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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 objective of the current investigation was to explore the reno- protective impact of 70% methanolic extract of Saussura lappa (coustus) against oxidative stress and oxidative DNA fragmentation induced renal damage in rat models in response to chronic exposure to the pesticide, deltamethrin. Deltamethrin was administered orally to rats at two doses (1/15 LD50 and 1/30 LD50) daily for 28 days. The results illustrated that oral intake of S lappa extract (300mg/Kg b.w) for 28 consecutive days to animals ingested by either of the two doses, significantly modulated the elevation in plasma malondialdehyde (MDA) and protein carbonyl as well as the decreases in plasma antioxidants markers, including protein thiol, glutathione S transferase (GST), catalase (CAT) and, superoxide dismutase (SOD) compared with control animal group. The plant extract could also reverse the inhibitory effect of deltamethrin on plasma ATPase in animals intoxicated by either of the two doses. In addition, the plant extract successfully modulated the oxidative DNA damage in kidneys of deltamethrin intoxicated rat groups. The beneficial renoprotective impact of the S lappa extract against deltamethrin toxicity was reflected by improvement in plasma renal function markers (urea and creatinine) and histomorphological pictures of renal tissues. Conclusion: The current investigation may suggest that early administration of S lappa extract may protect renal tissue from oxidative damage promoted by the toxic effects of deltamethrin pesticide. [ABSTRACT FROM AUTHOR]