Structural Changes in the Ventral Lobe of the Prostate of Diabetic Rat

Background: Streptozotocin has been widely used to induce type-1 diabetes in animal models. Aim of the Work: This study was conducted to delineate the effects of streptozotocin (STZ)-induced diabetes on the ultrastructure of the secretory epithelium of the ventral lobe of the prostate of adult albino rats. Material and Methods: Healthy thirty adult male albino rats were divided into two groups. Group I is the control and group II is the STZ-experiment group of healthy rats treated with five intraperitoneal injections STZ for 7-day intervals. The first three doses were 75 mg/kg body weight and the remaining two doses were 150 mg/kg per animal. The control group received only 0.1 ml 0.1 M citrate buffer, pH 4.4, by the intraperitoneal route. Thirty days after the detection of the diabetic status, the animals of the two groups were anaesthetized with ether inhalation and sacrificed. The ventral lobes of their prostate were removed and processed for microscopic examination. Results: The histological study of the experimental group revealed a reduction in the cell height of glandular epithelium, remarkable atrophy of secretory epithelial cells with an increase in the thickness of the glandular stroma as compared with the control group. The ultrastructural distinctive features of secretory epithelial cells of the ventral lobe of the prostate of the experimental group showed ruptured microvilli, homogeneous chromatin throughout the enlarged nucleus, thickened extracelluar matrix, dilated concentric cisterns of the granular endoplasmic reticulum and swollen mitochondria with disturbed cristae. The disorganized ultrastructural features of the experimental group were clear as compared with the control group. Conclusions: Our results suggested adverse effects of STZ-induced diabetes on the secretory epithelium of the ventral lobe of the prostate and emphasized remarkable drastic changes in the secretory epithelial cells that consequently lead to impaired glandular function and development of prostatic pathology