- Author:
Eun Hui BAE
1
;
Jong Un LEE
;
Soo Wan KIM
Author Information
- Publication Type:Review
- Keywords: Aquaporins; Reperfusion injury; Sodium transporters; Thioctic acid
- MeSH: Acute Kidney Injury*; Animals; Antioxidants; Aquaporins; Chelating Agents; Cisplatin; Down-Regulation; Iron; Rats*; Reactive Oxygen Species; Reperfusion Injury; Sodium; Thioctic Acid
- From:Electrolytes & Blood Pressure 2007;5(1):23-27
- CountryRepublic of Korea
- Language:English
- Abstract: Acute renal failure is mainly caused by ischemia/reperfusion (I/R) injury or nephrotoxic drugs, in which reactive oxygen species (ROS) may play an important role. Therefore, antioxidants are expected to decrease the vulnerability of renal injury associated with oxidative challenges. alpha-Lipoic acid (alpha-LA), potent antioxidant, could act as ROS scavengers, iron chelators and enzyme modulators. In rats with acute renal injury, dysregulation of aquaporin (AQP) water channels and sodium transporters has been noted. I/R injury or cisplatin induced marked down-regulation of AQP1, AQP2 and AQP3 water channels, and type-3 Na-H exchanger, Na,K-ATPase, and Na-K-2Cl cotransporters, in association with impairment of urinary concentration and tubular sodium reabsorption. Treatment with alpha-LA prevented the dysregulation of AQP channels and sodium transporters, along with improved urinary concentrating capability and renal sodium reabsorption.