Intermediates of peroxisomal beta-oxidation of [U-14C]hexadecanedionoate. A study of the acyl-CoA esters which accumulate during peroxisomal beta-oxidation of [U-14C]hexadecanedionate and [U-14C]hexadecanedionoyl-mono-CoA.
1. The oxidation of [U-14C]hexadecanedionoyl-mono-CoA was stimulated by CoA, by carnitine in the absence of CoA and by the presence of an NAD(+)-regenerating system. 2. Substrate inhibition was observed with respect to [U-14C]hexadecanedionoyl-mono-CoA at concentrations greater than 35 microM. 3. Acetyl-CoA and the dicarboxyl-CoA esters of chain length C6-16 were detected by HPLC under standard incubation conditions. 4. In the absence of the NAD(+)-regenerating system, 2-enoyl-CoA and 3-hydroxacyl-CoA esters were detected. 5. In general, the peroxisomal beta-oxidation of dicarboxylates is very similar to that of monocarboxylates [Bartlett, K., Hovik, R., Eaton, S., Watmough, N. J. & Osmundsen, H. (1990) Biochem. J. 270, 175-180] except that chain shortening does not proceed beyond C6. 6. We conclude that the peroxisomal beta-oxidation of dicarboxylates is regulated by the redox state of the peroxisomal matrix and CoA availability.
Pourfarzam
M
M
Department of Child Health, University of Newcastle upon Tyne, England.
Bartlett
K
K
D000105:Acetyl Coenzyme A / Q000378:metabolism; D000214:Acyl Coenzyme A / Q000378:metabolism*; D000818:Animals; D002331:Carnitine / Q000494:pharmacology; D002851:Chromatography, High Pressure Liquid; D003065:Coenzyme A / Q000494:pharmacology; D007700:Kinetics; D008099:Liver / Q000648:ultrastructure*; D008297:Male; D008830:Microbodies / Q000378:metabolism*; D009243:NAD / Q000378:metabolism; D010084:Oxidation-Reduction; D010168:Palmitates / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains
D000214:Acyl Coenzyme A; D010168:Palmitates; C066987:hexadecanedionyl-mono-coenzyme A; D009243:NAD; D000105:Acetyl Coenzyme A; D002331:Carnitine; D003065:Coenzyme A