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Once formed, GSNO can release NO and cause intracellular death of the pathogen [70,71,72,73]

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Pei et al (64) revealed a close relationship between pathological injury of renal tissues following renal ischemia-reperfusion, increased GPX3 expression (a marker of oxidative stress) and various processes (including GSH metabolism, oxidative stress pathways and regulation of T-cell activation)