Hasselbacher P
J Rheumatol. 1981 Jan-Feb;8(1):57-61.
The effect of gold sodium thiomalate on C3 and factor B activation by monosodium urate monohydrate (MSUM) and zymosan was studied using a quantitative immunoelectrophoretic assay for complement activation. C3 and factor B conversion by the classical pathway activator MSUM, was inhibited 50% and 100% by 3.2 x 10(-4)M and 10(-3)M gold sodium thiomalate, respectively. C3 and factor B conversion by the alternative pathway activator, zymosan, was much less susceptible to inhibition by gold. Gold at 10(-3)M, inhibited alternative pathway activation by only 30%. A 50% inhibition would have required 10(-2)M gold. There was no significant inhibition of complement activation through either pathway by less than 10(-4)M gold. Sodium thiomalate alone showed no inhibition. Studies using other crystals and immune complexes were confirmatory. Thus, there was no appreciable inhibition of the complement system at concentrations of gold attainable in the serum of patients receiving chrysotherapy. The in vivo significance of these findings is unknown.
采用补体激活定量免疫电泳分析法,研究了硫代苹果酸金钠对单水尿酸钠(MSUM)和酵母聚糖激活C3及B因子的影响。经典途径激活剂MSUM引起的C3和B因子转化,分别被3.2×10⁻⁴M和10⁻³M硫代苹果酸金钠抑制50%和100%。替代途径激活剂酵母聚糖引起的C3和B因子转化,对金的抑制作用更不敏感。10⁻³M的金仅抑制替代途径激活30%。50%的抑制率需要10⁻²M的金。低于10⁻⁴M的金对两条途径的补体激活均无明显抑制作用。单独的硫代苹果酸钠无抑制作用。使用其他晶体和免疫复合物的研究具有证实性。因此,在接受金疗法的患者血清中可达到的金浓度下,补体系统没有明显抑制。这些发现的体内意义尚不清楚。