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Article Abstract
Ischemia-mediated lipidomic changes in rat brains were explored by matrix-assisted laser desorption/ionization-mass spectrometry (MALDI-MS) profiling and imaging after in situ desalting which drastically simplified the spectral presentation of tissue lipids. Removal of interference from the massively changed cations in response to tissue damage permitted the revelation of subtle yet important lipidomic changes. The identities of the detected lipids were confirmed by MALDI tandem mass spectrometry (MALDI-MS/MS). The MALDI-MS imaging (MALDI-MSI) result of lysophosphatidylcholine 16:0 (LPC 16:0) in the desalted brain section appeared essentially identical to that of sodiated LPC 16:0 in the adjacent undesalted section and verified the suitability of the desalting method for the MALDI-MSI studies of lipids in tissue. Other than the consistently decreased phosphatidylcholine (PC) 16:0/18:1, images of PCs containing all saturated, or combined saturated and monounsaturated fatty acyl (MUFA) residues revealed their parenchymal increase by ischemia. Images of PCs containing polyunsaturated fatty acyl (PUFA) residues in normal cortex showed laminated patterns similar to cortical lamina. Ischemia reduced the abundance of PC 16:0/20:4 and PC 16:0/22:6 and disrupted the laminated distribution of the former. However, ischemia increased the subcortical abundance of PUFA-PCs containing stearoyl residue and confined their cortical increase within limited areas. Image of parenchymal sphingomyelin 18:0 (SM 18:0) showed its consistent decrease by ischemia that paralleled the increase of ceramide 18:0-H(2)O in region of moderate to high SM abundance. The above results presented the lipidomic changes largely different from previous MALDI-MSI results and suggested a window of intervention that may benefit the management of cerebrovascular accident and other brain injuries.
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| http://dx.doi.org/10.1007/s00216-012-6077-5 | DOI Listing |
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