Mansour H, Levacher M, Gougerot-Pocidalo M A, Rouveix B, Pocidalo J J
J Pharmacol Exp Ther. 1986 Feb;236(2):476-80.
Prolonged exposure of C57B16 mice to pure O2 at 1 ATA induced pulmonary edema associated with involution of lymphoid system and depressed immunity. The consequences of these toxic events were evaluated by 1) mortality rate, 2) determination of pulmonary water, 3) thymic and splenic cellularity, and 4) humoral (primary antibodies) and cellular (mitogenic) immune responses. Pretreatment of mice with 125 mg kg-1 of diethyldithiocarbamate (DDC) several days before exposure to O2 resulted in 1) an increase in animal survival (92-100% vs. 59% O2 controls), 2) a reduction in pulmonary edema, 3) partial stabilization of thymus and spleen lymphocyte populations, and 4) restoration of the humoral response (specific antibodies appeared earlier than in O2 control animals) and improvement of the mitogenic proliferative response of the spleen cells after hyperoxia. None of these effects were observed when DDC treatment coincided with the beginning of exposure. Our results indicated that DDC protects mice from both pulmonary and lymphoid hyperoxic injury, but only in a partial manner. It is suggested that the mechanism of this antioxidative property is indirect.
将C57B16小鼠在1个绝对大气压下长时间暴露于纯氧会诱发肺水肿，同时伴有淋巴系统退化和免疫力下降。通过以下方面评估这些毒性事件的后果：1）死亡率；2）肺含水量测定；3）胸腺和脾脏细胞数量；4）体液免疫（主要抗体）和细胞免疫（促有丝分裂）反应。在暴露于氧气前几天，用125 mg kg-1二乙基二硫代氨基甲酸盐（DDC）对小鼠进行预处理，结果如下：1）动物存活率提高（92 - 100%，而氧气对照组为59%）；2）肺水肿减轻；3）胸腺和脾脏淋巴细胞群体部分稳定；4）体液免疫反应恢复（特异性抗体比氧气对照组动物出现更早），并且高氧后脾脏细胞的促有丝分裂增殖反应得到改善。当DDC治疗与暴露开始同时进行时，未观察到这些效应。我们的结果表明，DDC可保护小鼠免受肺部和淋巴系统的高氧损伤，但只是部分保护。提示这种抗氧化特性的机制是间接的。
