Furthermore, EDS was cytotoxic to adult LCs in the testis of the guinea pig, frog, rabbit, and lizard. LCs in the adult Syrian hamster and immature rat exhibit significant effects of EdS exposure, although they are considered less sensitive than adult rat LCs based on the relative decrease in T production by LCs incubated in vitro with EDS.
Additional effects of EDS, on targets other than LCs, have also been identified. For example, EDS is not cytotoxic to adult LCs in quail, mouse, and goat, although spermatogenesis is still disrupted by exposure in these species, creating a state of temporary infertility. In the adult mouse, EDS treatment induces partial sper-matogenic disruption, evidenced by a loss of germ cells in the seminiferous tubules (STs) and expanded extracellular space between surviving germ cells, all without affecting LCs in the interstitium. Furthermore, Klinefelter et al. identified multiple effects of EDS exposure on the rat epididymis that are unrelated to androgen deprivation. The formation of sperm granulomas, morphological alterations of the epididymis, modification of sperm membrane proteins, and decreases in progressive motility and velocity of sperm could not be prevented with exogenous T. Furthermore, in vitro analysis revealed that EDS acts directly on the epididymal epithelium to mediate changes in sperm membrane proteins responsible for sperm motility.