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Sepsis is a complex pathophysiological condition resulting from a systemic inflammatory response to infection and is the leading cause of death in critically ill patients (1). In this condition, phagocytic cells firstly react with the lipopolysaccharide (LPS) or endotoxin (2). In response to LPS, macrophages excrete proinflammatory cytokines including tumor necrosis factor-α (TNF-α) and interleukin-1β (IL1β). Tumor necrosis factor-alpha seems to be important for diverse effects, which stimulates inducible nitric oxide synthase (iNOS) excretion (3). Nitric oxide can interact with superoxide (O 2) to compose the peroxynitrite (ONOO -) leading to septic shock with high mortality after a number of mechanisms. The measurement of 3-nitrotyrosine (3-NT) can mirror the stage of ONOOinduced tissue damage (4). The relationship between 3-NT and nitrosative tissue damage in sepsis has also been documented in recent studies using experimental models of endotoxemia (4, 5).

Lipoic acid decreases 3-nitrotyrosine and cytokine levels in a rat sepsis model