Kidney Failure and Brain Function"Antioxidants (N-acetylcysteine, NAC and deferoxamine, DFX) prevented
such effect"
Neurosci Lett. 2008 Mar 21;434(1):139-43. Epub 2008 Jan 31. Inhibition
of brain creatine kinase activity after renal ischemia is attenuated
by N-acetylcysteine and deferoxamine administration.
Di-Pietro PB, Dias ML, Scaini G, Burigo M, Constantino L, Machado RA,
Dal-Pizzol F, Streck EL.
Laboratório de Fisiopatologia Experimental, Programa de Pós-graduaçã=
o
em Ciências da Saúde, Unidade Acadêmica de Ciências da Saúde,
Universidade do Extremo Sul Catarinense, 88806-000 Criciúma, SC,
Brazil.
Encephalopathy may accompany acute or chronic renal failure, and the
mechanisms responsible for neurological complications in patients with
renal failure are poorly known. Considering that creatine kinase (CK)
is important for brain energy homeostasis and is inhibited by free
radicals, and that oxidative stress is probably involved in the
pathogenesis of uremic encephalopathy, we measured CK activity
(hippocampus, striatum, cerebellum, cerebral cortex and prefrontal
cortex) in brain if rats submitted to renal ischemia and the effect of
administration of antioxidants (N-acetylcysteine, NAC and
deferoxamine, DFX) on this enzyme. We verified that CK activity was
not altered in cerebellum and striatum of rats. CK activity was
inhibited in prefrontal cortex and hippocampus of rats 12h after renal
ischemia. The treatment with antioxidants prevented such effect.
Cerebral cortex was also affected, but in this area CK activity was
inhibited 6 and 12h after renal ischemia. Moreover, only NAC or NAC
plus DFX were able to prevent the inhibition on the enzyme. Although
it is difficult to extrapolate our findings to the human condition,
the inhibition of brain CK activity after renal failure may be
associated to neuronal loss and may be involved in the pathogenesis of
uremic encephalopathy.
PMID: 18304734 [PubMed - in process]
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