Ricinoleic Acid Catabolism in Peroxisomes

Peroxisomes from castor bean endosperm and mung bean hypocotyl completely degrade ricinoleic acid (12‐D‐hydroxy‐9‐cis‐octadecenoic acid) to acetyl‐CoA. Concomitant NADH formation occurred with a stoichiometry of 9 nmol NADH formed per 1 nmol ricinoleate degraded. At the C8‐intermediate level, where the hydroxy group of ricinoleic acid forms a barrier to β‐oxidation, 2‐hydroxyoctanoate and 2‐oxooctanoate were detected as intermediates. 2‐Hydroxyoctanoate was oxidized to 2‐oxooctanoate with H2O2 producing a reaction exhibiting 1:1 stoichiometry of the products. The peroxisomes appeared to oxidize both isomers of racemic 2‐hydroxyoctanoate. 2‐Oxooctanoate was metabolized to heptanoyl‐CoA (propionyl‐CoA and acetyl‐CoA) in a NAD‐dependent, but ATP‐independent, reaction. Heptanoate was not detected as an intermediate. Imidazole, an inhibitor of α‐oxidation, did not effect the degradation of ricinoleate or 2‐oxooctanoate. Arsenite, an inhibitor of oxidative decarboxylation, inhibited the metabolism of ricinoleate at the C8‐intermediate level, according to the accumulation of 2‐oxooctanoate and the stoichiometry of concomitant NADH formation. Arsenite completely inhibited the metabolism of 2‐oxooctanoate. It is concluded that the barrier caused by the hydroxy group of ricinoleic acid and prevention of β‐oxidation at the C8‐intermediate level, is circumvented by an α‐hydroxy acid oxidase reaction followed by an oxidative decarboxylation allowing return to the β‐oxidation track.