Histological study of the effect of induced diabetes on the zona glomerulosa of the adrenal cortex of adult male albino rat

Diabetes is one of the chronic diseases affecting many organs in the body. However, studies concerning its effect on the zona glomenilosa are limited. This work is concerned with studying the histological effects of streptozotocin [STZ]-induced diabetes on the zona glomenilosa of the adrenal gland of adult male albino rats Thirty healthy adult male albino rats were utilized, divided into two groups; Group A: Control and Group B: Experimental group. Rats of experimental group treated with five intra-peritoneal injections of [STZ] with 7-day intervals. The first three doses were 75 mg/kg and the remaining two doses were 150 mg/kg body weight. The control group received only 0.1 ml of 0.1 M citrate buffer, pH 4.4, by the intra-peritoneal route, Thirty days after the detection of the diabetic status, the animals of the two groups were anaesthetized with ether inhalation and the suprarenal glands were removed and processed for light and electron microscopy examination. Plasma level of aldosterone was measured by radioimmunoassay. At light microscopic level, the zona glomerulosa cells of the STZ-induced diabetic rats showed apparent increase in the cytoplasmic vacuolation and pyknotic nuclei. Electron microscopic study of the cells in the previous group revealed degenerative changes in the form of an apparent increase in the number of lipid droplets associated with mitochondrial degeneration. Plasma aldosterone decreased in STZ-induced diabetic rats. The results of this work suggested that streptozotocin induced diabetes changed the ultrastructures of the zona glomerulosa cells which may consequently lead to disturbance of their functions

Detrusor morphology and pathology in relation to bladder outflow obstruction in bilharzial patients

The light and electron microscopic structure of detrusor muscle of trabeculated urinary bladder from patients with urodynamically proved bilharzial outflow obstruction had been compared with normal detrusor muscle, In bilharzial outflow obstruction, the detrusor muscle bundles were formed of relatively smaller smooth muscle cells widely separated by dense connective tissue, fatty infiltration, bilharzial ova, inflammatory cells and hyalinosis. No evidence of smooth muscle hyperplasia, mitosis, or fibroblastic proliferation. At the level of electron microscopy. The connective tissue infiltration was proved to be microfibriles apparently in continuity of the basal lamina of the smooth muscle. These pathological changes can explain both the morphological and urodynamic changes in bilharzial urinary bladder outflow obstruction