Abstract
For a long time, it has been recognized that the effects of excessive production of reactive oxygen species leading to oxidative stress are damaging to cellular constituents with subsequent tissue necrosis. There is now evidence that reactive oxygen species can alter cell functions by acting as ‘second messengers’ [1] or by affecting proteins of the signal transduction pathway that leads to gene expression or to apoptosis [2–4]. But many questions remain about the role of reactive oxygen and nitrogen compounds: how and where do they act? Do they act by themselves or by way of secondary products like nitroso- or nitrated compounds, oxidized forms of thiol compounds such as GSSG (the oxidized form of gluthatione), α,β-unsaturated aldehydes or carbonylated proteins? Do they alter specific proteins of the signal transduction pathway or intervene in Ca2+ metabolism? Do they act at the level of the nucleus by oxidation of thiol proteins involved in the activation of gene expression? Do specific reactive oxygen species (ROS) such as nitric oxide (NO) or peroxynitrite, have specific activity on selected biomolecules? And, above all else, what can be transposed from in vitro studies or laboratory models to in vivo situations?
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Lamy, M., Nys, M., Deby-Dupont, G. (2001). Reactive Nitrogen and Oxygen Species: Role and Evidence of their Production in Humans. In: Vincent, JL. (eds) Yearbook of Intensive Care and Emergency Medicine 2001. Yearbook of Intensive Care and Emergency Medicine 2001, vol 2001. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-59467-0_25
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DOI: https://doi.org/10.1007/978-3-642-59467-0_25
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