Mitochondrial Reactive Oxygen Species and Nephrolithiasis

Mitochondrial redox/oxidative balance are vital for cellular life and death. Mitochondria are considered as the most important sub cellular site of reactive oxygen species production in mammalian organs. Reactive oxygen species produced by mitochondria can cause damage to mitochondrial components and initiate degradative processes. The kidney requires ample amount of mitochondria to remove waste from the blood and regulate fluid and electrolyte balance. Adverse conditions of organelle stress such as decreased altered energy metabolism in mitochondria contribute in the progression and development of kidney diseases. Nephrolithiasis is a kidney disease in which solid urinary components form crystals, precipitated out of the urine and shaped into stones. Studies have suggested that oxidative stress and associated renal injury paved the way for crystal deposition in the renal tissue. Mitochondria are anticipated as the foremost source of intracellular reactive oxygen species under oxalate induced nephrolithiasis. Persistent mitochondrial dysfunction results in the progression of nephrolithiasis. Although different approaches to minimize mitochondrial dysfunction through regulation of mitochondrial ROS production using antioxidants have been accomplished yet mitochondria specific antioxidants are the prerequisite. This review offers a glimpse into the role of mitochondrial reactive oxygen species in nephrolithiasis and the future perspective of potential antioxidant therapies.