Khillar M, Uong D S, Stolts D
Biokhimiia. 1977 Apr;42(4):589-97.
The effect of lysine-rich histone on mitochondria was studied with respect to the cation transport and proton uptake across the membrane. Histone does not affect Ca2+ uptake or level in mitochondria. It extrudes Mg2+ by 30% with the utilization of substrates; in the presence of rotenone extrusion drops to about 18%. Dinitrophenol and ADP prevent the effect of histone. Mg2+ uptake is inhibited by 12% by histone. K+ extrusion by histone (by 50%) which depends on the oxidation of substrates, is enhanced by phosphate, and Mg2+ decreases (by 50%) the K+ extrusion. Histone prevents to some extent extrusion of K+ by Ca2+. Histone does not affect Na+ level in mitochondria, it blocks (by 50%) Na+ uptake in the presence of gramicidin, probably by forming a gramicidin-histone complex. Histone blocks proton uptake by mitochondria incubated in the presence of valinomycin or DNP. In the presence of DNP valinomycin-induced H+ uptake is not affected by histone. H+ uptake induced by nigericin is not affected by histone as well.
就阳离子转运和跨膜质子摄取方面,研究了富含赖氨酸的组蛋白对线粒体的影响。组蛋白不影响线粒体对Ca2+的摄取或其在其中的水平。利用底物时,它会使Mg2+排出30%;在鱼藤酮存在的情况下,排出量降至约18%。二硝基苯酚和ADP可阻止组蛋白的作用。组蛋白会使Mg2+摄取受到12%的抑制。组蛋白引起的K+排出(达50%)依赖于底物的氧化,磷酸盐可增强此作用,而Mg2+会使K+排出减少(50%)。组蛋白在一定程度上可阻止Ca2+引起的K+排出。组蛋白不影响线粒体中Na+的水平,在短杆菌肽存在时,它会使Na+摄取受阻(50%),可能是通过形成短杆菌肽 - 组蛋白复合物。组蛋白会阻止在缬氨霉素或二硝基苯酚存在下孵育的线粒体摄取质子。在二硝基苯酚存在时,缬氨霉素诱导的H+摄取不受组蛋白影响。尼日利亚菌素诱导的H+摄取也不受组蛋白影响。