Nie Aifang, Meng Ziqiang
Institute of Environmental Medicine and Toxicology, Shanxi University, Taiyuan, China.
Food Chem Toxicol. 2006 Mar;44(3):355-63. doi: 10.1016/j.fct.2005.08.006. Epub 2005 Sep 21.
The effects of sulfur dioxide (SO(2)) derivatives (bisulfite and sulfite, 1:3M/M) on voltage-dependent L-type calcium current (I(Ca,L)) in isolated rat ventricular myocytes were studied using the whole cell patch-clamp technique. SO(2) derivatives increased I(Ca,L) in a concentration-dependent manner. SO(2) derivatives shifted both the steady-state activation and the inactivation curves of I(Ca,L) to more positive potentials, the effect on the latter being more pronounced. SO(2) derivatives markedly accelerated the recovery of I(Ca,L) from inactivation. SO(2) derivatives also significantly shortened the fast and slow time constants of inactivation. These results suggested that SO(2) inhalation might cause cardiac myocyte injury through increasing intracellular calcium via voltage-gated calcium channels.
采用全细胞膜片钳技术,研究了二氧化硫(SO₂)衍生物(亚硫酸氢盐和亚硫酸盐,摩尔比1:3)对离体大鼠心室肌细胞电压依赖性L型钙电流(I(Ca,L))的影响。SO₂衍生物以浓度依赖性方式增加I(Ca,L)。SO₂衍生物使I(Ca,L)的稳态激活曲线和失活曲线均向更正电位移动,对后者的影响更明显。SO₂衍生物显著加速I(Ca,L)从失活状态的恢复。SO₂衍生物还显著缩短了失活的快时间常数和慢时间常数。这些结果提示,吸入SO₂可能通过电压门控钙通道增加细胞内钙,从而导致心肌细胞损伤。