During spermatogenesis, head-tail cell polarity, apico-basal cell polarity and planar cell polarity (PCP) are remarkably noted in the seminiferous epithelium in which the heads of developing haploid spermatids are pointed to the basement membrane, and with their tails to the tubule lumen. Furthermore, these polarized spermatids are laid unidirectionally across the plane of the seminiferous epithelium, mimicking PCP noted in hair cells of the inner ear. Treatment of rodents with environmental toxicants that lead to germ cell exfoliation, however, are associated with notable changes in spermatid polarity, and defects in spermatid polarity always precede spermatid loss from the epithelium. Studies have also shown that environmental toxicant-induced Sertoli cell or testis injury is mediated through changes in actin and/or microtubule (MT) cytoskeletons. Emerging evidence has illustrated that cell polarity and PCP also exert their regulatory effects through changes in cytoskeletal organization. Herein, we discuss and critically evaluate these recent findings, hoping that better efforts can be coordinated by investigators to address this rapidly developing field regarding the role of cell polarity and PCP proteins in toxicant-induced male reproductive dysfunction.