Investigation of the Protective Role of N-Acetylcysteine Against Amikacin-Induced Systemic Toxicity and Anxiety Behavior in Mice

This dataset confirm the results of our findings that Amikacin-treated mice showed clear anxiety-like behavior, including reduced time in the light area, an effect was improved by NAC.  Amikacin altered liver function markers such increasing the levels of alanine transferase and aspartate transferase.  NAC attenuated these changes indicating hepatoprotective effects.  Metabolic markers such as lactate dehydrogenase, and uric acid were increased after amikacin treatments. Amikacin caused marked increase in inflammatory cytokines and chemokines, including IL-6, TNF-α, IL-12p70, IL-22, CXCL10 and CCL7.  NAC lowered IL-6, IL-12p70, IL-22, and CXCL10 indicating potential effects of NAC in reducing the systemic inflammatory responses associated with amikacin exposure. Principle compartment and heatmap analysis of serum biochemistry and inflammatory profiles revealed a clear segregation between amikacin compared to other three groups.