Publication: Histological recovery of the hepatocytes is based on the redox system upregulation in
the animal models of mutant superoxide dismutase
(SOD)1-linked amyotrophic lateral sclerosis
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Date
2006
Authors
Kato, Massuo J. ; Kato, S. ; Abe, Y. ; Nishino, T. ; Ohama, E. ; Aoki, M. ; Itoyama, Y.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Histological rescue of superoxide dismutase1
(SOD1)-mutated hepatocytes from mutant SOD1 stress
is investigated from the viewpoint of upregulation of the
redox system [peroxiredoxin (Prx) and glutathione
peroxidase (GPx)]. Histopathological and immunohistochemical
studies using antibodies against
PrxI/PrxII/GPxI were carried out on specimens from
four different strains of animal models of mutant SOD1-
linked familial amyotrophic lateral sclerosis (ALS). In
the livers of the ALS animal models in the
presymptomatic stage without motor neuron loss, both
swollen and eosinophilic hepatocytes with vacuolation
pathology were observed. After developing motor
deficits, this swelling and vacuolation ceased to be
apparent. In the terminal stage when severe motor
neuron loss was observed, these hepatocytes recovered
and appeared normal. In redox system-related
immunohistochemical preparations, almost all of the
normal hepatocytes expressed the redox system-related
enzymes PrxI/PrxII/GPxI. In the presymptomatic stage,
some hepatocytes did not express redox system-related
enzymes. After clinical onset, over 75% of hepatocytes
showed overexpression of PrxI/PrxII/GPxI, i. e.,
upregulation of the redox system. At the end stage, near
normal PrxI/PrxII/GPxI expression was observed again
in the hepatocytes. Redox system upregulation in SOD1-
mutated hepatocytes rescues hepatocytes from the
mutant SOD1 stress that leads to motor neuron death.
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