Ogata M
Department of Public Health, Okayama University Medical School, Japan.
Hum Genet. 1991 Feb;86(4):331-40. doi: 10.1007/BF00201829.
The abnormalities in acatalasemia at the gene level as well as properties of the residual catalase in Japanese acatalasemia are historically reviewed. The replacement of the fifth nucleic acid, guanine, in the fourth intron by adenine in the acatalasemic gene causes a splicing mutation and hence a deficiency of mRNA. The guanine-to-adenine substitution was detected in two Japanese acatalasemic cases from different families. The properties of the residual catalase are similar to those of normal catalase; the exons are identical. The properties of the residual catalase and the molecular defect in the catalase gene are compared among Japanese, Swiss, and mouse acatalasemias. The physiological role of catalase, as judged from human acatalasemic blood and acatalasemic mice, is also described.
本文对日本无过氧化氢酶血症在基因水平上的异常以及日本无过氧化氢酶血症中残余过氧化氢酶的特性进行了历史回顾。无过氧化氢酶血症基因中第四个内含子的第五个核酸鸟嘌呤被腺嘌呤取代,导致剪接突变,进而导致mRNA缺乏。在来自不同家族的两例日本无过氧化氢酶血症病例中检测到了鸟嘌呤到腺嘌呤的替换。残余过氧化氢酶的特性与正常过氧化氢酶相似;外显子是相同的。比较了日本、瑞士和小鼠无过氧化氢酶血症中残余过氧化氢酶的特性和过氧化氢酶基因中的分子缺陷。还描述了从人类无过氧化氢酶血症血液和无过氧化氢酶血症小鼠判断出的过氧化氢酶的生理作用。