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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