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Fig. 3 | Environmental Health

Fig. 3

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

Fig. 3

The major ways used by environmental pollutants to induce defaults in folliculogenesis leading to POI. Environmental pollutants can act through several mechanisms. • actions as endocrine disruptors as ligands to nuclear estrogen receptors (ER, salmon arrows) and aryl hydrocarbon receptors (AhR, blue arrows). Once linked to AhR, they can bind to AhR nuclear translocator (ARNT) to interfere with xenobiotoc responsive elements (XRE) from promotors and affect gene expression, notably promoting pro-apoptotic genes and inhibiting anti-apopototic genes. • creation of an imbalance between oxydative defenses and oxydative stress favoring apoptosis at different follicular stages (green arrows). • Modification of epigenetic marks such as DNA methylation () or histones post-traductional modifications (, , ) affecting the transcriptional state of chromatin and therefore gene expression. • binding to several membrane receptors suchs as membrane bound ER (mER) or receptor protein tyrosine kinases (RPTK) activating the PI3 Kinase pathway are suspected (grey dotted arrows)

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