this change in redox status promotes a leukocyte mediated pro-inflammatory response that ultimately leads to the exacerbation of secondary damage (Hulsebosch et al., 2011)
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The first was Fdh3, a putative glutathione-dependent S-nitrosoglutathione reductase (GSNOR), which catalyses the generation of GSSG during the recycling of GSNO adducts
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