Enzymatic antioxidant defence mechanism in rat intestinal tissue is changed after ischemia-reperfusion. Effects of an allopurinol plus antioxidant combination.
OBJECTIVE
To establish the antioxidant status of rat intestinal tissues after ischemia-reperfusion and to determine if pretreatment with an allopurinol and antioxidant vitamin combination gives any protection against mucosal injury.


METHODS
Twenty rats were divided into 4 groups of 5 animals each.


METHODS
Group 1 (control) rats were not subjected to ischemia-reperfusion and received no allopurinol plus vitamin combination; group 2 rats received vitamins C (200 mg/kg) and E (100 mg/kg) and allopurinol (50 mg/kg) combination daily for 3 days preoperatively; group 3 rats were subjected to ischemia-reperfusion only; and group 4 rats were subjected to ischemia-reperfusion and received the vitamin and allopurinol combination.


METHODS
Activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) enzymes, the level of thiobarbituric acid-reagent substances (TBARS) and histologic grading of tissue samples.


RESULTS
SOD and GSH-Px activities were decreased, but the CAT activity and TBARS level increased. Pretreatment of the rats with the allopurinol-vitamin C-vitamin E combination did not have any significant effect on the enzyme activities. However, it resulted in important reductions in the TBARS tissue levels. Histologic investigation revealed significant mucosal injury in group 3 rats compared with group 4 rats (mean [and standard deviation] for grading, 4.6 [0.5] versus 1.8 [0.4]).


CONCLUSIONS
The enzymatic antioxidant defence system was significantly changed after ischemia-reperfusion and intestinal tissue was exposed to increased oxidant stress, the results of which were peroxidation of some cellular structures and increased concentrations of oxidative products. Although antioxidant treatment did not drastically affect the enzyme activities or afford complete protection of cellular structures against deformation, it apparently could eliminate oxygen radicals and prevent peroxidative reactions.
Kaçmaz
M
M
Department of Biochemistry, Ibn-I Hospital, Ankara, Turkey.
Oztürk
H S
HS
Karaayvaz
M
M
Güven
C
C
Durak
I
I
D000493:Allopurinol / Q000494:pharmacology*; D000818:Animals; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology; D002374:Catalase / Q000097:blood*; D004359:Drug Therapy, Combination; D005609:Free Radicals / Q000378:metabolism; D005979:Glutathione Peroxidase / Q000097:blood*; D007413:Intestinal Mucosa / Q000098:blood supply* / Q000201:enzymology / Q000473:pathology; D015227:Lipid Peroxidation / Q000187:drug effects; D018384:Oxidative Stress / Q000502:physiology*; D011292:Premedication; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000201:enzymology* / Q000473:pathology; D013482:Superoxide Dismutase / Q000097:blood*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000494:pharmacology
D000975:Antioxidants; D005609:Free Radicals; D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D000493:Allopurinol; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D001205:Ascorbic Acid