Fish/flaxseed oil protect against nitric oxide-induced hepatotoxicity and cell death in the rat liver

被引:4
作者
Khan, M. W. [1 ,2 ]
Priyamvada, S. [1 ,3 ]
Khan, S. A. [1 ,4 ]
Khan, S. [1 ]
Gangopadhyay, A. [5 ]
Yusufi, A. N. K. [1 ]
机构
[1] Aligarh Muslim Univ, Dept Biochem, Fac Life Sci, Aligarh 202002, Uttar Pradesh, India
[2] Indian Inst Chem Biol, CSIR, Cell Biol & Physiol Div, Kolkata, W Bengal, India
[3] Univ Illinois, Dept Med, Chicago, IL USA
[4] SVKMs Mithibai Coll, Bhakti Vedanta Marg, Bombay, Maharashtra, India
[5] Indian Inst Chem Biol, CSIR, Kolkata, W Bengal, India
关键词
Fish oil; flaxseed oil; sodium nitroprusside; liver; carbohydrate metabolism; hepatotoxicity; POLYUNSATURATED FATTY-ACIDS; BRUSH-BORDER MEMBRANE; INDUCED NEPHROTOXICITY; OXIDATIVE DAMAGE; CARBOHYDRATE-METABOLISM; GLUTATHIONE-PEROXIDASE; ENERGY-METABOLISM; DNA-DAMAGE; FISH-OIL; KIDNEY;
D O I
10.1177/0960327115586207
中图分类号
R99 [毒物学(毒理学)];
学科分类号
100405 ;
摘要
Sodium nitroprusside (SNP) is an antihypertensive drug with proven toxic effects attributed mainly to the production of nitric oxide (NO). Polyunsaturated fatty acids (PUFAs) are widely regarded as functional foods and have been shown to ameliorate the harmful effects of many toxicants. This study examined whether feeding of fish oil (FO)/flaxseed oil (FXO) would have any protective effect against SNP-induced hepatotoxicity and cell death. Male Wistar rats were fed either on normal diet or with 15% FO/FXO for 15 days, following which SNP (1.5 mg/kg body weight) was administered intraperitoneally for 7 days. Animals were killed after treatment, and livers were collected for further analysis. We observed that SNP significantly elevated tissue nitrite levels and lipid peroxidation (LPO) with concomitant perturbation in antioxidant defense systems accompanied with dysregulated glucose metabolism and pronounced cellular death. FO/FXO supplementation to SNP-treated rats caused reversal of tissue injury/cell death and markedly decreased LPO and improved antioxidant defense systems. FO/FXO appear to protect against SNP-induced hepatotoxicity by improving energy metabolism and antioxidant defense mechanism.
引用
收藏
页码:302 / 311
页数:10
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