Alcohol and Aldehyde Metabolizing Systems-Iv 1980
DOI: 10.1007/978-1-4757-1419-7_38
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Effects of Chronic Ethanol Consumption on the Respiratory Chain of Rat Liver Submitochondrial Particles

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Cited by 24 publications
(28 citation statements)
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“…In agreement with previous studies that reported a decline in electron transport components [5,10,[22][23][24][25][26], the rate of generation of ∆p (the respiratory subsystem) with different substrates was inhibited after 2 months of ethanol consumption. With NAD + -dependent substrates and TMPD\ascorbate a significant suppression of the respiratory subsystem was observed at all values of the mitochondrial membrane potential examined, with more pronounced inhibition in State 3 than State 4.…”
Section: Discussionsupporting
confidence: 92%
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“…In agreement with previous studies that reported a decline in electron transport components [5,10,[22][23][24][25][26], the rate of generation of ∆p (the respiratory subsystem) with different substrates was inhibited after 2 months of ethanol consumption. With NAD + -dependent substrates and TMPD\ascorbate a significant suppression of the respiratory subsystem was observed at all values of the mitochondrial membrane potential examined, with more pronounced inhibition in State 3 than State 4.…”
Section: Discussionsupporting
confidence: 92%
“…The results presented in Table 1 demonstrate that 2 months of chronic alcohol treatment diminished the activities of the bc " complex, cytochrome oxidase and ATPase in rat liver mitochondria by 41p5 %, 40p6 % and 36p4 % respectively (Table 1). These data are consistent with previous studies [5,10,[22][23][24][25][26]. The alterations in the component activities bring about the differential responses of each block of reactions R, L and P to changes in ∆Ψ.…”
Section: Activities and Kinetic Responses Of The Components Of Oxidatsupporting
confidence: 93%
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“…However, there are no data regarding the zonal effects of ethanol on mitochondria functionality along the liver acinus (21)(22)(23)(24)(25). Since ethanol causes preferential necrosis and fibrosis in the centrilobular zone of the liver (26), the purpose of this study was to examine the hepatic acinar distribution of mitochondrial GSH in control and ethanol-fed rats and the relationship of changes to mitochondria functionality.…”
Section: Introductionmentioning
confidence: 99%