Table 1.

Summary of the major studies of CYP2E1 and JNK in alcohol-induced oxidative stress.

Experimental system	Model	Read out	Mechanism	Effect	Reference
CYP2E1 knockout mice	Chronic ethanol	Liver injury, oxidative stress, steatosis	Increased oxidative stress	Increased steatosis and injury	[40]
C57BL/6 mice	Pyrazole±LPS	Liver injury and oxidative stress	MAPK activation	Increased injury	[41]
C57BL/6 mice	Ethanol±Jo2 antibody	Liver injury and oxidative stress	Mitochondrial dysfunction	Increased injury	[44]
JNK1 and JNK2 knockout mice	Pyrazole±TNF	Liver injury, oxidative stress, mitochondrial dysfunction	JNK1 activation	Decreased injury in jnk1−/− mice	[45]
C57BL/6 mice	Pyrazole±TNF	Liver injury, oxidative stress, MAPK activation	ASK-1 activation	Increased injury	[41]
CYP2E1 knockout mice	Ethanol±Jo2 antibody	Liver injury, MAPK activation	Increased death receptor signaling	increased injury	[68]
C57BL/6 mice and CYP2E1 overexpressing HepG2 cells	Ethanol gavage in mice and ethanol treatment in cells	Cellular injury, oxidative stress, hepatic steatosis	Increased autophagy	Decreased steatosis	[58]
CYP2E1 overexpressing HepG2 cells	siRNA knockdown of thioredoxin	MAPK activation, cell survival	ASK-1 and JNK activation	Increased cell death	[48]
CYP2E1 overexpressing HepG2 cells	3-Methyladenine or Atg 7 siRNA	Oxidative stress, MAPK activation, cell survival	Decreased autophagy	Increased injury	[57]