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Gold nanoparticles (AuNPs) have many biomedical applications. However, the toxic impacts of these nanomaterials, due to their nanosize, surface area, and much particle number, on human health are still unclear. The present study was undertaken to explore the adverse toxic impacts of AuNPs (about 20nm) on the livers of experimental animals and the potential protective and therapeutic roles of N-3 polyunsaturated fatty acids (N-3 PUFA). Forty male adult rats were partitioned into four groups, G I normal animals; G II rats were injected with a suspension of AuNPs (20µg/Kg b.w.) for six days; GIII rats were injected with Au-NPs and co-administered orally with N-3 PUFA (100 mg/Kg b. w.) for six successive days; G IV: rats were ingested orally with N-3 PUFA for 6 successive days, followed by injection with AuNPs daily for 6 days. The results showed that either protective or therapeutic administration of N-3 PUFA to AuNPs intoxicated rats, significantly decreased the increases in hepatic nitric oxide (NO) and malondialdehyde (MDA). N-3 PUFA also aggravated the elevation in the expressions of hepatic transcription factors, nuclear factor erythroid 2-related factor 2 (Nrf2) and hemeoxygenase-1 (HO-1) and significantly up-modulated the depletion in the hepatic expression of peroxisome proliferator-activated receptors-γ (PPAR γ). In addition, the present data revealed that protective or therapeutic treatment of AuNPs intoxicated rats with N-3 PUFA, markedly ameliorated the alterations in the serum hepatic function markers, including alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total and direct bilirubin and albumin. The current biochemical investigations were documented by histopathological observation. Conclusion, the present results may support the use of N-3 PUFA as a protective or a therapeutic agent against liver damage caused by AuNPs toxicity. [ABSTRACT FROM AUTHOR]

Background: Diabetic nephropathy and cardiomyopathy are the main complications induced by chronic hyperglycemia through production of advanced glycation end products (AGEs), connective tissue growth factor (CTGF) and the creation of a proinflammatory mediators. The present study was designed to investigate the effect of quercetin (Qr) and/or lactoferrin (LF) in down regulation of advanced glycation end product, connective tissue growth factor and inflammatory cytokines expressions in diabetic nephropathy and cardiomyopathy induced rats. Materials and Methods: Diabetes was induced in rats by intraperitoneal injection of streptozotocin (40 mg/kg). Rats were allocated into five groups; (G1) Normal non-diabetic rats; (G2) Diabetic rats; (G3) Diabetic rats injected with Qr (10 mg/ kg / day); (G4) Diabetic rats treated with Bovine LF (50 mg/kg /day); (G5) Diabetic rats injected with the combination of Qr and Bovine LF (as in groups 3,4).Serum fasting glucose level, blood hemoglobin, serum biomarkers of heart (AST, LDH and CPK). and kidney damage (cystatin C, creatinine albumin andurea), inflammatory cytokines, as interleukin-6 ( IL-6) and tumor necrosis factor (TNF)-α as well as AGEs and CTGF in heart and kidney tissues were determined. Significant differences among different groups were analyzed using oneway analysis of variance (ANOVA) followed by Bonferroni's test. Results: Induction of diabetes in rats dramatically led to increase in the levels of AGEP and CTGF in both kidney and heart tissues of diabetic rats. Serum TNFα and IL-6, albumin, urea and cystatin C, AST, LDH and CPK levels were significantly increased in diabetic group. The administration of Qr and/or LF to the diabetic rats significantly down-modulated the alterations in the above parameters in relation to diabetic untreated animals. Conclusion: The current two agents possess significant therapeutic effects against diabetic nephropathy and cardiomyopathy by down regulation of the studied parameters. Moreover, the results proved that bovine LF alone and particularly its combination with Qr were effective in controlling the hyperglycemic induced renal and cardiac damage. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the protective and therapeutic roles of red grape juice (Vitis vinifera fruit juice) against tissue damage in rats under the effect of ethanol toxicity. 10% ethanol was administered orally (2ml/kg body weight) to rats for two weeks. The results revealed that oral administration of red grape juice (2ml/ rat) daily for four weeks to rats either along with or after ethanol intoxication markedly ameliorated the alteration in the serum biomarkers of hepatic and cardiac functions, including L-alanine aminotransaminase (ALT) and albumin as biomarkers of hepatic function, aspartate aminotransaminase (AST) and lactate dehydrogenase (LDH) as markers of hepatic and cardiac functions, and creatine kinase (CK) as a marker of cardiac muscle damage. However, non significant change in serum alkaline phosphatase (ALP), bilirubin and total protein was observed between intoxicated rats and normal healthy ones. The red grape juice also successfully modulated the decrease in the serum total antioxidant capacity and nitric oxide (NO) levels as well as the alteration in the serum lipid profiles namely, triglycerides (TGs), total cholesterol (TCh), low density lipoprotein (LDL-C) and high density lipoprotein (HDL-C), in rats under the effect of ethanol with respect to intoxicated untreated ones. However, non-significant change in the serum kidney function biomarkers (creatinine, urea and uric acid) in ethanol intoxicated rats versus normal healthy animals was observed. In conclusion, treatment with red grape juice along with (as protective agent) or after (as therapeutic) ethanol intoxication may protect or recover liver and cardiac tissue damage induced by the toxic effects of ethanol. [ABSTRACT FROM AUTHOR]