Renal Oxidative Stress Induced by Long-Term Hyperuricemia Alters Mitochondrial Function and Maintains Systemic Hypertension

Figure 2

Antioxidant treatment successfully prevented long-term hyperuricemia induced renal biochemical and mitochondrial abnormalities. Long-term OA-induced increased oxidative stress and mitochondrial accumulation of UA. These changes were associated with renal cortical mitochondrial dysfunction characterized by oxidative phosphorylation uncoupling (decreased RC) and decreased aconitase activity and diminished ATP renal content. Tempol and allopurinol treatments prevented those changes. a: versus Control; b: versus OA.