Endocrine Disruptors Acting on Estrogen and Androgen Pathways Cause Reproductive Disorders through Multiple Mechanisms: A Review.
Level 5 - mechanism / opinion, no new human data
Narrative review summarizing in vitro, in vivo, and in silico mechanistic research
PubMed 33557243 · doi:10.3390/ijerph18041464
What was done
A narrative review evaluated in vitro, in vivo, and in silico studies published over the prior decade (retrieved via PubMed and PubChem). The authors summarized molecular mechanisms by which endocrine disrupting chemicals (EDCs) act via estrogen and androgen receptor pathways to trigger reproductive defects.
What was found
The abstract reports no quantitative metrics or effect estimates. It outlines that EDCs (such as bisphenol A, DDT, DDE, polychlorinated biphenyls, and phthalates) bind classic estrogen (ERα, ERβ) and androgen receptors or alternative targets (GPR30, GPCRs, ERRγ). These interactions alter downstream kinase signaling and induce reproductive toxicity through spermatozoid DNA damage, altered DNA methylation patterns, histone modifications, and aberrant miRNA expression.
Why it matters
The review maps the diverse receptor-level and epigenetic pathways through which common environmental toxicants disrupt reproductive physiology in both sexes.
Limits
No quantitative synthesis, systematic screening methodology, or study counts are reported in the abstract. The findings rely on preclinical (in vitro, in vivo, in silico) mechanistic models rather than direct human clinical evidence.
Cited by
- supports Phthalates lower testosterone levels, while bisphenols raise estrogen levels.