Archive \ Volume.9 2018 Issue 1

Beneficial Impacts of N-3 Polyunsaturated Fatty Acids On Gold Nanoparticles -Induced Liver Injury by Activating Ppar? and Nrf2/Ho-1 Signaling Pathway

Najla O. Ayaz
Abstract

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 AuNPs 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.

 


[PDF]