Extra virgin olive oil enhances the hepatic antioxidant defense and inhibits cytogenotoxic effects evoked by 5-hydroxymethylfurfural in mice

被引:11
|
作者
El Bohi, Khlood M. [1 ]
Ghoniem, Mervat H. [1 ]
Azab, Haidy H. [1 ]
Ali, Haytham [2 ]
Farag, Mayada R. [1 ]
机构
[1] Zagazig Univ, Dept Forens Med & Toxicol, Zagazig 44511, Egypt
[2] Zagazig Univ, Fac Vet Med, Dept Pathol, Zagazig 44511, Egypt
关键词
5-HMF; EVOO; Genotoxicity; Antioxidant status; Mice; HUMAN SULFOTRANSFERASES 1A1; PHENOLIC-COMPOUNDS; DNA-DAMAGE; HYPERLIPEMIC RABBITS; HEXAVALENT CHROMIUM; LIPID-PEROXIDATION; HYDROXYTYROSOL; GENOTOXICITY; MOUSE; MUTAGENICITY;
D O I
10.1007/s11356-020-07659-x
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
This study was performed to assess the ability of the food genotoxicant 5-hydroxymethylfurfural (5-HMF) to induce DNA damage and oxidative injuries in the liver of mice as a possible mechanism of toxic action and to evaluate the role of extra virgin olive oil (EVOO) in inhibiting these injuries. For this purpose, 80 mice were assigned into four equal groups of 20 mice each. Group 1 was kept as control and group 2 was given 5-HMF (250 mg/kg bw) by intraperitoneal (IP) injection 3 times weekly for 4 weeks. Group 3 received EVOO (300 mu l/kg bw) orally daily for 4 weeks. Group 4 was co-treated with both 5-HMF (250 mg/kg bw) with IP injection and EVOO (300 mu l/kg bw) orally 3 times weekly for 4 weeks. IP injection of 5-HMF resulted in a significant decrease in albumin, globulin, and total protein contents and significant increases in alanine transaminase, aspartate transaminase, and alkaline phosphatase activities. Administration of EVOO alone or with 5-HMF reduced the 5-HMF-induced alterations and restored the liver function biomarkers, antioxidant defense system, and histoarchitecture of the liver to normal values. EVOO also inhibited the genotoxic and apoptotic effects of 5-HMF suggesting that EVOO could provide liver protection through its powerful antioxidant and confirm its good nutriceutical and pharmacological properties.
引用
收藏
页码:11882 / 11891
页数:10
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