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. 2013 Oct 25;63(8):1313–1324. doi: 10.1136/gutjnl-2012-304058

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Importance of non-oxidative metabolism of ethanol and oxidative metabolism of ethanol in pancreatic acinar cell death. (A) Levels of apoptosis (caspase; green) and necrosis (PI; red) were increased by palmitoleic acid ethyl ester (POAEE;50–200 μmol/L) compared with controls, whereas acetaldehyde (ACETAL, 100–200 μmol/L) was without effect. (B) Ethanol (EtOH; 10 mmol/L), palmitoleic acid (POA;20 μmol/L) or 4-methylpyrazole (4-MP;100 μmol/L), applied alone, did not increase caspase activation (green) or PI uptake (red). However, a combination significantly increased apoptotic and necrotic cell death pathway activation. (C) Inhibition of carboxylester lipase with 3-benzyl-6-chloro-2-pyrone (3-BCP;10 μmol/L) reversed ethanol/POA-induced cell death precipitated by 4-MP (expressed as % total cells; mean±SE; numbers in parentheses indicate cells assessed for each experimental condition, *p<0.05 compared to control values).