Efecto del tratamiento antioxidante sobre parámetros de bioenergética mitocondrial

Abstract

Acute renal failure has been defined as a sudden decrease in glomerular filtration with an accumulation of nitrogenous products and the inability of the kidneys to maintain hydroelectrolytic homeostasis. The kidney is one of the organs with the highest energy demand, which is why it is rich in mitochondria, it has been demonstrated by previous studies the relation of the mitochondrial bioenergetics and the alterations in the chain of transport of electrons in the acute renal failure caused by compounds Nephrotoxic. In rats it has been shown that folic acid at doses higher than 200 mg / kg causes damage to the nephrons, so the present study seeks to demonstrate that N-acetylcysteine (NAC) as an antioxidant can prevent the nephrotoxic effect produced by the Folic acid (AF). Therefore, alterations of mitochondrial bioenergetics were determined in a model of folic acid-induced renal damage (AF) at a dose of 300 mg / kg rat, and a treatment with 300 mg/kg n-acetylcysteine (NAC) in male Wistar rats. This showed a decrease in membrane potential, a complex I and ATPsinase (CV) damage, and an increase in peroxide production, affecting the electron transport chain, Increasing the oxidative stress and reducing the energy supply by the mitochondria. However, damage is prevented with NAC treatment, which in future studies can demonstrate the protective effect of antioxidants in acute renal failure as a prevention method.