Factors controlling the rate of fatty acid β-oxidation in rat liver mitochondria

Bremer, Jon; Wojtczak, Andrzej

doi:10.1016/0005-2760(72)90131-2

Cited by 169 publications

(71 citation statements)

References 26 publications

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“…The latter would predict the acyl-CoA dehydrogenases to have by far the greatest control strength since their measured activities are the lowest of the four steps of P-oxidation (Melde et al, 1991). Such a role of the redox state has been postulated previously (Bremer and Wojtczak, 1972 ;Lopez-Cardozo et al, 1978;Latipaa et al, 1986), although only when respiratory-chain activity was decreased. Kunz (1 991) found significant control to reside with the respiratory chain under all conditions, although it is important to note that the concentration of CoA esters never attained a steady state in our experiments, as found by Tubbs (1974, 1975), even though flux measured as acid-soluble radioactivity would suggest steady-state conditions to be prevailing.…”

Section: Discussionsupporting

confidence: 57%

“…Production of 3-enoyl-CoA esters by rat liver mitochondria has not been directly demonstrated previously, although work by Davidoff and Korn (1965), Bremer and Wojtczak (1972), Stanley and Tubbs (1975), Lopez-Cardozo et al (1978) and Jin et al (1992) suggested that such a CoA ester might be formed in situations in which the NAD+/ NADH ratio is held artificially low, either by succinate-induced reversed electron flow (Chance and Hollunger, 1957 ;Ernster and Lee, 1967) or by rotenone inhibition of complex I (Slater, 1967), The 3-enoyl-CoA derivatives probably arise from the action of 3,2-enoyl-CoA isomerase (Stoffel and Ecker, 1969) on trans-2-enoyl-CoA formed by the acyl-CoA dehydrogenases. The stereospecificity of the 3-enoyl-CoA esters could not be determined here, although Jin et al (1 992) found approximately equal amounts of cis-and trans-acids.…”

Section: Discussionmentioning

confidence: 95%

“…However the formation of 2-enoyl-CoA and 3-hydroxyacylCoA esters from [U-'4C]hexadecanoate is different to previous studies of liver mitochondria. These either used insensitive methods (Bremer and Wojtczak, 1972;Stanley and Tubbs, 1975 ;Lopez-Cardozo et al, 1978) or low-specificactivity substrate with uncoupled mitochondria in the presence of the citrate-cycle inhibitor fluorocitrate (Watmough et al, 1989). The present work extends that of Watmough et al (1989) to a more physiological situation i.e.…”

Section: Discussionmentioning

confidence: 99%

“…Inhibition of respiratory-chain activity at the level of complex I leads to diminished P-oxidation flux and the accumulation of 3-hydroxyacyl-CoA and 2-enoyl-CoA and carnitine esters (Bremer and Wojtczak, 1972;Tubbs, 1974, 1975;LopezCardozo et al, 1978;Latipaa et al, 1986;Watmough et al, 1989) which may lead to further inhibition of flux at the level of the acyl-CoA dehydrogenases (Davidson and Schulz, 1982;Powell et al, 1987). Similarly deficiency of ETF or ETF: QO leads to diminished P-oxidation flux and an accumulation of long-chain saturated acyl-CoA and and acylcarnitine esters (Singh Kler et al, 1991).…”

mentioning

confidence: 99%

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Redox control of β‐oxidation in rat liver mitochondria

Eaton

Turnbull

Bartlett

1994

European Journal of Biochemistry

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Coupled rat liver mitochondria were incubated with [U-i4C]hexadecanoate and carnitine which resulted in the formation of acyl-, 2-enoyl-and 3-hydroxyacyl-CoA and carnitine esters. The production of 2-enoyl-CoA and 3-hydroxyacyl-CoA esters was associated with a significant lowering of the NAD'NADH ratio, in contrast to rat muscle mitochondria [Eaton, S., Bhuiyan, A. K. M. J., Kler, R. S., Turnbull, D. M. & Bartlett, K. (1993) Biochem. J. 289, 161-1721, suggesting that control by the respiratory chain is important under normal conditions. When NAD'NADH ratios were held low by succinate-induced reverse electron flow, 3-enoyl-CoA esters were also detected, probably formed by the action of 3,2-enoyl-CoA isomerase. Measurement of the flux of P-oxidation at different osmolalities showed that flux was strongly dependent on osmolality changes in the physiological range. Measurement of the CoA and carnitine esters resulting from incubations made at different osmolalities showed that there was an increase in the amounts of the saturated acyl-CoA esters with respect to 2-enoyl-CoA and 3-hydroxyacyl-CoA esters, consistent with control by the electron-transfer flavoprotein-ubiquinone segment [Halestrap, A. P. & Dunlop, J. L. (1986) Biochem. J. 239, 559-5651. This however could not be the only factor operating as indicated by the continued presence of 2-enoyl-CoA and 3-hydroxyacyl-CoA esters at high osmolalities.Mitochondria1 P-oxidation is linked to the respiratory chain at two stages ; the 3-hydroxyacyl-CoA dehydrogenases to complex I via NAD'DJADH and the acyl-CoA dehydrogenases to ubiquinone via electron-transfer flavoprotein (ETF) and its oxidoreductase (ETF: QO). Inhibition of respiratory-chain activity at the level of complex I leads to diminished P-oxidation flux and the accumulation of 3-hydroxyacyl-CoA and 2-enoyl-CoA and carnitine esters (Bremer and

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 95%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

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Redox control of β‐oxidation in rat liver mitochondria

Eaton

Turnbull

Bartlett

1994

European Journal of Biochemistry

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“…If the mitochondria were to be incubated in a KC1 containing medium, they were given a final wash in that medium. 1-[14C] Palmitoylcarnitine was prepared as described by Bremer et al [8], and had a specific activity of 1.2 × 103 c.p.m./ nmol.…”

Section: Methodsmentioning

confidence: 99%