation. This suggests that employing antioxidants may be a promising strategy to relieve BPA-induced disturbances.Epidemiological studies have also provided data indicating that BPA alters male reproductive function in humans. These investigations revealed that men occupationally exposed to BPA had high blood/urinary BPA levels, and abnormal semen parameters. BPA-exposed men also showed reduced libido and erectile ejaculatory difficulties; moreover, the overall BPA effects on male reproduction appear to be more harmful if exposure occurs in utero. The regulation of BPA and BPA-related products should be reinforced, particularly where exposure during the fetal period can occur. The current TDI for BPA is proposed as 25 and 50 1-1g/kg bwt/day (European Food Safety Authority and Health Canada, respectively). Based on the evidence available, we believe that a TDI value of 5 1-1g/kg bwt/day is more appropriate (the endpoint is modulation of rat testicular function). Certain BPA derivatives are being considered as alternatives to BPA. However, certain of these related products display adverse effects that are similar to those of BPA. These effects should be carefully considered before using them as final alternatives to BPA in plastic production.

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Section: Effects Of In Utero Exposure To Bisphenol a On Male Reproducmentioning

confidence: 64%

Adverse Effects of Bisphenol A on Male Reproductive Function

Manfo

Jubendradass

Nantia

et al. 2013

Reviews of Environmental Contamination and Toxicology

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“…By contrast, mature OVX rats fed purified equol (400 mg/kg) or injected with purified genistein (54 mg/kg) displayed mild estrogen-like uterine stimulation (Rachon et al 2007a, Rimoldi et al 2007. Studies utilizing purified soy isoflavones were shown to regulate gene expression similar to estrogens in female (Naciff et al 2002) and male reproductive tissues (Naciff et al 2004(Naciff et al , 2005. However, other studies comparing SPI with genistein at the gene expression level in female reproductive tissues revealed a completely different set of genes expressed following SPI feeding compared with feeding purified genistein at the same levels present in SPI (Eason et al 2005, Su et al 2007.…”

Section: Discussionmentioning

confidence: 99%

Hepatic gene expression following consumption of soy protein isolate in female Sprague–Dawley rats differs from that produced by 17β-estradiol treatment

Singhal¹,

Shankar²,

Badger³

et al. 2009

Journal of Endocrinology

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Although soy foods have been recognized as an excellent source of protein, there have been recent concerns regarding potential adverse effects of isoflavone phytochemicals found in soy products, which are known to bind and activate estrogen receptors. Here, we used global hepatic gene expression profiles in ovariectomized female SpragueDawley rats treated with 17b-estradiol (E 2 ) or fed with soy protein isolate (SPI) as a means of estimating potential estrogenicity of SPI. Female Sprague-Dawley rats were fed AIN-93G diets containing casein (CAS) or SPI starting at postnatal day (PND) 30. Rats were ovariectomized on PND 50 and infused with E 2 or vehicle in osmotic pumps for 14 d. Microarray analysis was performed on liver using Affymetrix GeneChip Rat 230 2.0. Serum E 2 levels were within normal ranges for the rat and SPI feeding did not increase uterine wet weight in the absence or presence of E 2 . SPI feeding altered (P!0 . 05, RG1 . 5-fold) the expression of 82 genes, while E 2 treatment altered 892 genes. Moreover, only 4% of E 2 -affected genes were also modulated by SPI, including some whose expression was reversed by SPI feeding. The interaction between E 2 and SPI uniquely modulated the expression profile of 225 genes including the reduction of those involved in fatty acid biosynthesis or glucocorticoid signaling and an induction of those involved in cholesterol metabolism. The different hepatic gene signatures produced by SPI feeding compared with E 2 and the lack of increase in uterine wet weight in rats fed with SPI suggest that SPI is not estrogenic in these tissues.

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“…Naciff et al (2005), from The Procter and Gamble Company, examined the effect of prenatal bisphenol A exposure on male rat reproductive organ histology and gene expression. Pregnant Sprague-Dawley rats were fed Purina 5K96, a casein-based soy-and alfalfa-free diet.…”

Section: Experimental Animalmentioning

confidence: 99%