Abstract
Azelate (C9) and glutarate (C5) are odd‐chain dicarboxylates. Azelate, derived from the oxidation of oleate, is an inhibitor of tyrosinase and thioredoxin reductase. The compartmentation of azelate metabolism and its final metabolic fates are not known. We investigated the metabolism of azelate in rat liver using a combination of metabolomics and mass isotopomer analysis. Isolated rat livers were perfused with 2 mM (un)labeled azelate or glutarate ([13C9]azelate or [13C5]glutarate) for 2 h in recirculating mode. Perfusate and liver were analyzed by GC‐MS and LC‐MS/MS. The data showed that: (i) azelate oxidation starts in peroxisomes, and ends in mitochondria; (ii) glutarate oxidation occurs only in mitochondria; (iii) azelate forms pimeloyl‐CoA and glutaryl‐CoA, but not malonyl‐CoA, (iv) an unknown reaction removes one carbon from azelaoyl‐CoA forming octanedioyl‐CoA, then hexanedioyl‐CoA, (v) the metabolism of glutarate to acetyl‐CoA via 3‐hydroxyglutaryl‐CoA, crotonyl‐CoA and S‐3‐hydroxybutyryl‐CoA is confirmed.Grant Funding Source: NIH R33DK07029 and Cleveland Mt. Sinai Health Care Foundation
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