Lipid‑disrupting effects of an organochlorine mixture in Sertoli TM4 cells reveal testicular obesogen mechanisms. (PubMed, Arch Toxicol)
These responses differed from those elicited by a fatty acid mixture or the lipotoxicant amiodarone and did not appear to involve androgen receptor, aryl hydrocarbon receptor, or peroxisome proliferator‑activated α signaling, suggesting distinct lipid‑centered mechanisms...Notably, OC‑MIX selectively altered phospholipid and lysophospholipid species in Sertoli TM4 cells, indicating interference with membrane remodeling and lipid‑dependent signaling. Overall, these findings support the hypothesis that persistent organochlorines act as testicular obesogens, contributing to male reproductive dysfunction through selective, lipid‑disrupting mechanisms.