5-fluorouracil (5-FU) is a potent antineoplastic agent used for the treatment of various malignancies. The L-arginine nitric oxide (NO) pathway involved in the pathogenesis of chemotherapy induced kidney damage. This work investigated the beneficial mechanism of L-arginine supplementation in 5-FU induced nephropathy. Eighty male Wistar rats were divided into four equal groups: control group; L-arginine group (378 mg/rat/day for 4 weeks); 5-FU group (189 mg/rat/week for 4 weeks) and L-arginine for 1 week before and 4 weeks concomitant with 5-FU group. At the end of experiment, the kidney functions were assessed and kidneys specimens were processed for paraffin sections and stained with haematoxylin and eosin (H&E), Masson's trichome (MT) and periodic acid-Schiff (PAS) stains. Other sections were processed for immunohistochemical demonstration of caspase-3 and inducible NO synthase (iNOS). Image analyser was used to analyse the results morphometrically and statistically. L-arginine administration to 5-FU treated animals elicited significant reduction in serum urea and creatinine levels, urine volume, urinary protein excretion and kidney/body weight ratio in comparison to fluorouracil treated group. L-arginine improved glomeruloscelerosis, degeneration of convoluted tubules and interstitial fibrosis in 5-FU treated animals. L-arginine attenuated effectively some biochemical and histological changes in 5-FU nephrotoxicity.

Introductions:Smoking is an important cause of increased mortality and morbidity in the developing countries. Nicotine in cigarette smoke is one of the toxic substances which impair the fertility. So, the aim of this work was to study the histological changes induced by nicotine hydrogen tartrate on the endometrium of albino rat and the possible ameliorative effect of human chorionic gonadotropin (hCG). Material and Methods: Forty females of Wister albino rats in the normal estrous cycle were selected and used for the experiment. The experimental animals were randomly divided into four groups, each one including 10 female rats. The experiment period was extended to four weeks. Group I was (control group). Group II (Nicotine treated group) was subcutaneously (SC) injected by nicotine hydrogen tartrate as 8 mg/rat three times/week for four weeks. Group III (Nicotine and hCG) was subcutaneously injected with the previous dose of nicotine together with hCG (pregnyl). HCG was subcutaneously injected as 2 IU/rat/day for four weeks. Group IV (hCG group) was subcutaneously injected only with hCG as 2.0 IU/rat/day for four weeks. The specimens were prepared for light and scanning electron microscopic examinations, and morphometric measurements. Results: Nicotine induced decrease in the thickness of the endometrium. The height of the surface epithelium was decreased, the endometrial stromal cells were disrupted and had congested blood vessels. The endometrial glands became small and atrophied. The endometrium showed apparent increase in collagen fibers, a weak PAS reaction and highly positive immunohistochemical staining KI 67. Scanning electron microscopic examination revealed flattening of the surface epithelial cells with absent apical microvilli and apparent decrease in the number of pits of the glands. Concomitant administration of nicotine and hCG showed marked improvement in the structures of the endometrium as compared with that of the nicotine-treated group. Conclusion: Nicotine altered the structure of the endometrium and concomitant administration of hCG with nicotine improved it.

Background: Bisphenol A is the most commercially used of bisphenol groups in plastic industry. It induces oxidative damage in the brain of rats. Aim of Study: The present work investigates the adverse effects of bisphenol A (5mg/kg/day) on the cerebellar cortex of albino rat's offspring of treated mothers throughout pregnancy and lactation and the possible protective effect of omega 3. Material and Methods: Fifty pregnant albino rats were used in this work. They were divided into 4 groups: I-Control group (Group C); half of them did not receive any substance with their pallets (Group CN). The other half were given 0.54ml of corn oil/rat (Group CR). II-Omega 3 treated group (Group O); each rat was given 0.54ml of corn oil (contained 54mg of omega 3). III-Bisphenol A treated group (Group B); each rat was given 0.54ml of corn oil (contained 6.3mg of bisphenol A). IV-Bisphenol A and omega 3 treated group (Group BO); each rat was given the same dose of bisphenol A in Group B plus the dose of omega 3 in Group O. The treatments were given as a single daily dose orally by gastric tube throughout pregnancy and for 2 weeks after delivery. The cerebelli of the offspring of all groups were extracted at the ends of the 2nd and 8th weeks and prepared for light and electron microscopic examination and morphometric study. Results: Light and electron microscopic examinations and morphometric study showed that bisphenol A induced various signs of delayed development in the cerebellar cortex. It also induced degeneration and necrosis of the cerebellar cells and nerve fibers in the form of cytoplasmic vacuoles, dilated rough endoplasmic reticulum, swollen and degenerated mitochondria with destructed cristae. Nuclear changes were observed also in form of karyolysis, pyknosis, karyorrhexis and finally nuclear disappearance. Beside that there was decrease in the number of Purkinje cells. The deleterious effects of bisphenol A on the cerebellar cortex were irreversible on stoppage of its administration. However, combined administration of omega 3 with bisphenol A alleviated the majority of its adverse effects.