Cigarette smoking prevalence is still increasing in the developing world especially among men mainly in central Asia, east Europe and Africa. Furthermore, maternal cigarette smoking during pregnancy has multiple deleterious effects on the offspring, which may persist into adulthood. The present work aims at clarifying whether the prenatal exposure to either nicotine or thiocyanate could be the responsible factor in induction of the possible effect of smoking on spermatogenesis and the cytoarchitecture of the testis and hence influencing the male fertility later on. Twenty pregnant rats were randomly divided into four groups from gestational day 4. Groups Ia and b served as control. Group II animals were injected with nicotine (6 mg/kg/day) subcutaneously as a single dose. Group III Animals were treated with oral potassium thiocyanate (25 mg/rat/day) as a single dose through gastric gavages. Five male litters from each group (one/each pregnant rat) were sacrificed at the age of 1 month. Pituitary and testicular tissue samples were subjected to histological and electron microscopic study. The counts of different cells of seminiferous tubules were statistically analyzed for significance. Results revealed apoptotic changes at the subcellular level of the pituitary gonadotrophs and different spermatogenic and Sertoli cells of the testis. The number of Sertoli and different spermatogenic cells- rather than spermatogonia- showed a very highly significant decrease in the nicotine treated group in comparison to the control. The dense cells revealed a very highly significant increase in the nicotine treated group. In conclusion, the results of the present study were more consistent with a suggested dual effect of nicotine on the pituitary-testicular axis rather than a purely direct effect on the testis. On the other hand, thiocyanate induced subcellular effect on the testicular histology with minimal affection of gonadotrophs.