Cheng P T, Pritzker K P
Department of Pathology, Mount Sinai Hospital, Toronto, Canada.
J Rheumatol. 1988 Feb;15(2):321-4.
To determine the physical-chemical effects of [Fe++] and [Fe ] on calcium pyrophosphate dihydrate (CPPD) crystal formation de novo, we studied CPPD crystal formation in an established model aqueous solution mixture system using physiological concentrations of Na+, Mg++, Ca++, C1-. We found that [Fe++] greater than 1 microM or [Fe ] greater than or equal to 100 microM inhibits CPPD crystal formation under conditions of [Ca++] = 1.5 mM, [Pi] = 0.1 mM, and [PPi] = 0.1 mM that simulate CPPD formation in vivo. These experiments suggest that at biological concentrations, Fe++ acts to inhibit CPPD formation but that [Fe++] depletion therapy by removal of inhibition effects may facilitate CPPD crystal formation in articular tissues.
为了确定亚铁离子(Fe++)和铁离子(Fe )对二水焦磷酸钙(CPPD)晶体从头形成的物理化学作用,我们在一个既定的模型水溶液混合体系中,使用生理浓度的钠离子(Na+)、镁离子(Mg++)、钙离子(Ca++)、氯离子(C1-)研究了CPPD晶体的形成。我们发现,在模拟体内CPPD形成的[Ca++] = 1.5 mM、[Pi] = 0.1 mM和[PPi] = 0.1 mM条件下,大于1微摩尔/升的Fe++或大于或等于100微摩尔/升的Fe 会抑制CPPD晶体的形成。这些实验表明,在生物浓度下,Fe++起到抑制CPPD形成的作用,但通过消除抑制作用的Fe++消耗疗法可能会促进关节组织中CPPD晶体的形成。