To account for differences in susceptibility
to alcoholic liver disease (ALD), tobacco smoking should be evaluated as a
potential cofactor given the very high percentage of heavy drinkers also smoke,
and the NNK tobacco-specific nitrosamine was shown to cause steatohepatitis and
exacerbate molecular and biochemical effects of alcohol on the liver.
Since one
of the key factors linked to ALD progression is dysregulated lipid
metabolism, we examined effects of cigarette smoke (CS) exposures on hepatic
lipid profiles using matrix-assisted laser desorption and ionization imaging
mass spectrometry (MALDI-IMS).
Adult male A/J mice were exposed to air (8
weeks; A8), CS for 4 (CS4) or 8 (CS8) weeks; or CS8 with 2 weeks recovery
(CS8+R). MALDI-IMS demonstrated broad CS-associated reductions in hepatic
phospholipids that were partly ameliorated by short-term recovery.
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