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relationship between oxidative stress and hepatic glutathione levels in
ethanol-mediated apoptosis of
polarized hepatic cells
Glutathione Articles - Additional Usages
Relationship between oxidative stress and hepatic glutathione levels in
ethanol-mediated apoptosis of
polarized hepatic cells
McVicker B., Tuma P., Kharbanda K.,
Lee S., Tuma D.
World J Gastroenterol 2009 June 7; 15(21): 2609-2616
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AIM: To investigate the role of
reactive oxygen species (ROS) in ethanol-mediated cell death of
polarized hepatic (WIF-B) cells.
METHODS: In this work, WIF-B cultures were treated with pyrazole
(inducer of cytochrome P4502E1, CYP2E1) and/or L-buthionine sulfoximine
(BSO), a known inhibitor of hepatic glutathione (GSH), followed by
evaluation of ROS production, antioxidant levels, and measures of cell
injury (apoptosis and necrosis).
RESULTS: The results revealed that ethanol treatment alone caused a
significant two-fold increase in the activation of caspase-3 as well as
a similar doubling in ROS. When the activity of the CYP2E1 was increased
by pyrazole pretreatment, an additional two-fold elevation in ROS was
detected. However, the CYP2E1-
related ROS elevation was not accompanied with a correlative increase in
apoptotic cell injury, but rather was found to be associated with an
increase in necrotic cell death. Interestingly, when the thiol status of
the cells was manipulated using BSO, the ethanol-induced activation of
caspase-3 was abrogated. Additionally,
ethanol-treated cells displayed enhanced susceptibility to Fas-mediated
apoptosis that was blocked by GSH depletion as a result of diminished
caspase-8 activity.
CONCLUSION: Apoptotic cell death induced as a consequence of ethanol
metabolism is not completely dependent upon ROS status but is dependent
on sustained GSH levels.
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