SM(d16:1/18:2(10E,12Z)+=O(9))

(2-{[(2S,3R,4E)-3-hydroxy-2-[(10E,12Z)-9-oxooctadeca-10,12-dienamido]hexadec-4-en-1-yl phosphono]oxy}ethyl)trimethylazanium

Formula: C39H73N2O7P (712.5155)
Chinese Name:
BioDeep ID: BioDeep_00000215272 ( View LC/MS Profile)
SMILES: [H][C@@](COP([O-])(=O)OCC[N+](C)(C)C)(NC(=O)CCCCCCCC(=O)\C=C\C=C/CCCCC)[C@H](O)\C=C\CCCCCCCCCCC



Found 4 Sample Hits

m/z Adducts Species Organ Scanning Sample
713.5304 [M+H]+
PPM:10.7
Mus musculus Lung MALDI (DHB)
image1 - MTBLS2075
Resolution: 40μm, 187x165

Description

Fig. 2 MALDI-MSI data from the same mouse lung tissue analyzed in Fig. 1. A: Optical image of the post-MSI, H&E-stained tissue section. B–D, F–G: Ion images of (B) m/z 796.6855 ([U13C-DPPC+Na]+), (C) m/z 756.5514 ([PC32:0+Na]+), (D) m/z 765.6079 ([D9-PC32:0+Na]+), (F) m/z 754.5359 ([PC32:1+Na]+), and (G) m/z 763.5923 ([D9-PC32:1+Na]+). E, H: Ratio images of (E) [D9-PC32:0+Na]+:[PC32:0+Na]+ and (H) [D9-PC32:1+Na]+:[PC32:1+Na]+. Part-per-million (ppm) mass errors are indicated in parentheses. All images were visualized using total-ion-current normalization and using hotspot removal (high quantile = 99%). DPPC = PC16:0/16:0. U13C-DPPC, universally 13C-labeled dipalmitoyl PC; PC, phosphatidylcholine; MSI, mass spectrometry imaging; H&E, hematoxylin and eosin. Fig 1-3, Fig S1-S3, S5

713.5326 [M+H]+
PPM:13.8
Homo sapiens esophagus DESI ()
LNTO29_16_2 - MTBLS385
Resolution: 17μm, 95x101

Description

713.5342 [M+H]+
PPM:16
Homo sapiens esophagus DESI ()
LNTO22_1_9 - MTBLS385
Resolution: 75μm, 89x74

Description

695.5204 [M+H-H2O]+
PPM:11.8
Mus musculus Liver MALDI (CHCA)
Salmonella_final_pos_recal - MTBLS2671
Resolution: 17μm, 691x430

Description

A more complete and holistic view on host–microbe interactions is needed to understand the physiological and cellular barriers that affect the efficacy of drug treatments and allow the discovery and development of new therapeutics. Here, we developed a multimodal imaging approach combining histopathology with mass spectrometry imaging (MSI) and same section imaging mass cytometry (IMC) to study the effects of Salmonella Typhimurium infection in the liver of a mouse model using the S. Typhimurium strains SL3261 and SL1344. This approach enables correlation of tissue morphology and specific cell phenotypes with molecular images of tissue metabolism. IMC revealed a marked increase in immune cell markers and localization in immune aggregates in infected tissues. A correlative computational method (network analysis) was deployed to find metabolic features associated with infection and revealed metabolic clusters of acetyl carnitines, as well as phosphatidylcholine and phosphatidylethanolamine plasmalogen species, which could be associated with pro-inflammatory immune cell types. By developing an IMC marker for the detection of Salmonella LPS, we were further able to identify and characterize those cell types which contained S. Typhimurium. [dataset] Nicole Strittmatter. Holistic Characterization of a Salmonella Typhimurium Infection Model Using Integrated Molecular Imaging, metabolights_dataset, V1; 2022. https://www.ebi.ac.uk/metabolights/MTBLS2671.


SM(d16:1/18:2(10E,12Z)+=O(9)) is a type of oxidized sphingolipid found in animal cell membranes. It usually consists of phosphorylcholine and ceramide. SM(d16:1/18:2(10E,12Z)+=O(9)) consists of a sphingosine backbone and a 9-oxo-octadecadienoyl chain. In humans, sphingomyelin is the only membrane phospholipid not derived from glycerol. Like all sphingolipids, SM has a ceramide core (sphingosine bonded to a fatty acid via an amide linkage). In addition, it contains one polar head group, which is either phosphocholine or phosphoethanolamine. The plasma membrane of cells is highly enriched in sphingomyelin and is considered largely to be found in the exoplasmic leaflet of the cell membrane. However, there is some evidence that there may also be a sphingomyelin pool in the inner leaflet of the membrane. Moreover, neutral sphingomyelinase-2, an enzyme that breaks down sphingomyelin into ceramide, has been found to localize exclusively to the inner leaflet further suggesting that there may be sphingomyelin present there. Sphingomyelin can accumulate in a rare hereditary disease called Niemann-Pick Disease, types A and B. Niemann-Pick disease is a genetically-inherited disease caused by a deficiency in the enzyme sphingomyelinase, which causes the accumulation of sphingomyelin in spleen, liver, lungs, bone marrow, and the brain, causing irreversible neurological damage. SMs play a role in signal transduction. Sphingomyelins are synthesized by the transfer of phosphorylcholine from phosphatidylcholine to a ceramide in a reaction catalyzed by sphingomyelin synthase.