ABSTRACT
Background: Sodium arsenate (Na 3As0 4, Sodium As) is an important toxic substance that leads to nephrotoxicity. Due to having bioactive molecules, such as polyphenols and tyrosol, olive oil plays a significant role in scavenging free radicals. This study aimed to investigate the effects of olive oil and tyrosol on As-induced nephrotoxicity. Methods: In our study, 42 adult male BALB/c mice were randomly divided into six groups: control (normal saline), olive oil (0.4 ml/d, gavage), tyrosol (5 mg/kg/d), Sodium As (15 mg/kg), olive oil + Sodium As, and tyrosol + Sodium As (olive oil and tyrosol received one hour before Sodium As). Drugs were administreted once daily for 30 consecutive days. On the 31st day of the study, oxidative stress parameters in kidney tissue, FRAP in plasma, renal function parameters in serum, and histopathological assays were performed. Results: Sodium As-induced renal damage as characterized by a significant increase of creatinine and BUN (P < 0.001) and histopathological changes. Also, Sodium As markedly altered oxidative stress biomarkers such as a significant increase in MDA (P < 0.001) and significantly decreased in FRAP and GSH (P < 0.01). Olive oil and tyrosol administration significantly improved the renal antioxidant defense system and decreased MDA concentration, markedly preserving the tissue structure and functional markers of kidney. However, these effects were more effective for tyrosol than olive oil. Conclusions: Our results suggest that olive oil and tyrosol can be used as a protective agent in preventing Sodium As-induced nephrotoxicity due to antioxidant property.
ABSTRACT
BACKGROUND: Sodium arsenate (As), a toxic substance with induced oxidative stress, lead to hepatotoxicity. Olive oil (OO) with antioxidant property has protective effect on toxicity. The aim of this study was to investigate protective effect of OO on sodium As-induced hepatotoxicity in mice. SUBJECTS AND METHODS: In this experimental study, 32 adult male BALB/c mice were divided randomly into four groups: control group (received only normal saline, the same volume as other groups), OO (0.4 mL/day, gavage), sodium As (15 mg/kg, gavage), and OO + sodium As (received OO 1 h before sodium As). Drugs were given for 30 consecutive days. After the last receipt of the drugs, oxidative stress parameters [malondialdehyde (MDA), glutathione (GSH)] in tissue, liver function parameters [alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphatase (ALP)] in serum, ferric reducing ability of plasma (FRAP) in plasma, and histopathological assays were performed. RESULTS: Sodium As induced hepatic injury as indicated by significant increase in AST, ALT, ALP, and LDH in serum and pathologic evidences. It also induces hepatic oxidative stress biomarkers as indicated by significant increase in levels of MDA and significant decrease in FRAP and GSH concentration. OO administration significantly improved oxidative stress parameters, histopathological changes, and enzymatic markers of liver injury. CONCLUSIONS: It was concluded that antioxidant activity of OO has hepatoprotective effect on As-induced hepatic injury.
