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The peroxisomal fatty acid β-oxidation pathway is a cellular metabolic process responsible for the initial breakdown and shortening of very long-chain and branched-chain fatty acids. Its function is distinct from mitochondrial β-oxidation, as it specializes in substrates that cannot be processed by mitochondria, generating acetyl-CoA and hydrogen peroxide (H₂O₂) as byproducts. Key enzymes include acyl-CoA oxidase, bifunctional proteins, and thiolase, with regulation governed by peroxisome proliferator-activated receptor alpha (PPARα). Disruption or dysregulation of this pathway contributes to metabolic diseases such as fatty liver, steatohepatitis, liver cancer, and certain neurological disorders due to accumulation of substrate fatty acids or excessive ROS production[1][2][3][5].
Induction of pathway activity by peroxisome proliferators (drugs increase enzyme expression/activity) Attenuation of oxidative stress via antioxidants
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