1.
Alcohol Alcohol Suppl
; 1: 241-4, 1987.
Artigo
em Inglês
| MEDLINE
| ID: mdl-2827693
RESUMO
Two hours after an acute ethanol load (50 mmol/kg, i.p.), brain mitochondrial superoxide production was unchanged. This is contrary to our previous findings concerning liver mitochondria. On the other hand, the ethanol treatment caused a marked inhibition of respiration stimulated by phosphate plus ADP (with succinate or pyruvate plus malate as substrates) (state 3) in the brain mitochondria, whereas it did not exert any modification on the hepatic mitochondrial electron transport chain.