Differential lipid profiles in experimental steatohepatitis : role of imaging mass spectrometry as a diagnostic festival

Abstract EN

Background.

Ethanol, tobacco-specific nitrosamine ketone (NNK), and ethanol+NNK exposures cause steatohepatitis, suggesting that smoking can be a cofactor in alcoholic liver disease.

Study design.

We used MALDI-TOF imaging mass spectrometry (IMS) to characterize hepatic lipid profiles in steatohepatitis caused by ethanol, NNK, and ethanol+NNK.

Results.

Ethanol, NNK, and ethanol+NNK increased levels and altered the profiles of hepatic phospholipids.

Ethanol caused striking accumulations of m/z 932.7 phosphatidylinositol (PI).

NNK increased hepatic levels of PIs with m/z’s of 934.8, 960.8, and 962.7.

Relative abundance of PIs with m/z’s of 857.9 or 883.7 increased progressively from control to NNK, then ethanol, and finally ethanol+NNK, indicating differential and additive effects of these exposures.

In contrast, no differences occurred with respect to phosphatidylethanolamine (m/z 766.9), phosphatidylserine (m/z 810.9) or PIs with m/z of 960.8 or 962.7.

Principal component analysis generated distinct exposure-related hepatic lipid profiles.

Conclusion.

MALDI-IMS could serve as a complementary diagnostic aid for differentiating underlying causes of steatohepatitis.