Advanced age heightens hepatic damage in a murine model of scald burn injury.

Background: Elderly burn patients exhibit a lower survival rate compared with younger counterparts. The liver is susceptible to damage after burn injury, which predisposes to poor outcomes. Lipid homeostasis and the antioxidant glutathione system play fundamental roles in preserving liver integrity. Herein, we explored changes in these major pathways associated with liver damage in the aging animals after burn injury.

Methods: We compared liver enzymes, histology, lipid-peroxidation, and glutathione-metabolism profiles from young and aged female mice after a 15% total body surface area burn. Mice were euthanized at 24 hours after injury, and livers and serum were collected.

Results: Aged burn animals exhibited elevated (p < 0.05) aspartate aminotransferase and alanine aminotransferase levels and increased inflammatory cell infiltration, edema, and necrosis compared with their younger counterparts. The percentage of adipophilin-stained area in livers from young sham, young burn, aged sham, and aged burn groups was 10%, 44%, 16%, and 78% (p < 0.05), respectively. Liver malondialdehyde levels were 1.4 ± 0.5 nmol/mg, 2.06 ± 0.2 nmol/mg, 1.81 ± 0.12 nmol/mg, and 3.45 ± 0.2 nmol/mg (p < 0.05) in young sham, young burn, aged sham, and aged burn mice, respectively. Oxidized glutathione (GSSG) content increased 50% in the young burn, and 88% in aged burn animals compared with the young sham group (p < 0.05). The reduced glutathione GSH/GSSG ratio was significantly reduced by 54% in aged burn mice compared with young sham animals (p < 0.05). Furthermore, glutathione peroxidase gene expression showed a 96% decrease in the aged burn group compared with young sham mice (p < 0.05).

Conclusion: Aged burn animals exhibit severe liver damage from heightened lipid peroxidation and inadequate antioxidative response. The increased peroxidation is associated with abundant lipid deposits in hepatic tissue postburn and a weak antioxidative response due to hepatic glutathione peroxidase downregulation. Further studies will focus on the functional significance of these findings concerning hepatic homeostasis.