Changes in catalase activity in lung and liver after endotoxemia in sheep.
R Daryani, Cheryl Lalonde, Daling Zhu, Demling Rh
Abstract
R Daryani, Cheryl Lalonde, Daling Zhu, Demling Rh
Abstract
Endotoxemia in the sheep produces oxidant-induced cardiopulmonary dysfunction and lung and liver lipid peroxidation, which can be prevented with exogenous catalase, indicating a role for hydrogen peroxide. We determined whether endotoxin-induced oxidant release altered endogenous catalase activity to help explain the lipid peroxidation. Unanesthetized sheep were given 2 micrograms/kg Escherichia coli endotoxin and killed at 5 hr or 24 hr. Lung and liver lipid peroxidation, measured as malondialdehyde, and catalase activity were determined after endotoxin and compared with controls. Lung tissue MDA increased by 100% at 5 hr and was still elevated by 50% at 24 hr, while catalase activity decreased by 50% at 5 hr and remained decreased, suggesting irreversible inactivation. Liver MDA was also doubled at both 5 and 24 hr, but catalase activity remained unchanged. We conclude that endotoxemia results in a significant inactivation of endogenous catalase activity in lung, but not in liver. The lung may be more prone to a subsequent H2O2 injury before restoration of catalase activity.
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Endotoxemia in the sheep produces oxidant-induced cardiopulmonary dysfunction and lung and liver lipid peroxidation, which can be prevented with exogenous catalase, indicating a role for hydrogen peroxide. We determined whether endotoxin-induced oxidant release altered endogenous catalase activity to help explain the lipid peroxidation. Unanesthetized sheep were given 2 micrograms/kg Escherichia coli endotoxin and killed at 5 hr or 24 hr. Lung and liver lipid peroxidation, measured as malondialdehyde, and catalase activity were determined after endotoxin and compared with controls. Lung tissue MDA increased by 100% at 5 hr and was still elevated by 50% at 24 hr, while catalase activity decreased by 50% at 5 hr and remained decreased, suggesting irreversible inactivation. Liver MDA was also doubled at both 5 and 24 hr, but catalase activity remained unchanged. We conclude that endotoxemia results in a significant inactivation of endogenous catalase activity in lung, but not in liver. The lung may be more prone to a subsequent H2O2 injury before restoration of catalase activity.
Key concepts: Catalase, Lipid peroxidation, Malondialdehyde, Endogeny, Hydrogen peroxide, Internal medicine, Endocrinology, Lung