Protective effect and mechanism of CoQ10 in mitochondrial dysfunction in diquat-induced renal proximal tubular injury

Coenzyme Q10 (CoQ10) plays an important role in improving mitochondrial function and has many beneficial effects on the kidney. However, whether CoQ10 protects against diquat (DQ)-induced acute kidney injury (AKI) remains unclear. In this study, we investigated the protective effects and mechanism of action of CoQ10 against DQ-induced AKI. Institute of Cancer Research (ICR) mice were intraperitoneally injected with DQ to induce AKI. The expression levels of serum creatinine (Cr), urea, and kidney injury molecule-1 (KIM-1) increased, those of Aquaporin 1 (AQP-1) decreased, and those of mitochondrial Reactive Oxygen Species (ROS) increased with increased depolarization of mitochondrial membranes and mitochondrial rupture. In contrast, treatment with CoQ10 significantly improved DQ-induced AKI. CoQ10 treatment reduced serum Cr, urea, and KIM-1 contents, increased the AQP-1 expression, and reduced ROS contents in mice with DQ poisoning. Our results suggest that AKI caused by DQ poisoning may be related to the disruption of mitochondrial homeostasis and that CoQ10 treatment protects against AKI caused by DQ poisoning by improving mitochondrial kinetic homeostasis. Thus, CoQ10 represents a new therapeutic option for the prevention and treatment of AKI caused by DQ poisoning.

Coenzyme Q10; Diquat; kidney injury; mitochondrial dynamics; mitochondrial membrane potential.