Piletz J E, Herschman H R
Biochem Genet. 1983 Jun;21(5-6):465-75. doi: 10.1007/BF00484439.
Mottled-brindled mutant mice did not display the elevated hepatic metallothionein synthesis normally observed in 2- to 6-day-old wild-type mice. This difference between normal and mutant mice was not due to a decreased ability to synthesize metallothionein in the liver, since hepatic metallothionein synthesis was inducible in response to copper, cadmium, zinc, or hydrocortisone administration to neonatal mutant mice. Hydrocortisone treatment resulted in increased metallothionein synthesis in liver of mutant mice but had no ameliorative effect on the mottled-brindled disease.
斑驳-虎斑突变小鼠未表现出在2至6日龄野生型小鼠中通常观察到的肝脏金属硫蛋白合成升高的情况。正常小鼠与突变小鼠之间的这种差异并非由于肝脏中合成金属硫蛋白的能力下降,因为对新生突变小鼠给予铜、镉、锌或氢化可的松后,肝脏金属硫蛋白的合成是可诱导的。氢化可的松治疗导致突变小鼠肝脏中金属硫蛋白合成增加,但对斑驳-虎斑病没有改善作用。