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Biological Chemistry

Editor-in-Chief: Brüne, Bernhard

Editorial Board: Buchner, Johannes / Lei, Ming / Ludwig, Stephan / Thomas, Douglas D. / Turk, Boris / Wittinghofer, Alfred

IMPACT FACTOR 2018: 3.014
5-year IMPACT FACTOR: 3.162

CiteScore 2018: 3.09

SCImago Journal Rank (SJR) 2018: 1.482
Source Normalized Impact per Paper (SNIP) 2018: 0.820

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Volume 383, Issue 3-4


Mammalian Cell Injury Induced by Hypothermia the Emerging Role for Reactive Oxygen Species

U. Rauen / H. de Groot
Published Online: 2005-06-01 | DOI: https://doi.org/10.1515/BC.2002.050


Hypothermia is a wellknown strategem to protect biological material against injurious or degradative processes and is widely used in experimental and especially in clinical applications. However, hypothermia has also proved to be strongly injurious to a variety of cell types. Hypothermic injury to mammalian cells has long been attributed predominantly to disturbances of cellular ion homeostasis, especially of sodium homeostasis. For many years, reactive oxygen species have hardly been considered in the pathogenesis of hypothermic injury to mammalian cells. In recent years, however, increasing evidence for a role of reactive oxygen species in hypothermic injury to these cells has accumulated. Today there seems to be little doubt that reactive oxygen species decisively contribute to hypothermic injury in diverse mammalian cells. In some cell types, such as liver and kidney cells, they even appear to play the central role in hypothermic injury, outruling by far a contribution of the cellular ion homeostasis. In these cells, the cellular chelatable, redoxactive iron pool appears to be decisively involved in the pathogenesis of hypothermic injury and of coldinduced apoptosis that occurs upon rewarming of the cells after a (sublethal) period of cold incubation.

About the article

Published Online: 2005-06-01

Published in Print: 2002-04-12

Citation Information: Biological Chemistry, Volume 383, Issue 3-4, Pages 477–488, ISSN (Print) 1431-6730, DOI: https://doi.org/10.1515/BC.2002.050.

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