INVESTIGADORES
LORES ARNAIZ Silvia
artículos
Título:
Mitochondrial dysfunction in brain cortex mitochondria of STZ-diabetic rats. Effect of L-arginine.
Autor/es:
ORTIZ, M.C.; LORES-ARNAIZ, S.; ALBERTONI BORGHESE, M.F.; BALONGA, S.; LAVAGNA, A.; FILIPUZZI, A.L.; CICERCHIA, D.; MAJOWICZ, M. ; BUSTAMANTE, J.
Revista:
NEUROCHEMICAL RESEARCH
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Lugar: New York; Año: 2013 vol. 38 p. 2570 - 2580
ISSN:
0364-3190
Resumen:
Mitochondrial dysfunction has been implicated
in many diseases, including diabetes. It is well known that
oxygen free radical species are produced endogenously by
mitochondria, and also nitric oxide (NO) by nitric oxide
synthases (NOS) associated to mitochondrial membranes,
in consequence these organelles constitute main targets for
oxidative damage. The aim of this study was to analyze
mitochondrial physiology and NO production in brain
cortex mitochondria of streptozotocin (STZ) diabetic rats
in an early stage of diabetes and the potential effect of
L-arginine administration. The diabetic condition was
characterized by a clear hyperglycaemic state with loose of
body weight after 4 days of STZ injection. This hyperglycaemic
state was associated with mitochondrial dysfunction
that was evident by an impairment of the
respiratory activity, increased production of superoxide
anion and a clear mitochondrial depolarization. In addition,
the alteration in mitochondrial physiology was associated
with a significant decrease in both NO production and
nitric oxide synthase type I (NOS I) expression associated
to the mitochondrial membranes. An increased level of
thiobarbituric acid-reactive substances (TBARS) in brain
cortex homogenates from STZ-diabetic rats indicated the
presence of lipid peroxidation. L-arginine treatment to
diabetic rats did not change blood glucose levels but significantly
ameliorated the oxidative stress evidenced by
lower TBARS and a lower level of superoxide anion. This
effect was paralleled by improvement of mitochondrial
respiratory function and a partial mitochondrial repolarization.
In addition, the administration of L-arginine to diabetic
rats prevented the decrease in NO production and
NOSI expression. These results could indicate that exogenously
administered L-arginine may have beneficial effects
on mitochondrial function, oxidative stress and NO production
in brain cortex mitochondria of STZ-diabetic rats.