Histological and ultrastructural changes of the brain, pancreas and ileum of diabetic and nondiabetic mice under heat stress with special reference to heat shock proteins

The current study was designed to evaluate the thermal stress effect on brain, pancreas and ileum in normal and alloxan-diabetic mice by studying the structural changes at both light and electron microscopical levels and by studying the molecular changes expressed through the examination of protein banding pattern in the electrophorograms of the different groups . The animals were divided into four main groups; control mice, alloxan diabetic mice, heat-stressed nondiabetic mice and heat-stressed diabetic mice. No remarkable changes could be detected in nonstressed diabetic animals except the ultrastructural changes noticed in B cells of islets of Langerhans in pancreas. The heat-stressed nondiabetic animals displayed various cellular and subcellular changes in the organs of study, which were focal in most of the cases. Signs of restitution were also noted in the three selected organs in this group. On the other hand, heat stress was so much destructive in diabetic mice and that was so clear specially in pancreas. The difference in degree of cellular injury between diabetics and nondiabetics is correlated with data of protein studies which demonstrated more expression of heat stress proteins [HSPs] in nondiabetics and attenuation of this expression in diabetics. These stress proteins are suggested to play an important role in protection against thermal stress injury. Consistent with this, the brain which showed more expression of HSPs was the least affected of the three organs. Moreover, the attenuated expression of these HSPs in diabetics highlights the suggestion that diabetes deranged the stress response and delayed the expression of the protective HSPs. In conclusion further studies are needed to characterize the molecular structure of the HSPs and the genes responsible for the expression of these proteins in these tissues and the other body tissues

Adrenal suppression induced by megestrol acetate and the possible protective role of selenium a histological, histochemical and ultrastructural study

The anticancer drug megestrol acetate [MA] is suspected to cause adrenal insufficiency. Several clinical reports indicated that suppressed adrenal function might be possible in long term administration of MA . The present study was designed to evaluate this issue by using the histological, histochemical and ultrastructural techniques. The data obtained from the present study indicated that MA caused various cellular and subcellular damages in most of the cells of the three zones of adrenal cortex. Histochemical investigations indicated increased lipid content associated with increased storage of ascorbic acid and acid phosphatase, and all these data might reflect a state of suppressed steroidogenesis. The results also indicated that selenium might have a protective role against the cytotoxicity of megestrol acetate on adrenocortical cells. All the results were discussed and it is concluded that more followup of adrenal function should be done during the long term treatment with MA, and an additional protective supplement

Ultrastructural study of renal tubular damage induced by captopril in adult and fetal mice

The present study has been designed to evaluate the possible nephrotoxicity of the angiotensin converting enzyme inhibitor, captopril on renal tubules of adult and maternally treated fetuses of CD-1 mice. The study included the effect of captopril administration for one month up to three months in adults, while in fetuses, they were exposed to the drug through their mothers in two periods. The first was from 6th-12th days of pregnancy, while the second was from 6th-18th day of pregnancy. The dose used in the present study represents the dose equivalent to the therapeutic daily dose taken by human. All the recorded tissue damage was found to be time dependent. The first remarkable feature noticed in all the treated adult animals was the presence of hyaline casts that obstructed most of the renal tubules. The second remarkable feature was the increase of the intertubular space associated with irregularity of the tubules due to the degeneration and vacuolation of the basal regions of the cells. Renal tubule cells showed large blebs, accumulaton of lipids, degeneration and necrosis. In maternally treated fetuses, the proximal convoluted tubule cells displayed moderate vacuolation and marked increase of lysosomes while some of the distal convoluted tubules revealed atrophy and their cells showed loss of mitochondria. In addition, the collecting tubules showed loss of microprojections. Worthy to mention that there was apparent increase of mesenchymal cells as well as fibroblasts in the fetuses maternally treated with captopril. The significance of these changes was discussed and it should be emphasized that captopril must be taken with caution for pregnant women and those who suffer from renal troubles. Moreover, kidney function should be monitored during therapy