The role of oxygen-free radical in the apoptosis of enterocytes in scalded rats after delayed resuscitation.
BACKGROUND
This study aimed to evaluate the relation between apoptosis of enterocytes and oxygen-free radical injury in scalded rats with delayed resuscitation as well as the role of antioxidants in the prevention of enterocyte apoptosis.


METHODS
For this study, 150 male Wistar rats were divided randomly into four groups representing early resuscitation (ER), delayed resuscitation (DR), N-acetylcysteine (NAC) treatment, and allopurinol (Allo) treatment. The animals were subjected to a 30% total body surface area, full-thickness scald. Fluid therapy was started 6 hours after the injury in the DR and treatment groups. Apoptosis of enterocytes was identified by DNA fragmentation (ap%), DNA agarose gel electrophoresis, and terminal deoxynucleotidyl transferace (TdT)-mediated dUPT-biotin nick end labeling (TUNEL). The contents of malondialdehyde (MDA), total sulfhydryl (TSH), and nonprotein sulfhydryl (NPSH) and the activity of xanthine oxidase in intestinal mucosa were determined after the burn in the four groups.


RESULTS
Apoptosis of enterocytes increased significantly in all the groups. The animals in the DR group showed an earlier and greater increase in ap% than the animals in the ER group. Similar results were seen for electrophoresis, TUNEL assay, and levels of MDA, xanthine oxidase (XO), TSH, and NPSH. Treatment with NAC was associated with a decrease in ap% and MDA, but not XO, as compared with the levels in the DR group, whereas treatment with Allo was associated with a decrease in MDA and XO, but not ap%. Delayed resuscitation was associated with significant decreases in TSH and NPSH, as compared with the levels in the ER group, whereas both the NAC and Allo groups had significantly higher levels of TSH and NPSH than the DR group.


CONCLUSIONS
Significant apoptosis of enterocytes was induced by oxidative stress in the intestinal mucosa after a burn in rats. The findings show that NAC blunted intestinal apoptosis induced by oxygen-free radical, which was generated in the process of ischemia-reperfusion injury after a burn because of delayed resuscitation.
Zhang
Cheng
C
Department of Burns and Plastic Surgery, Lanzhou General Hospital, Lanzhou 730050, Gansu Province, China. zc5976@yahoo.com
Sheng
Zhi-Yong
ZY
Hu
Sen
S
Gao
Jian-Chuan
JC
Li
Jun-You
JY
Liu
Y
Y
D000111:Acetylcysteine / Q000494:pharmacology; D000493:Allopurinol / Q000494:pharmacology; D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D002056:Burns / Q000503:physiopathology*; D053938:DNA Fragmentation; D020895:Enterocytes / Q000502:physiology*; D005978:Glutathione / Q000378:metabolism; D007085:Ilium / Q000098:blood supply; D020287:In Situ Nick-End Labeling; D007413:Intestinal Mucosa / Q000098:blood supply; D008297:Male; D018384:Oxidative Stress / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000378:metabolism*; D015427:Reperfusion Injury / Q000503:physiopathology; D012151:Resuscitation; D012769:Shock / Q000503:physiopathology; D014969:Xanthine Oxidase / Q000378:metabolism
D017382:Reactive Oxygen Species; D000493:Allopurinol; D014969:Xanthine Oxidase; D005978:Glutathione; D000111:Acetylcysteine