A side effect of cyclophosphamide (CP), an alkylating agent widely used to treat tumors and autoimmune disorders is the alteration of male reproductive function. CP is extremely dangerous to the germinal epithelium and damage to spermatogenesis. High doses can cause azoospermia which can result infertility in humans. This study is focused on the evaluation of toxicological effect of cyclophosphamide on male rat testis and the possible reversibility of these toxic effects. Thirty adult male rats were divided into three groups: vehicle-treated (control), CP-treated and rehabilitated groups. CP was administrated intraperitoneally (100mg/kg/week) for five successive weeks, and semithin sections from testicular tissue were prepared and examined after last injection (treated group) and six weeks later (rehabilitated group). A quantitative morphometric study and statistical analysis were applied for accurate and efficient assessment of spermatogenic impairment induced by CP. The CP treated group showed various morphological alterations in the testis such as reduction in the size and distortion in the shape of the seminiferous tubules with degeneration and vacuolation in spermatogonia, spermatocytes and spermatids associated with marked interstitial oedema. In addition, the CP induced significant decreases in volume proportion, diameter and epithelial height of the seminiferous tubules together with a significant reduction in the number of different germ cells in the treated animals. Interestingly, spermatogonia A appeared to be target cells for the damaging effect of CP in the testis that presented severe degenerative changes in structure along with significant reduction in number in the treated group animals. Furthermore, the number of primary spermatocytes and round spermatids decreased significantly in CP- treated group. The Sertoli and Leydig cells, however, appeared to be less affected to CP toxicity; exhibiting insignificant decrease in number as well as less morphological alterations. The Interstitial spaces of treated group animals showed a highly significant increase in its volume proportion, when compared to the control animals. Meanwhile, the rehabilitated group showed significant increases for aforementioned variables in comparison to the CP- treated group, associated with reversal of morphological changes towards normalcy. Based on the results from the present study it is concluded that the morphological alterations induced by CP toxicity were further substantiated by morphometric findings in the testicular tissue of rat. A direct toxicity of CP to the number and quality of spermatogenic compartment may be considered as one of the mechanisms of action of CP in producing the abnormal and dead sperms that alter fertility. By the reversal of morphological and stereological changes towards normalcy, the role of rehabilitation is illuminated in CP induced testicular damage.