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Int J Clin Exp Pathol 2(2),182-189;2009

Original Article
The Double Danger of Ethanol and Hypoxia: Their Effects on a Hepatoma Cell Line

Stephanie M. Wang and Rongqian Wu

The Feinstein Institute for Medical Research, Manhasset, NY 11030, USA

Received 2 July 2008; Accepted 18 July 2008; Available online 25 July 2008

Abstract: Alcohol use has become far too prevalent in our society. Alcohol kills 6.5 times more youth than all other illicit drugs combined. In
combination with traumatic and hemorrhagic injuries, alcohol results in a much higher mortality rate. Alcohol, alone and in high dosages, also
causes great damage to the body, often leading to death as well. Thus, it is of utmost importance that research is conducted to help explain the
pathological mechanism of high fatalities and injuries associated with alcohol use. In order to simulate this complex situation in vitro, a rat
hepatoma cell line (H-II-4-E) was exposed to various concentrations of ethanol as well as the condition of hypoxia. Hypoxia mimics the primary
level of tissue damage caused by hemorrhage after impact in a car accident. In this way, we tested the hypothesis that the presence of ethanol
in combination with hypoxia causes greater cellular damage compared to conditions of ethanol or hypoxia alone. Ethanol, alone and in high
concentrations, was found to greatly affect cell function as shown by decreased cellular ATP levels, increased LDH release, and a
downregulated expression of CYP2E1 gene. By adding the condition of hypoxia to low concentrations of ethanol, cellular damage increased
dramatically as well. Decreased gene expression and protein levels of CYP2E1 correlated with increased hepatocyte injury and thus, this
enzyme may significantly contribute to the severity of cellular damage. These results provide useful information for future research on the effects
of ethanol in combination with hemorrhage on cells in vitro, simulating the condition of driving while intoxicated and binge drinking.
(IJCEP807001 ).

Key Words: Ethanol, hypoxia, adenosine triphosphate, cytochrome P450 2E1, lactate dehydrogenase

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Address all correspondence to: Rongqian Wu, MD, PhD, The Feinstein Institute for Medical Research, 350 Community Drive, Manhasset, NY
11030, USA. Tel: 516-562-2390; Fax: 516-562-2396; Email:
rwu@nshs.edu