An in vivo assessment of the genotoxic potential of bisphenol A and 4-tert-octylphenol in rats

Ulutaş, Onur Kenan; Yıldız, Nurçin; Durmaz, Emre; Ahbab, Müfide Aydoğan; Barlas, Nurhayat; Çok, İsmet

doi:10.1007/s00204-010-0620-y

Cited by 44 publications

(25 citation statements)

References 51 publications

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“…36 These results suggest that exposure to a low dose of BPA may lead to the persistence of mDSBs by inhibiting their repair, although high doses of BPA have been reported to be genotoxic. 37 Subsequently, these unresolved mDSBs in pachytene spermatocytes result in the disruption of meiotic progression and chromosome abnormalities, such as asynapsis, chromosomal aberrations, and interrupted regions of SYCP3 staining, as also demonstrated by previous studies. 9, 14 …”

Section: Discussionsupporting

confidence: 59%

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

et al. 2013

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The effect of bisphenol A (BPA) on the reproductive system is highly debated but has been associated with meiotic abnormalities. However, evidence is lacking with regard to the mechanisms involved. In order to explore the underlying mechanisms of BPA-induced meiotic abnormalities in adult male rats, we exposed 9-week-old male Wistar rats to BPA by gavage at 0, 2, 20 or 200 μg/kg body weight (bw)/day for 60 consecutive days. 17β-Estradiol (E2) was administered at 10 μg/kg bw/day as the estrogenic positive control. Treatments with 200 μg/kg bw/day of BPA and E2 significantly decreased sperm counts and inhibited spermiation, characterized by an increase in stage VII and decrease in stage VIII in the seminiferous epithelium. This was concomitant with a disruption in the progression of meiosis I and the persistence of meiotic DNA strand breaks in pachytene spermatocytes,and the ataxia–telangiectasia-mutated and checkpoint kinase 2 signal pathway was also activated; Eventually, germ cell apoptosis was triggered as evaluated by terminal dUTP nick-end labeling assay and western blot for caspase 3. Using the estrogen receptor (ER) antagonist ICI 182780, we determined that ER signaling mediated BPA-induced meiotic disruption and reproductive impairment. Our results suggest that ER signaling-mediated meiotic disruption may be a major contributor to the molecular events leading to BPA-related male reproductive disorders. These rodent data support the growing association between BPA exposure and the rapid increase in the incidence of male reproductive disorders.

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Section: Discussionsupporting

confidence: 59%

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

et al. 2013

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“…Furthermore, Tyl et al ( 2002 ) investigated physiological parameters, but did not assess biochemical changes. Other authors have studied BPA and have reported that it caused various effects, including genotoxicity and clastogenicity in blood cells (Ulutaş et al 2010 ;Dobrzyńska and Radzikowska 2013 ;Tiwari et al 2012 ), increased susceptibility to chemically induced mammary carcinogenesis (Jenkins et al 2012 ), and induced meiotic aneuploidy in oocytes (Hunt et al 2003 ), suggesting possible modifi cation of the DNA in male germ cells that may be transmitted to the next generation (Salian et al 2011 ).…”

Section: Effects Of Bisphenol a On Spermatogenesismentioning

confidence: 99%

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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“…The worldwide distribution of BPA in various environments was considered as the sources of BPA exposure to human beings (Kang et al 2006b;Ulutao et al 2011). Another way of exposure to BPA occurred through ingestion followed by accumulation in the fatty tissues (Oehlmann et al 2008;Sanchez-Avila et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Bacteria-mediated bisphenol A degradation

Zhang

Yin

Chen

2013

Appl Microbiol Biotechnol

179

100

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Bisphenol A (BPA) is an important monomer in the manufacture of polycarbonate plastics, food cans, and other daily used chemicals. Daily and worldwide usage of BPA and BPA-contained products led to its ubiquitous distribution in water, sediment/soil, and atmosphere. Moreover, BPA has been identified as an environmental endocrine disruptor for its estrogenic and genotoxic activity. Thus, BPA contamination in the environment is an increasingly worldwide concern, and methods to efficiently remove BPA from the environment are urgently recommended. Although many factors affect the fate of BPA in the environment, BPA degradation is mainly depended on the metabolism of bacteria. Many BPA-degrading bacteria have been identified from water, sediment/soil, and wastewater treatment plants. Metabolic pathways of BPA degradation in specific bacterial strains were proposed, based on the metabolic intermediates detected during the degradation process. In this review, the BPA-degrading bacteria were summarized, and the (proposed) BPA degradation pathway mediated by bacteria were referred.

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An in vivo assessment of the genotoxic potential of bisphenol A and 4-tert-octylphenol in rats

Cited by 44 publications

References 51 publications

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

Exposure to bisphenol A disrupts meiotic progression during spermatogenesis in adult rats through estrogen-like activity

Adverse Effects of Bisphenol A on Male Reproductive Function

Bacteria-mediated bisphenol A degradation

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