At adulthood, EDS-exposed mice still manifest incomplete spermatogenesis and numerous tubule cross sections still lacked germ cells. Similar disruption of spermatogenesis was previously observed in adult EDS-exposed mice 3 wk after five daily treatments (25 mg EDS/100 g BW) in the absence of apparent effects on the interstitium or LCs.
It is well accepted that fertility end points in individuals are relatively insensitive measures of reproductive competence as mice with a 90% reduction in sperm counts have been shown to reproduce normally. We evaluated fertility with a continuous 10-day mating regimen to enhance the sensitivity of fertility by natural mating. The observed decreases in the mating ratio suggest dysfunctional mating behavior in the male mice.
This may be due to persistent effects of EDS on the brain, erectile responsiveness, or merely a consequence of decreased body weight and the resulting size incompatibility with the females. The observed decrease in fertility ratio, as well as the smaller litter sizes, is likely a direct result of the body weight-independent reduction in epididymal sperm reserves, a consequence of the incomplete spermatogenesis we observed by histological evaluation of the adult testis.
The sustained effects of EDS may not be confined to LCs. Indeed, EDS may exert a direct effect on the seminiferous tubules because studies have demonstrated that EDS exerts direct effects on organs (i.e., epididymis) and cells (i.e., Sertoli cells) other than the LC.