Background: Monosodium glutamate (MSG) has been recognized as flavor enhancer that adversely affects male reproductive systems. Objective: The study was conducted to explore the conceivable protective effects of vitamin C and/or vitamin E on testicular toxicity induced by MSG in rats. Materials and Methods: Thirty male Wistar albino rats were divided (six per group) into: control, MSG, MSG + Vitamin C, MSG + Vitamin E and MSG + Vitamin C + Vitamin E groups. The duration of the study was three weeks. Assessment of serum testosterone, leuteinizing hormone (LH), malondialdehyde (MDA), glutathione peroxidase (GPX), interleukin-10 (IL-10) ,and tumor necrosis factor (TNF-α) were done. Histopathological examination of the testes of the rats was performed using histological, histochemical (Periodic Acid Schiff reaction (PAS)), and immunohistochemical (Proliferating cell nuclear antigen (PCNA), androgen receptors (ARs), Caspase-3) techniques. Results: MSG-group was associated with significant decrease in serum testosterone, LH, GPX, and IL-10 (P < 0.05) and significant increase in serum MDA and TNF-α (P < 0.05) when compared with control group. MSG-group revealed many histopathological changes in the testis including degeneration of the germinal epithelium, absence of sperms in the lumina of tubules, widened vacuolated interstitium, marked deposition of the collagen fibers, very strong PAS reaction and marked immunohistochemical changes. Administration of vitamin C or vitamin E significantly reduced these changes; however, the combination of vitamin C and vitamin E provided more potent protection against the toxic effect of MSG than using each vitamin alone. Also, there was insignificant difference (P > 0.05) between MSG +Vitamin C and MSG +Vitamin E groups. Conclusion: Vitamin C and Vitamin E act synergistically in reducing MSG-induced testicular toxicity via antioxidant, anti-inflammatory and antiapoptotic effects of both vitamins.

Background: Skin ulcers and poor healing are serious problems in diabetic patients. Products of citrus herbal are promising in new studies. Many benefits of hesperidin especially for cutaneous functions including skin healing have been demonstrated. Aim of the Study: The aim of this work was to evaluate the possible healing effect of hesperidin on diabetic skin injury in adult male albino rats. Materials and Methods: Forty adult male albino rats were randomly divided into four equal groups (10 rats, each). Group I: the control; group II: hesperidin; group III: untreated diabetic rats; and group IV, diabetic rats treated with hesperidin. Skin specimens were obtained and processed for histological study using Hematoxylin and Eosin (H & E), Mallory trichrome (M.T) and immunohistochemical study using vascular endothelial growth factor (VEGF) Electron microscopic examination was done. Morphometric measurements of epidermal thickness and area percentage of collagen fibers were carried out followed by statistical analysis. Results: The untreated diabetic group showed incomplete closure and scab covering proliferating epidermis. Another area of self-healed malformed skin revealed reepithelization with increased thickness of epidermis significantly. Epidermal cells showed loss of polarity and in between hyaline material. The underlying dermis revealed a significantly increased disorganized collagen fibers and massive inflammatory cells infiltration. Also, moderate VEGF immunoexpression was observed. Diabetic skin treated with hesperidin revealed complete closure of the wounds with thin apparently normal epidermis. The underlying dermis revealed normal amount of well-organized collagen fibers with few inflammatory cells infiltration and spaces between collagen fibers. Strong positive VEGF immunoexpression was observed reflecting enhanced angiogenesis. Conclusion: Diabetic skin injuries are healing badly in relatively prolonged time. Hesperidin can be used as an adjunctive or alternative agent in diabetic wound giving good cosmetic results.

This study is aiming to investigate the protective effect of glucosamine, risedronate (alone or in combination) on articular cartilage in experimental model of immobilized rat knee. Twenty-five adult male albino rats were divided into five groups (five rats each): control group, immobilized group, glucosamine-treated group, risedronate-treated group, and group treated by a combination of glucosamine and risedronate. The articular cartilage was obtained for histological, immunohistochemical and morphometric studies. The immobilized group showed manifestations of osteoarthritis in the form of significant decrease of articular cartilage thickness with surface erosions, shrunken chondrocytes with pyknotic nuclei and marked manifested fall of chondrocyte number. There was manifested reduction of collagen contents of the articular cartilage using Masson trichrome stain. Safranin O-Fast Green revealed low proteoglycan contents. The collagen type II was also declined. The manikin score was 7.8. Risedronate improved this manifestation slightly more than glucosamine, but combination of booth drugs caused significant improvement of the damaged articular cartilage caused by immobilization. Oral administration of glucosamine and risedronate improved the degenerative changes of rat knee articular cartilage that follow immobilization. This improvement was more remarkable when both drugs were used in combination.

Acrylamide (ACR) is a cytotoxic and carcinogenic material. It is a product of a Maillard reaction during the cooking of many types of fried fast food, e.g. potato chip fries, and chicken nuggets. ACR has a severe toxic effect on different body organs. This study investigates the hepatotoxic effect of ACR, and the protective effect of ascorbic acid and silymarin. For this purpose, forty adult, male, albino rats were divided into four groups and received the following treatments for fourteen days: Group I: (the control) normal saline; Group II: ACR only; Group III: ACR and ascorbic acid; and Group IV: ACR and silymarin. Under a light microscope, the liver from rats treated with ACR only presented disturbed liver architecture, degenerated hepatocytes, reduced glycogen contents, congested central vein, and increased collagen fibres with areas of fibrosis. Immunohistochemical examination revealed an increased mean number of CD68-, and α-SMA-positive cells. This indicates the presence of large numbers of stellate macrophages (Kupffer cells) and Hepatic stellate cells (HSCs). The combination of ACR with either ascorbic acid or silymarin resulted in less hepatic degeneration, less fibrosis and fewer CD68 and α-SMA positive cells compared to the ACR only group. In conclusion, treatment with silymarin or ascorbic acid along with ACR appears to alleviate ACR-induced hepatotoxicity with more protection in silymarin treated rats.

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