Van Den Broeke L T, Gräslund A, Larsson P H, Nilsson J L, Wahlberg J E, Scheynius A, Karlberg A T
Department of Occupational Health, National Institute for Working Life, Solna, Sweden.
Acta Derm Venereol. 1998 Mar;78(2):95-8. doi: 10.1080/000155598433395.
A possible free radical mechanism in metal allergy was investigated in peripheral blood mononuclear cell (PBMC) cultures from 6 subjects, contact allergic to Ni2+ and Co2+, and 6 control individuals. Ni2+ and Co(2+)-mediated free radical generation was studied with electron spin resonance spectroscopy. The immune response was characterized by cellular [methyl-3H]thymidine uptake and interferon-gamma (IFN-gamma) production Ni2+ and Co2+ (10-50 microM) significantly increased lymphocyte proliferation and IFN-gamma production in PBMC cultures from contact allergic subjects in comparison with cultures from controls. Inhibition of Co(2+)-mediated free radical generation by ascorbic acid did not influence cellular [methyl-3H]thymidine uptake and IFN production. Detectable amounts of free radicals were not obtained with Ni2+. We therefore conclude that it is unlikely that free radicals are involved in contact allergy to Ni2+ and Co2+.
对6名对Ni2+和Co2+接触过敏的受试者以及6名对照个体的外周血单核细胞（PBMC）培养物中金属过敏可能的自由基机制进行了研究。采用电子自旋共振光谱法研究了Ni2+和Co(2+)介导的自由基生成。通过细胞[甲基-3H]胸腺嘧啶核苷摄取和干扰素-γ（IFN-γ）产生来表征免疫反应。与对照培养物相比，Ni2+和Co2+（10-50 microM）显著增加了接触过敏受试者PBMC培养物中的淋巴细胞增殖和IFN-γ产生。抗坏血酸对Co(2+)介导的自由基生成的抑制作用不影响细胞[甲基-3H]胸腺嘧啶核苷摄取和IFN产生。用Ni2+未获得可检测量的自由基。因此，我们得出结论，自由基不太可能参与对Ni2+和Co2+的接触过敏。
