which kind of fatty acids are the substrates for peroxisomal beta-oxidation?

Question

I need to know the differences between mitochondrial and peroxisomal beta-oxidation in mammals and also about beta-oxidation in yeast.

Answer 1

Straight from the web. . .



Beta-oxidation of fatty acids

Whereas the mitochondria are responsible for the oxidation of the bulk of dietary fatty acid (palmitate, oleate and linolate), peroxisomes oxidize VLCFA in addition to pristanic acid (from the dietary phytanic acid) and dihydroxycholestanoic acid (DHCA) or trihydroxycholestanoic acid (THCA). These last 2 compounds lead to the formation of bile acids, cholic acid, and chenodeoxycholic acid from cholesterol in the liver. Another major function of the peroxisomal beta-oxidation system is related to the biosynthesis of polyunsaturated fatty acid (C22:6w3). Peroxisomes also work in conjunction with mitochondria to shorten fatty acid chains, which are in turn degraded to completion in the mitochondria. The end result is the formation of acetylcoenzyme A (acetyl-CoA) units, which are degraded in the Krebs cycle to produce energy (adenosine triphosphate [ATP]).

Abnormal accumulation of VLCFAs (C24, C26) is the hallmark of peroxisomal disorders. VLCFAs have deleterious effects on membrane structure and function, increasing microviscosity of RBC membranes and impairing the capacity of cultured adrenal cells to respond to adrenocorticotropic hormone (ACTH).

In the CNS, VLCFA accumulation may cause demyelination associated with an intense inflammatory response in the white matter, with increased levels of leukotrienes due to beta-oxidation deficiency. Accompanying this response is a perivascular infiltration by T cells, B cells, and macrophages in a pattern suggestive of an autoimmune response. Levels of tumor necrosis factor and alpha immunoreactivity in astrocytes and macrophages at the outermost edge of the demyelinating lesion are increased, suggesting a cytokine-mediated mechanism. Furthermore, VLCFAs are postulated to be components of gangliosides and cell-adhesion molecules in growing axons and radial glia, and hence contribute to the migrational defect in the CNS.

Answer 2

This might help...
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6372785&dopt=Abstract

Answer 3

lactic acid