Content of liver and brain ubiquinol-9 and ubiquinol-10 after chronic ethanol intake in rats subjected to two levels of dietary alpha-tocopherol

Citation
Vbc. Junqueira et al., Content of liver and brain ubiquinol-9 and ubiquinol-10 after chronic ethanol intake in rats subjected to two levels of dietary alpha-tocopherol, FREE RAD RE, 33(3), 2000, pp. 313-319
Citations number
36
Categorie Soggetti
Biochemistry & Biophysics
Journal title
FREE RADICAL RESEARCH
ISSN journal
10715762 → ACNP
Volume
33
Issue
3
Year of publication
2000
Pages
313 - 319
Database
ISI
SICI code
1071-5762(2000)33:3<313:COLABU>2.0.ZU;2-9
Abstract
To assess the effect of chronic ethanol ingestion in the content of the red uced forms of coenzymes Q(9) (ubiquinol-9) and Q(10) (ubiquinol-10) as a fa ctor contributing to oxidative stress in liver and brain, male Wistar rats were fed ad libitum a basal diet containing either 10 or 2.5 mg alpha-tocop herol/100% diet (controls), or the same basal diet plus a 32% ethanol-25% s ucrose solution. After three months treatment, ethanol chronically-treated rats showed identical growth rates to the isocalorically pair-fed controls, irrespectively of alpha-tocopherol dietary level. Lowering dietary alpha-t ocopherol led to a decreased content of this vitamin in the liver and brain of control rats, without changes in that of ubiquinol-9, and increased lev els of hepatic ubiquinol-10 and total glutathione (tGSH), accompanied by a decrease in brain tGSH. At the two levels of dietary alpha-tocopherol, etha nol treatment significantly decreased the content of hepatic alpha-tocopher ol and ubiquinols 9 and 10. This effect was significantly greater at 10 mg alpha-tocopherol/100% diet than at 2.5, whereas those of tGSH were signific antly elevated by 43% and 9%, respectively. Chronic ethanol intake did not alter the content of brain alpha-tocopherol and tGSH, whereas those of ubiq uinol-9 were significantly lowered by 20% and 14% in rats subjected to 10 a nd 2.5 mg alpha-tocopherol/100 g diet, respectively. It is concluded that c hronic ethanol intake at two levels of dietary alpha-tocopherol induces a d epletion of hepatic alpha-tocopherol and ubiquinols 9 and 10, thus contribu ting to ethanol-induced oxidative stress in the liver tissue. This effect o f ethanol is dependent upon the dietary level of alpha-tocopherol, involves a compensatory enhancement in hepatic tGSH availability, and is not observ ed in the brain tissue, probably due to its limited capacity for ethanol bi otransformation and glutathione synthesis.