Abstract
It has been proven by numerous investigations that in hypoxic and shock states the purine breakdown by XO is the main source of the superoxide-mediated reperfusion injury of cells. Grant et al. have demonstrated that after caffeine intake the molar ratio of methyluric acid (MU) and methylxanthine (MX) measured by HPLC in urine reflects the XO activity in vivo. The results of such measurements (x ± S.D.) in various groups of children were as follows: 15 controls: 1.11 ± 0.52; 17 newborns with RDS first day: 16.9 ± 4.90; third day: 10.5 ± 6.9; 18 critically ill children, in acute phase: 11.5 ± 14.4 (range 1.9 - 50.0); in reparation: 2.3 ± 3.7; in 6 so-called shock-tolerant patients: 0.38 ± 0.25. The MU/MX ratio and the serum uric acid value showed a significant correlation (r: 0,57, n = 44, p < 0,001) in various groups. In conclusion: The XO activity in vivo is extremely increased in severe acute clinical states and - presumably by an adaptive process -, it rapidly decreases in reparation and becomes extremely low in shock-tolerant states. These results explain the favourable effect of allopurinol in experimental and clinical shock states.
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Boda, D., Németh, I. IN VIVO XANTHINE OXIDASE (XO) ACTIVITY IN PREMATURE INFANTS WITH RDS AND IN HYPOXIC STATES OF CHILDREN MEASURED BY URINARY CAFFEINE METABOLITES. Pediatr Res 26, 511 (1989). https://doi.org/10.1203/00006450-198911000-00070
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DOI: https://doi.org/10.1203/00006450-198911000-00070