PMC

Schematic representation of beta oxidation and the enzymes involved

Spectra of extracts from triolein aged with titanium dioxide measured in positive mode highlighting products of hydrolysis, oxidation, and β scission. Products of oxidation and β scission pathways of MAG (a), DAG (b), and TAG (c). The dark vertical lines in the upper part of each spectrum highlight the peaks that were matched with oxidation products, and the dark vertical lines on the lower mirrored spectrum highlight the peaks that were matched to the products formed after β scission reaction. The light gray areas in the upper part of each spectrum correspond to the approximate regions for oxidation products, and the light gray areas in the lower part of each spectrum correspond to the approximate regions for β scission products.

(A) Accumulation of S-PTGS siRNAs from GUS transgene (L1 locus) in the wild-type (Col) before and after the oxidation and β elimination reactions (+β) and in hen1-4 and hen1-6 (SALK_090960).
(B) Accumulation of IR-PTGS siRNAs from an AP1 hairpin transgene in the wild-type (Col) and hen1-4 before and after (+β) the oxidation and β elimination reactions.
(C) Accumulation of a ta-siRNA in the wild-type (Ler) and hen1-1 before and after (+β) the oxidation and β elimination reactions. Images of ethidium-bromide-stained gels in the region of tRNAs are shown at the bottom.

Proposed model of HNE disposal pathways. In addition to the well-established detoxification pathways for HNE, catabolism through fatty acid β oxidation serves as an important downstream pathway of HNE disposal. The catabolism of HNE is blocked under conditions where fatty acid β oxidation is inhibited under pathological conditions such as ischemia/reperfusion or when the heart is exposed to elevated concentrations of lipid. Diminished catabolism of HNE through β oxidation leads to a greater burden of disposal through detoxification pathways and an enhanced accumulation of HNE-modified protein, lipid and DNA. CAC; citric acid cycle.