Abstract | OBJECTIVE: The purpose of this study was to investigate whether ischemia and subsequent reperfusion would affect xanthine oxidase activity in fetal rat brain capillaries. STUDY DESIGN: We used rats on day 19 of pregnancy. Fetal ischemia was induced by bilateral occlusion of the utero-ovarian artery for 20 minutes. Reperfusion was achieved by releasing the occlusion to restore the circulation for 30 minutes. Control rats underwent a sham operation. Fetal brain capillaries were isolated for measurement of concentrations of hypoxanthine, xanthine, and uric acid, as well as of concentrations of thiobarbituric acid-reactive substances. The brain capillaries were incubated with hypoxanthine for 1-5 hours at 25 degrees C. The activity of xanthine oxidase was estimated by measuring the amount of xanthine converted from hypoxanthine. RESULTS: CONCLUSION: Ischemic insult led to the accumulation of hypoxanthine and stimulated xanthine oxidase activity in fetal brain capillaries. Subsequent reperfusion enhanced the degradation of hypoxanthine to uric acid, which may induce cerebral lipid peroxidation.
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Authors | A Wakatsuki, Y Okatani, C Izumiya, N Ikenoue |
Journal | American journal of obstetrics and gynecology
(Am J Obstet Gynecol)
Vol. 181
Issue 3
Pg. 731-5
(Sep 1999)
ISSN: 0002-9378 [Print] United States |
PMID | 10486491
(Publication Type: Journal Article)
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Chemical References |
- Thiobarbituric Acid Reactive Substances
- Xanthine
- Uric Acid
- Hypoxanthine
- Xanthine Oxidase
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Topics |
- Animals
- Arteries
- Brain
(blood supply, embryology)
- Capillaries
(enzymology)
- Constriction
- Female
- Fetus
(blood supply)
- Hypoxanthine
(metabolism)
- Ischemia
(enzymology)
- Ovary
(blood supply)
- Pregnancy
- Rats
- Rats, Wistar
- Reperfusion
- Thiobarbituric Acid Reactive Substances
(metabolism)
- Uric Acid
(metabolism)
- Uterus
(blood supply)
- Xanthine
(metabolism)
- Xanthine Oxidase
(metabolism)
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