Recombinant Human Growth Hormone Decreases Lung and Liver Tissue Lipid Peroxidation and Increases Antioxidant Activity After Thermal Injury in Rats

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Abstract

The combination of increased oxidant with decreased endogenous polypeptide and protein antioxidant activity corresponds to a decrease in cellular energetics and cell membrane lipid peroxidation. Providing large doses of growth hormone has been shown to preserve cell mass and organ function after burn injury. The role of growth hormone in oxidant injury has not been defined. We determined whether growth hormone altered the degree of lung and liver lipid peroxidation and the activity of glutathione and catalase in lung and liver tissue after burn injury. Four groups of 40 rats each were studied for 48 hours, with 1 group receiving a 20% full-thickness burn, 1 group treated with growth hormone after 20% full-thickness burn injury, a control group, and a growth hormone alone-treated group. We found increased lipid peroxidation, measured as malondialdehyde, in lung and liver tissue, and a decrease in glutathione and catalase activities during the 48-hour post-burn period. The addition of growth hormone prevented the lipid peroxidation and significantly increased tissue glutathione and catalase activities with respect to control values. Growth hormone alone also increased endogenous antioxidant levels. We conclude that growth hormone given after burn injury decreases oxidant stress by producing a significant increase in the endogenous antioxidants glutathione and catalase.

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