摘要
本文报道了氧化/还原型谷胱甘肽对Ni^(2+)激活的钙调神经磷酸酶(Calcineurin,CaN)活性的影响。GSSG和CaN预保温导致CaN活性丧失,并且其失活过程依赖于GSSG的浓度。10mmol/L的GSSG和CaN在4℃保温,48个小时后,酶活性即全部丧失,其它实验表明,不含GSSG的酶液和含5mmol/L β—ME的酶液在4℃保温48小时后酶活性无明显变化。和GSSG保温的酶液当酶活性降至Ni^(2+)、CaM最大激活活性的20%时,透析除去GSSG,再加入GSH又能使失活的CaN活性恢复。48小时后酶活性全部丧失时GSH不能再使失活的CaN活性恢复。本文结果说明CaN是一疏基敏感酶。
Calcineurin incubated with 10 mmol/L oxidized glutathione(GSSG) at 4℃ for 48 hours can fully inactivate the enzyme. A short incubation of the GSSG partially inactivated enzyme (remained 20% activity) with glu-tathione (GSH) can restor 95% enzyme actiuity, GSH has no effect oa the GSSG fully inactivated enzyme. The inactivation of calcineurin by GSSG may be due to the forming of some mixed disulfides between the glutathione and function sulfhydryl groups of the enzyme. These facts may help to explain the mechanisms of activation to calcineurin by Hg2+ .
出处
《徐州医学院学报》
CAS
1990年第2期133-136,共4页
Acta Academiae Medicinae Xuzhou
关键词
CAM
谷胱甘肽
重金属中毒
calcineurin
GSSG
GSH
sulphydryl groups
heavy metal toxicity