Endocrine-Disrupting Chemicals: Some Actions of POPs on Female Reproduction

Abstract

Persistent organic pollutants (POPs), such as polychlorinated dibenzo-p-dioxins (PCDDs) and dibenzofurans (PCDFs), polychlorinated biphenyls (PCBs), and polybrominated ethers (PBDEs), chloronaftalens (PCNs), and bisphenol A (BPA), are stable, lipophilic pollutants that affect fertility and cause serious reproductive problems, including ovotoxic action, lack of ovulation, premature ovarian failure (POF), or polycystic ovarian syndrome (PCOS). Most of the representatives of POPs influence the activation of transcription factors, not only activation of aromatic hydrocarbon receptor (AhR), but also the steroid hormone receptors. This minireview will focus on a variety of PAH activities in oocyte, ovary, placenta, and mammary gland. The complexity and diversity of factors belonging to POPs and disorders of the reproductive function of women indicate that the impact of environmental pollution as an important determinant factor in fertility should not be minimize.

Environmental pollutants, a possible etiology for premature ovarian insufficiency: a narrative review of animal and human data

“…According to the animal review from Camlin [62], cigarette smoking has negative effects on female fertility. Exposure to tobacco induces a depletion in follicle stock [75–78], according to a mechanism of apoptosis and oxidative stress [75–78]. This depletion in follicle stock seems to persist, even in the case of discontinuing smoking [79].…”

Expression of aryl hydrocarbon receptor 1 (AHR1), AHR1 nuclear translocator 1 (ARNT1) and CYP1 family monooxygenase mRNAs and their activity in chicken ovarian follicles following in vitro exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

“…AHR-knockout mice display a number of defects suggesting that in addition to transducing xenobiotic signals, AHR is involved in the regulation of fundamental physiological processes (Benedict et al, 2003;Nebert et al, 2000). In mammals, the AHR physiological role is supported by the presence of AHR in several tissues, including the reproductive system (Baldridge and Hutz, 2007;Bussmann and Bara nao, 2006;Gregoraszczuk et al, 2001;Gregoraszczuk and Ptak, 2013;Jablonska et al, 2011;Pocar et al, 2004;Schlecht et al, 2004;Wojtowicz et al, 2005). Lee et al (2009) have revealed that both AHRs are expressed in chicken tissues, although only AHR1 mediates TCDD action.…”

Stanowisko Polskiego Towarzystwa Endokrynologicznego dotyczące związków endokrynnie czynnych (EDC)

“…Animal studies have also shown their impact on the maturation of the ovarian follicles [35]. PCB153 congener (2,2',4,4',5,5'-hexachlorobiphenyl) could accumulate in the antral follicles and as a consequence reduce oestradiol secretion [36]. Similar to dioxin, the toxicity of coplanar PCBs and monoortho-PCBs is thought to be primarily mediated via binding to the aryl hydrocarbon receptor (AhR) [37], but they may also act via ER.…”

“…Badania na zwierzętach wykazały ich wpływ na zahamowanie dojrzewania pęcherzyków Graafa [35]. Kongener PCB153 (2,2'4,4',5,5'-heksachlorobifenyl) może kumulować się w pęcherzykach jajnikowych i w konsekwencji hamować wydzielanie 17b-estradiolu [36]. Toksyczność zarówno koplanarnych PCB, jak i mono-orto-PCB wydaje się być głównie mediowana poprzez receptory arylowęglowodorowe (AhR) [37] lub poprzez receptory estrogenowe (ER).…”