Smolen A, Petersen D R, Collins A C
Dev Pharmacol Ther. 1981;3(1):31-49. doi: 10.1159/000457419.
A 3-fold increase in aldehyde dehydrogenase (A1DH) was found in the cytosolic fraction of mouse liver homogenates during pregnancy. The increase in A1DH activity began at day 10 of pregnancy, peaked at parturition, and declined in a biphasic manner with half-lives of 4.15 and 47.7 days. Enzymes from control (beta A1DH), pregnant (pi A1DH) and phenobarbital-treated (phi AlDH) were partially purified and compared. All had molecular weights of approximately 60,000 daltons. Substrate specificities were similar except that phi A1DH had a lower Km for propionaldehyde than beta or pi and both pi and phi oxidized 4-carboxybenzaldehyde poorly compared to beta. Electrophoretic and thermal denaturation studies showed some similarities between beta and pi, but phi A1DH behaved quite differently. It was concluded that pregnancy caused an increase in one of the A1DHs already present in control mice, while phenobarbital treatment resulted in induction of a unique cytosolic A1DH.
在孕期小鼠肝脏匀浆的胞质部分中，醛脱氢酶（A1DH）增加了3倍。A1DH活性的增加始于孕期第10天，在分娩时达到峰值，并以双相方式下降，半衰期分别为4.15天和47.7天。对来自对照组（β A1DH）、孕期组（π A1DH）和苯巴比妥处理组（φ A1DH）的酶进行了部分纯化并比较。所有酶的分子量均约为60,000道尔顿。底物特异性相似，只是φ A1DH对丙醛的Km值低于β或π，并且与β相比，π和φ对4-羧基苯甲醛的氧化能力较差。电泳和热变性研究表明β和π之间存在一些相似之处，但φ A1DH的表现却大不相同。得出的结论是，怀孕导致对照小鼠中已存在的一种A1DH增加，而苯巴比妥处理则导致诱导出一种独特的胞质A1DH。
