Chemotherapy treats many types of cancer effectively but it often causes side effects. Chemotherapy works on active cells, such as cancer cells, and some healthy cells. Side effects happen when chemotherapy damages these healthy cells. Today, many more drugs are available to treat side effects than in the past. Triptorelin (Decapeptyl) is a gonadotropin-releasing hormone agonist that is reported to have many therapeutic effects besides being an anti-cancer agent. In the current study, intraperitoneal cyclophosphamide (65 mg/kg/day) was administered for 4 weeks to induce marked dystrophic changes in the cerebral cortex and hippocampus of male albino rats. After 4 weeks, we observed significant degeneration of neurocytes with dystrophic changes. Subcutaneous triptorelin (0.05 mg/kg/day) for 4 weeks significantly improved histological signs of degeneration and apoptosis. Anti-Bcl2 staining of sections of the cerebral cortex and hippocampus showed that the apoptotic index was increased. This finding was confirmed by the anti-p53 staining, which showed a significant decrease in the apoptotic index. Ultimately, such improvements were accompanied by significant restoration of normal brain histology, as revealed by hematoxylin and eosin. In conclusion, triptorelin can reverse the apoptotic changes induced by cyclophosphamide therapy, which is more marked in the hippocampus than cerebral cortex.

<p class="abstract"><strong>Background:</strong> Diabetic nephropathy (DN) has become one of the most common causes of end stage renal disease (ESRD). Hyperglycemia induces oxidative stress in renal tubular epithelial cells that initiate tubulointerstitial fibrosis, which is a characteristic feature of diabetic nephropathy that becomes progressively complicated by renal failure. Aim: To assess the effect of spironolactone (SPL) on WT-1 protein expression and ultrastructural changes associated with the progression of experimental diabetic nephropathy (DN).</p><p class="abstract"><strong>Methods:</strong> Forty female albino rats were divided into five groups. Group I (control group), Group II (untreated diabetic rats), Group III (insulin-treated diabetic rats), Group IV (spironolactone-treated diabetic rats) and Group V (insulin and spironolactone-treated diabetic rats). At the 4^th and 8^th weeks, 4 rats from each group were sacrificed and renal tissue and blood samples were obtained. The rats were anaesthetized using ether inhalation. Each kidney was longitudinally divided and processed for immunohistochemical analysis with rabbit polyclonal anti-WT-1 Antibody and electron microscopic examination.</p><p class="abstract"><strong>Results:</strong> Treatment of STZ-induced diabetic rats with insulin and spironolactone (Group V) showed improvement in renal corpuscles as well as their capsular space, the basement membrane became normal with preserved minor and major processes and subpodocytic space, most of the proximal convoluted tubules retained their brush border, and their cells showed normal euchromatic nuclei and scattered mitochondria with apical microvilli, which is similar to the findings of the control group. Quantitative analyses showed significant increase in area of fibrosis and focal thickening of the glomerular basement membrane in non-SPL treated groups. There was a marked decrease in proteinuria compared to other treated groups. The results were better after 8 weeks compared to those after 4 weeks.</p><strong>Conclusions:</strong> The administration of SPL significantly prevented the extent of interstitial fibrosis in the diabetic kidney.

<p class="abstract"><strong>Background:</strong> Acrylamide (ACR) is a widely used chemical in industry and it accounts for major health problems as it has been detected in highly consumed food items, carbohydrate-rich food items cooked at high temperature. Accordingly the population is highly exposed to ACR. The aim of the study was to assess the effect of vitamin E on biochemical and ultrastructure changes in acrylamide-induced renal toxicity in wistar albino rats.</p><p class="abstract"><strong>Methods:</strong> Three groups of adult albino wistar rats weighing about (200-250 gm) were used in this study to investigate the effect of vitamin E on acrylamide induced renal toxicity; 10 rats in each group; Group I: Control group, Group II: Acrylamide treated and Group III: Acrylamide-Vit E treated group. Blood samples were collected for estimation of serum creatinine, blood urea nitrogen (BUN), lactic dehydrogenase (LDH) and albumin. Kidneys specimens were processed for light and electron microscopic studies. Kidney sections were stained with H&amp;E, MT, PAS and immuno-histochemical stains for detection of NF-kβp65 and Bcl-2. Morphometric study was done followed by biochemical and morphometric statistical analysiss.</p><p class="abstract"><strong>Results:</strong> Acrylamide treated rats showed degeneration of cells lining PCT and DCT, atrophy of glomeruli and fibrosis. Ultrastructurally; tubules lining cells showed loss of microvilli, basal membrane in foldings and mitochondrial changes. Podocytic changes include: Vacuolation, irregularity and disorientation of their processes and thinning of glomerular basement membrane. Significant increase in the mean number of NF-kβp65 positive cells and decrease in the mean area% of Bcl-2 immuno-expression, increase in the mean area % of collagen fibers and urinary space diameter and decrease in thickness of epithelial cells of PCT and DCT were also observed. Serum creatinine, BUN anLDH were increased whereas serum albumin was decreased. Vitamin E co-administration with ACR improve all these histological, ultrastructural and biochemical changes.</p><strong>Conclusions:</strong> Acrylamide induced renal toxicity could be ameliorated by vitamin E co-administration.