The role of the mitochondrial dynamic distribution in oocyte development arrest induced by F-53B

Chlorinated polyfluoroalkyl ether sulfonates (F-53B), an alternative to perfluorooctane sulfonate (PFOS), has gained attention for reproductive toxicity, but data on its specific effects on oocyte remain limited. We conducted in vitro maturation (IVM) experiments on ICR mouse oocytes exposed to F-53B at its medium inhibition of maturation concentration (IM 50 ). PFOS and 0.5 % dimethyl sulfoxide (DMSO) served as positive and negative control, respectively, during 16-hour treatments. For each sample, 50 GV oocytes were tested, with six replicates. Phenotypic assessments included oocyte maturation status, spindle architecture, and mitochondrial function, and single-cell transcriptomic analysis was conducted to investigate molecular mechanism. Mitochondrial ultrastructure was evaluated by transmission electron microscopy, and distribution patterns were tracked by live-cell imaging. In vitro , F-53B exposure led to meiotic arrest, spindle defects, chromosome misalignment, and mitochondrial dysfunction. Single-cell transcriptomic analysis revealed mitochondria as the primary organelle affected by F-53B exposure. Disrupted mitochondrial organization caused by F-53B contributed to spindle assembly abnormalities, with significant alterations observed in key genes related to mitochondrial distribution. Our findings provide new insights into the reproductive toxicity of F-53B, identifying disrupted mitochondrial distribution and function as key factors in oocyte maturation impairment caused by F-53B.