抄録
Platelet-activating factor (PAF) acetylhydrolase has been recognized as an enzyme to inactivate PAF. We developed the convenient method to determine human serum PAF acetylhydrolase activity, that was based on the measurement of [14C] -acetate from 1-O-alkyl-2- [14C] -acetyl-sn-glycero-3-phosphocholine on the precipitation of the complex of radioactive substrate and albumin by adding trichloro acetic acid to the incubation mixture. Thirty-two subjects with the deficiency of serum PAF acetylhydrolase were found in 816 healthy adult Japanese. The low PAF acetylhydrolase activity in the deficient serum was not due to the presence of the enzyme inhibitor. Both the sensitivity to PAF and the metabolism of PAF in platelets from subjects with PAF acetylhydrolase deficiency were almost the same as that of the normal subjects. The deficiency in serum PAF acetylhydrolase is apparently transmitted according to autosomal recessive heredity among four Japanese families.
Asthmatic children were grouped into five classes (Remission, Wheezy, Mild, Moderate and Severe groups) on the basis of symptoms according to the grade of bronchial asthma of Japanese Society of Pediatric Allergy and Clinitical Immunology. The probability of PAF acetylhydrolase deficiency in group with severe symptoms (Moderate and Severe, 5 subjects per 42) was significantly higher than that in a healthy group without a history of wheezy (one subject per 36), a group with slight symptoms (Remission and Wheezy, one subject per 100) and healthy adult Japanese (32 subjects per 816) .
These results suggest that the deficiency of serum PAF acetylhydrolase might be one of factors which lead asthmatic children to more severe state in respiratory symptoms.
