Lipid dysregulation has been implicated in
multiple sclerosis due to its involvement during and after
inflammation. In this study, we have profiled
fatty acids (FAs) in the mouse model of
multiple sclerosis with new capabilities of assigning
carbon-
carbon double bond (C=C) location(s) and quantifying C=C location isomers. These new capabilities are enabled by pairing the
solution phase Paternò-Büchi (PB) reaction that modifies C=C bonds in FAs, with tandem mass spectrometry (MS/MS), termed as PB-MS/MS. A series of unsaturated FAs and C=C location isomers have been identified, including FA17:1 (Δ10), FA18:1 (Δ9 and Δ11), FA18:2 (Δ9 and Δ12), and FA 20:4 (Δ5, Δ8, Δ11, Δ14). Notable differences in saturated and unsaturated FAs between normal and
experimental autoimmune encephalomyelitis (EAE) mice spinal cords have been detected. Furthermore, the effects of
hydralazine, a scavenger of
acrolein, on profile changes of FAs in mice were studied. Increased Δ11-to-Δ9 isomer ratios for FA 18:1 were noted in the diseased samples as compared to the control. The present work provides a facile and robust analytical method for the quantitation of unsaturated FAs as well as identification of FA C=C location isomers, which will facilitate discovering prospective
lipid markers in
multiple sclerosis.