Endocrine-active chemicals in mammary cancer causation and prevention

Jenkins, Sarah; Betancourt, Angela M.; Wang, Jun; Lamartiniere, Coral A.

doi:10.1016/j.jsbmb.2011.06.003

Cited by 55 publications

(55 citation statements)

References 101 publications

(130 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…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

View full text Add to dashboard Cite

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.

show abstract

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

View full text Add to dashboard Cite

show abstract

“…The level of genistein exposure in Asian populations consuming a soy-rich diet has been reported to range from ~1 to 30 mg/d, or ~0.02–0.55 mg/kg BW × d, and considerably less in Western populations [7]. Oral exposure to genistein during the early prepubertal period decreased susceptibility of the mammary gland to carcinogenesis [8-10], whereas exposure during the same period of time to BPA increased susceptibility to chemically-induced mammary cancer [9,11,12]. Although both BPA and genistein possess weak estrogenic properties, these chemicals appear to influence the mammary gland via unknown, yet different, mechanisms.…”

Section: Introductionmentioning

confidence: 99%

Cell proliferation and apoptosis in rat mammary glands following combinational exposure to bisphenol A and genistein

2014

Self Cite

View full text Add to dashboard Cite

BackgroundHumans are exposed to an array of both harmful and beneficial hormonally active compounds in the environment and through diet. Two such chemicals are Bisphenol A (BPA), a plasticizer, and genistein, a component of soy. Prepubertal exposure to BPA increased mammary carcinogenesis, while genistein suppressed cancer in a chemically-induced model of rodent mammary cancer. The purpose of this research was to determine the effects of combinational exposure to genistein and BPA on cell proliferation, apoptosis, and associated proteins as markers of cancer in mammary glands of rats exposed prepubertally to these environmental chemicals.MethodsPrepubertal rats (postpartum days (PND) 2–20) were exposed through lactation via nursing dams treated orally with sesame oil (SO), BPA, genistein, or a combination of BPA and genistein (BPA + Gen). Cell proliferation, apoptosis and protein expressions were investigated for mechanistic studies in mammary glands of rats exposed to these environmental chemicals.ResultsPrepubertal exposure to genistein increased cell proliferation in mammary glands of PND21 rats, while BPA increased cell proliferation in adult (PND50) rats. Prepubertal combinational exposure to BPA + Gen increased cell proliferation and reduced apoptosis in PND21 rats, but reduced cell proliferation and increased apoptosis in PND50 rats. The altered mechanisms behind these cellular responses appear to be centered on differential protein expression of caspases, PARP, Bad, p21, Akts, PTEN, ER-β and SRCs 1–3, in the rat mammary gland.ConclusionPrepubertal BPA exposure resulted in increased cell proliferation in mammary glands of PND50 rats, a process associated with increased risk of cancer development in a chemically-induced mammary cancer. On the other hand, genistein stimulated cell proliferation at PND21, a process that correlates with mammary gland maturation and chemoprevention. In contrast to single chemical exposure, combinational exposure to BPA + Gen performed most similarly to genistein exposure alone. BPA + Gen increased cell proliferation at PND21, suggesting mammary gland maturation, and decreased cell proliferation while increasing apoptosis in PND50 rats, suggesting mammary chemoprevention. Differential expression of proteins involved in regulating cell proliferation and apoptosis lend support to these chemicals, both alone and in combination, altering mammary gland cancer susceptibility.

show abstract

“…However, recent studies reported that multiple molecules and pathways could be targets of BPA action, including genes associated with tumorigenesis and the immune system (Jenkins et al, 2012;Clayton et al, 2011). Numerous studies have investigated the influence of BPA on human health, especially reproductive health, since the ovary is an active organ that is susceptible to harmful environmental exposure.…”

Section: Introductionmentioning

confidence: 99%