Chini E N, Liang M, Dousa T P
Mayo Clinic and Foundation, Department of Physiology and Biophysics and Department of Anesthesiology, 200 First Street, SW, 901 Guggenheim Bldg., Rochester, MN 55905, USA.
Biochem J. 1998 Nov 1;335 ( Pt 3)(Pt 3):499-504. doi: 10.1042/bj3350499.
We investigated the pH dependence and the effects of thimerosal and dithiothreitol (DTT) upon the Ca2+ release induced by cADP-ribose (cADPR) and nicotinate-adenine dinucleotide phosphate (NAADP) in sea urchin egg homogenates. Both Ca2+ release triggered by cADPR and the binding of [3H]cADPR to sea urchin egg homogenates were decreased by alkalization of the assay media from pH 7.2 to 8.9. In contrast, NAADP-triggered Ca2+ release was not influenced by changes in pH. The Ca2+ release induced by cADPR was potentiated by thimerosal and inhibited by DTT, but neither thimerosal nor DTT had any effect upon the Ca2+ release induced by NAADP. We conclude that cADPR-sensitive Ca2+-release mechanisms are dependent on pH of the assay media and are sensitive to thiol group modification. On the other hand, these functional properties are not shared by NAADP-regulated Ca2+ channels.
我们研究了pH依赖性以及硫柳汞和二硫苏糖醇（DTT）对海胆卵匀浆中cADP - 核糖（cADPR）和烟酰胺腺嘌呤二核苷酸磷酸（NAADP）诱导的Ca2+释放的影响。将测定介质的pH从7.2碱化至8.9时，cADPR触发的Ca2+释放以及[3H]cADPR与海胆卵匀浆的结合均减少。相比之下，NAADP触发的Ca2+释放不受pH变化的影响。硫柳汞增强了cADPR诱导的Ca2+释放，而DTT则抑制了该释放，但硫柳汞和DTT对NAADP诱导的Ca2+释放均无任何影响。我们得出结论，cADPR敏感的Ca2+释放机制取决于测定介质的pH，并且对巯基修饰敏感。另一方面，这些功能特性并非NAADP调节的Ca2+通道所共有。
