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用ＴＢＡ法测定了青蒿琥酯（Ｓｏｄｉｕｍａｒｔｅｓｕｎａｔｅ，ＳＡ）中毒大鼠骨髓脂质过氧化作用产物——丙二醛（ｍａｌｏｎａｌｄｅｈｙｄｅ，ＭＤＡ）含量以探济该药的造血毒性机制。结果表明，１００～３３３ｍｇ／ｋｇＳＡ引起骨髓ＭＤＡ含量与剂量呈正相关线性增高；相关系灵敏ｒ＝０．９５６６；骨髓ＭＤＡ增殖（ＩＭＤＡ）时间－反应曲线表明，达峰时间为１６．５ｈ，ＩＭＤＡ峰反应消除一半需７６．５ｈ。骨髓ＩＭＤＡ变化时程与骨髓细胞膜系结构损伤及造血抑制的发生、发展和恢复的时间规律基本一致，从而认为药物所致的自由基－膜指质过氧化作用可能是ＳＡ致骨髓等造血组织血液毒性和遗传毒性的作用机制
The TBA method was used to determine the content of malonaldehyde (MDA), a product of bone marrow lipid peroxidation in Sodiumartesunate (SA) -based rats, to explore the hematopoietic toxicity mechanism of the drug. The results showed that 100 ~ 333mg / kg SA resulted in a positive and linear correlation between MDA content and dose. The correlation was r = 0.9566. The IMDA time-response curve showed that the peak time was 16.5h, the IMDA peak Half of the reaction to be eliminated 76.5h. The time course of IMDA changes in bone marrow cell membrane structure damage and hematopoietic inhibition, development and recovery of the time rule is basically consistent, so that drug-induced free radical - membranous lipid peroxidation may be caused by bone marrow and other hematopoietic tissue blood Toxicity and genotoxicity mechanism of action