Arachidonic acid is a preferred acetyl donor among fatty acids in the acetylation of p-aminobenzoic acid by human lymphoid cells.

We have previously reported that human lymphoid cells, such as peripheral blood mononuclear leukocytes (PBML) and the T-cell leukemia line Jurcat, synthesize p-acetamidobenzoic acid from p-aminobenzoic acid (PABA) and a two carbon fragment from arachidonic acid (AA), conceivably derived from beta-oxidation. Here we demonstrate that AA is a preferred substrate in this acetylation reaction over other common fatty acids such as palmitic (PA), oleic, linoleic or linolenic. This was unexpected because AA is not considered as a fuel fatty acid. In Jurcat cells, AA is also preferred as a substrate for beta-oxidation over PA. In contrast, in PBML, PA was clearly preferred as substrate for beta-oxidation over AA, in accordance with previous observations. The difference between Jurcat cells and PBML was not dependent on culture conditions, because phytohemagglutinin and interleukin-2 activated PBML, kept in culture, showed the same PA preference as freshly prepared non-activated PBML. Furthermore, we observed differences between Jurcat cells and PBML in their relative content of fatty acids and in the incorporation of PA and AA into triacylglycerols and phospholipids. Taken together, our results show differences in beta-oxidation between Jurcat cells and PBML, and suggest the involvement of peroxisomal, besides mitochondrial, beta-oxidation, in the acetylation of PABA with fatty acids as acetyl donors.