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.

In vitro studies reveal antiurolithic effect of Terminalia arjuna using quantitative morphological information from computerized microscopy

ABSTRACT Purpose: For most cases, urolithiasis is a condition where excessive oxalate is present in the urine. Many reports have documented free radical generation followed by hyperoxaluria as a consequence of which calcium oxalate (CaOx) deposition occurs in the kidney tissue. The present study is aimed to exam the antilithiatic potency of the aqueous extract (AE) of Terminalia arjuna (T. arjuna). Materials and Methods: The antilithiatic activity of Terminalia arjuna was investigated in vitro nucleation, aggregation and growth of the CaOx crystals as well as the morphology of CaOx crystals using the inbuilt software ‘Image-Pro Plus 7.0’ of Olympus upright microscope (BX53). Antioxidant activity of AE of Terminalia arjuna bark was also determined in vitro. Results: Terminalia arjuna extract exhibited a concentration dependent inhibition of nucleation and aggregation of CaOx crystals. The AE of Terminalia arjuna bark also inhibited the growth of CaOx crystals. At the same time, the AE also modified the morphology of CaOx crystals from hexagonal to spherical shape with increasing concentrations of AE and reduced the dimensions such as area, perimeter, length and width of CaOx crystals in a dose dependent manner. Also, the Terminalia arjuna AE scavenged the DPPH (2, 2-diphenyl-1-picrylhydrazyl) radicals with an IC50 at 13.1µg/mL. Conclusions: The study suggests that Terminalia arjuna bark has the potential to scavenge DPPH radicals and inhibit CaOx crystallization in vitro. In the light of these studies, Terminalia arjuna can be regarded as a promising candidate from natural plant sources of antilithiatic and antioxidant activity with high value.

Prophylactic effect of coconut water (Cocos nucifera L.) on ethylene glycol induced nephrocalcinosis in male wistar rat

Purpose Many medicinal plants have been employed during ages to treat urinary stones though the rationale behind their use is not well established. Thus, the present study was proposed to evaluate the effect of coconut water as a prophylactic agent in experimentally induced nephrolithiasis in a rat model. Materials and Methods The male Wistar rats were divided randomly into three groups. Animals of group I (control) were fed standard rat diet. In group II, the animals were administrated 0.75% ethylene glycol in drinking water for the induction of nephrolithiasis. Group III animals were administrated coconut water in addition to ethylene glycol. All the treatments were continued for a total duration of seven weeks. Results and Conclusion Treatment with coconut water inhibited crystal deposition in renal tissue as well as reduced the number of crystals in urine. Furthermore, coconut water also protected against impaired renal function and development of oxidative stress in the kidneys. The results indicate that coconut water could be a potential candidate for phytotherapy against urolithiasis. .