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Introduction: Monosodium glutamate (MSG) is utilized to enhance appetite and there is rising solicitude that MSG has a role in the evolution of hepatic disturbances. Propolis has been notified to have a considerable role in the amelioration of hepatic toxicity. Aim: The aim of this study is to investigate the protective effect of propolis on hepatotoxicity induced by MSG. Materials and methods: Forty-eight male rats were divided into four equal groups (Gp). GpI was served as a control, GpII was treated orally with propolis (90mg/kg bw) and GpIII was treated with MSG (97 mg/kg bw). GpIV was treated with MSG and propolis in the same doses as GpII and GpIII. All agents were administrated orally once daily for 6 weeks. Then, rats were sacrificed and blood samples were collected for biochemical analysis. Liver tissues were harvested for histopathological and histochemical examinations with determination of oxidative markers. Results: The results showed that the levels of ALT, AST, and ALP significantly augmented in MSG-treated rats whereas serum albumin level significantly declined. Rats' exposure to MSG increased oxidative parameters; malondialdehyde (MDA) in the tissue, in parallel with decreased antioxidant enzymes levels as well as histopathological damages in the hepatic tissue. The administration of propolis highly mitigated the hepatotoxic influences of MSG based on biochemical and histological alterations. Conclusion: In summary, the study obviously indicates that MSG-induced hepatic toxicity could be protected by propolis administration and such beneficial properties could be attributed to the polyphenolic compounds present in these natural products.

Background: Hepatic and renal damage is a cisplatin (Cis)-induced deleterious effect that is a major limiting factor in clinical chemotherapy. Objectives: The current study was designed to investigate the influence of pretreatment with olive leaf extract (OLE), bone-marrow-derived mesenchymal stem cells (BM-MSC), and their conditioned media (CM-MSC) against genotoxicity, nephrotoxicity, hepatotoxicity, and immunotoxicity induced by cisplatin in rats. Methods: The rats were randomly divided into six groups (six rats each) as follows: Control; OLE group, treated with OLE; Cis group, treated with a single intraperitoneal dose of Cis (7 mg/kg bw); Cis + OLE group, treated with OLE and cisplatin; Cis + CM-MSC group, treated with BM-MSC conditioned media and Cis; and Cis + MSC group, treated with BM-MSC in addition to Cis. Results: Cis resulted in a significant deterioration in hepatic and renal functions and histological structures. Furthermore, it increased inflammatory markers (TNF-α, IL-6, and IL-1β) and malondialdehyde (MDA) levels and decreased glutathione (GSH) content, total antioxidant capacity (TAC), catalase (CAT), and superoxide dismutase (SOD) activity in hepatic and renal tissues. Furthermore, apoptosis was evident in rat tissues. A significant increase in serum 8-hydroxy-2-deoxyguanosine (8-OH-dG), nitric oxide (NO) and lactate dehydrogenase (LDH), and a decrease in lysozyme activity were detected in Cis-treated rats. OLE, CM-MSC, and BM-MSC have significantly ameliorated Cis-induced deterioration in hepatic and renal structure and function and improved oxidative stress and inflammatory markers, with preference to BM-MSC. Moreover, apoptosis was significantly inhibited, evident from the decreased expression of Bax and caspase-3 genes and upregulation of Bcl-2 proteins in protective groups as compared to Cis group. Conclusions: These findings indicate that BM-MSC, CM-MSC, and OLE have beneficial effects in ameliorating cisplatin-induced oxidative stress, inflammation, and apoptosis in the hepatotoxicity, nephrotoxicity, immunotoxicity, and genotoxicity in a rat model.

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The aim of this study was to investigate the possible protective effect of the antioxidant sodium selenite (0.1 mg/kg/day) via gavage once a day for 30 days for the first time in a model of malathion (27 mg/kg/day) via gavage once a day for 30 days induced testicular toxicity in mice. Results of this study revealed that concomitant administration of selenium has prevented the decrease in mean final and relative body weight as well as testicular and relative testicular weight as compared to malathion group. Concomitant selenium administration has also decreased malondialdehyde contents and increased serum levels of follicle stimulating hormone, luteinizing hormone, testosterone, acetylcholinesterase and testicular levels and activities of glutathione, glutathione peroxidase, catalase, superoxide dismutase and improved the testicular histopathological features as compared to malathion group.

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