Comparison of the effects of L: -carnitine and alpha-tocopherol on acute ureteral obstruction-induced renal oxidative imbalance and altered energy metabolism in rats.

The suppression of renal energy metabolism during ureteral obstruction is a well-known phenomenon; however, its exact responsible mechanism(s) and association with simultaneously induced renal oxidative stress have not been clarified. This study examined the improving effects of L: -carnitine, a facilitating cofactor for mitochondrial oxidation of fatty-acids as well as a scavenger of free-radicals, and alpha-tocopherol as the most potent antioxidant on renal metabolic defect and oxidative stress induced by acute unilateral ureteral obstruction (UUO). The left ureter was ligated in ether-anaesthetised rats, in which L: -carnitine, alpha-tocopherol or their vehicles were intraperitoneally injected in four different groups. After elapsing 24 h of UUO-induction, both kidneys were removed and stored at -80 degrees C. There were also two sham-operated and control groups. The kidney samples were assessed to measure the levels of ferric reducing/antioxidant power (FRAP) and malondialdehyde (MDA) for evaluating their redox state, as well as, their amounts of adenosine triphosphate (ATP) and adenosine diphosphate (ADP) by using luciferin-luciferase method. As much as 24 h of UUO in vehicle-treated groups caused increases in MDA and ADP, but decreases in FRAP, ATP, and ATP/ADP of the obstructed kidney with respect to those of the sham group. alpha-tocopherol normalised the levels of MDA and FRAP but did not affect the altered amounts of energy metabolic indices in the obstructed kidney, while L: -carnitine could ameliorate all of them. These findings suggest that oxidative stress may not involve in development of acute UUO-induced suppression of renal aerobic metabolism, and probably reduction of energy substrates is a responsible factor.