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P. K. M. Kim, B. S. Zuckerbraun, L. E. Otterbein, Y. Vodovotz, T. R. Billiar

Til cell death do us part: nitric oxide and mechanisms of hepatotoxicity

Like many juggernauts in biology, the elusive nature of nitric oxide (NO) sprints through the fields, sometimes the savior, at other times the scimitar. In the liver, which is the metabolic center of the organism, hepatocytes and immune cells trade blows using the reactive diatomic molecule NO to induce cellular damage under toxic conditions. In response, hepatocytes can utilize several mechanisms of NO to their protective advantage by prohibiting the activation of programmed cell death, a.k.a. apoptosis. The balance of these effects in this reactive milieu set the stage for the homeostatic response to cellular injury that determines whether hepatocytes will live, die, or regenerate. Insights that we and others have gained from the liver under pathologic conditions of stress can be applied to the understanding of cellular death mechanisms in other organs and tissues.

Biological Chemistry, Walter de Gruyter

Print ISSN: 1431-6730
Volume: 385, 02/2004
Pages: 11 - 15

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