BILIRUBIN ENCEPHALOPATHY IN THE GUNN RAT: A FINE STRUCTURE STUDY OF THE CEREBELLAR CORTEX
BILIRUBIN ENCEPHALOPATHY IN THE GUNN RAT: A FINE STRUCTURE STUDY OF THE CEREBELLAR CORTEX
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冈恩大鼠胆红素脑病：小脑皮质精细结构研究
DOI：
10.1097/00005072-196707000-00003
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发表时间：
1967
影响因子：
3.2
通讯作者：
L. Johnson
中科院分区：
文献类型：
--
作者：
H. Schutta;L. Johnson
非溶血性黄疸发生在被C.IK覆盖的Wistar大鼠品系中。冈恩(13)。黄疸特征是由一个突变的隐性常染色体基因传递的，代表符号“j”。“J”代表NorıNal基因。纯合子(JJ)动物LıAVC低到无肝葡萄糖醛酸基转移酶活性(31)。由于不能将胆红素与葡萄糖醛酸结合(31)，他们会发展成黄疸和核黄斑(3)。除了酶缺陷和由此导致的黄疸的影响外，大鼠基本上是正常的。具有黄疸特征的杂合子(JJ)大鼠不会发生高胆红素血症，尽管他们的肝性葡萄糖醛酸基转移酶活性显著低于正常(31)。
Non-hemolytic jaunlice occurs in a strain of Wistar rats liscovered by C. IK. Gunn (13). The jaundice trait is transmitted by a mutant recessive autosomal gene, represented ly the symbol “j”.“J” represents the norınal gene. Homozygous (jj) animals lı avc low to absent hepatic glucuronyl transferrase activity (31). They develop jaundice and kernicterus (3) as a consequence of their inability to conjugate bilirubin witlh glucuronic acid (31). Apart from the enzymatic defect and the cffccts of the resultant jaundice, the rats are essentially normal. Rats heterozygous (Jj) for the jaundice trait do not develop lhyperbilirubinemia, although their liepatic glucuronyl transferase activity is significantly lower than normal (31).