Fish oil prophylaxis attenuates rotenone-induced oxidative impairments and mitochondrial dysfunctions in rat brain
- 作者：K.M. Denny Joseph ; Mura Muralidhara ; mura16@yahoo.com
- 关键词：ROS ; reactive oxygen species ; TBARS ; thiobarbituric acid reactive substances ; MDA ; malondialdehyde ; DCF ; 2&prime ; 7&prime ; -dichlorofluorescein ; DCFH-DA ; 2&prime ; 7&prime ; -dichlorofluorescein diacetate ; n&minus ; 3 PUFAs ; n&minus ; 3 polyunsaturated fatty acid
- 刊名：Food and Chemical Toxicology
- 出版年：2012
- 期刊代码：20_02786915
- 类别：pha
- 出版时间：May, 2012
- 卷：50
- 期：5
- 页码：1529-1537
- 文件大小：1074 K
摘要
Studies describing the potential of fish oil (FO) prophylaxis to render neuroprotection in experimental model/s are limited. In the present study, we have examined the propensity of FO supplements to modulate endogenous markers of oxidative stress and attenuate neurotoxicant-induced oxidative stress and mitochondrial dysfunctions in rat brain. Prepubertal male rats given FO supplements (oral, 2 and 4 mL/kg bw/day, for 30 days) showed no alterations in malondialdehyde and reactive oxygen species in brain regions. However, FO supplements significantly enhanced the GSH levels in all brain regions examined, while differential effect was discernible in the activity levels of antioxidant enzymes. Further, we investigated whether FO prophylaxis could offset Rotenone (ROT, a well known neurotoxicant) induced early oxidative stress and mitochondrial dysfunctions. While ROT elicited marked oxidative stress as evidenced by the elevated levels of malondialdehyde, hydroperoxides and protein carbonyls in the cerebellum, FO prophylaxis significantly attenuated the effect. FO prophylaxis offered varying degree of protection against ROT-induced mitochondrial dysfunctions. Collectively, our findings in the ROT model allow us to hypothesize that the prophylactic protection offered by FO may be due to its ability to enhance GSH levels, antioxidant machinery, offset protein oxidation and specific modulatory effects on brain mitochondria.