Regulation of lung oxidative damage by endogenous superoxide dismutase in sepsis.
BACKGROUND
The purpose of this research is to study the relationship between superoxide dismutase (SOD) and lung redox state in an animal model of sepsis.


METHODS
Sepsis was induced in rats by the cecal ligation and perforation model (CLP). After 3, 6, and 12 h, CLP protein content and expression of SOD1, SOD2, and SOD3 were evaluated, and SOD activity was assessed. Oxidative damage was determined by quantifying nitrotyrosine content. Lung localization of SOD3 was performed by immunohistochemistry. The protective effect of a SOD mimetic on oxidative damage, inflammation, and lung permeability was assessed 12 and 24 h after sepsis induction.


RESULTS
Lung levels of SOD1 decreased 3 and 12 h after sepsis, but SOD2 and SOD3 increased, as well as SOD activity. These alterations were not associated with changes in sod gene expression. Nitrotyrosine levels increased 3 and 12 h after sepsis. The administration of a SOD mimetic decreased nitrotyrosine and proinflammatory cytokine levels and improved lung permeability.


CONCLUSIONS
SOD2 and SOD3 increased after sepsis induction, but this was insufficient to protect the lung. Treatments based on SOD mimetics could have a role in lung injury associated with sepsis.
Laboratório de Fisiopatologia Experimenta e Instituto Nacional de Ciência e Tecnologia Translacional em Medicina (INCT-TM), Programa de Pós-Graduação de Ciências da Saúde, Universidade do Extremo Sul Catarinense, Avenida Universitária, 1105, Criciúma, SC, 88806-000, Brazil, larissa.constantino@gmail.com.
Larissa
L
Constantino
Renata Casagrande
RC
Gonçalves
Vinícius Renê
VR
Giombelli
Cristiane Damiani
CD
Tomasi
Francieli
F
Vuolo
Luiza Wilges
LW
Kist
Giovanna Medeiros Tavares
GM
de Oliveira
Matheus Augusto de Bittencourt
MA
Pasquali
Maurício Reis
MR
Bogo
Thais
T
Mauad
Adolfo
A
Horn
Karen V
KV
Melo
Christiane
C
Fernandes
José Cláudio Fonseca
JC
Moreira
Cristiane
C
Ritter
Felipe
F
Dal-Pizzol