Original articleMitochondria-initiated apoptosis triggered by oxidative injury play a role in total parenteral nutrition–associated liver dysfunction in infant rabbit model
Section snippets
Animal model
Rabbits were selected as the animal model for this study because their biliary metabolism is similar to that of humans. Twenty New Zealand white rabbits (specific pathogen-free, age, 12-16 days; body weight, approximately 200-250 g) were obtained from the Animal Experiment Center of the Chinese Academy of Science. The rabbits were divided into 2 groups as follows: the control group (n = 10, maternal feed) and the TPN group (n = 10, TPN for 10 days). The rabbits were housed in individual cages
Liver function test
The liver function results are shown in Table 2. Because hemolysis can affect the assay of bile acid, γ-glutamyl transpeptidase, and direct bilirubin, hemolyzed samples were discarded (ie, one hemolyzed sample from a control rabbit was excluded). Both the bile acid and total bilirubin levels were significantly increased in the TPN group, but there were no between-group differences in aspartate transaminase, alanine transaminase, and γ-glutamyl transpeptidase.
Control group
Light microscopy revealed mild
Discussion
Recent studies have supported the hypothesis that the generation of reactive oxygen species (ROS) and an elevation of lipid hydroperoxides in the liver during cholestasis cause tissue injury. Animal studies using models of surgically induced extrahepatic biliary obstruction have shown that lipid peroxidation products—specifically, MDA—were increased in the cholestatic liver [11], [12]. This increase was associated with a decrease in tissue antioxidant activity, increased leukocyte infiltration,
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