HEMATOPOIETIC EFFECT OF OCHRATOXIN A(OCT A) IN MICE EXPOSED TO IRRADIATION

赭曲霉毒素A（OCT A）有可能导致骨髓毒性， 除了众所周知的对肝脏和肾脏的毒性作用之外。 这里报道的实验旨在确定小鼠是否 将从OCT A诱导的骨髓毒性作用中恢复 其次，先前注射OCT A的小鼠是否 对辐射诱导的骨髓毒性比溶剂敏感 对照 将6周龄雌性B6 C3 F1小鼠注射 在一周内隔日腹腔内注射，总剂量为 0、20或40 mg/kg OCT A，并监测骨髓参数 长达16周 骨髓粒细胞受到抑制- 巨噬细胞祖细胞（CFU-C）在OCT A治疗的动物， 2周（20 mg/kg组）或5周后恢复正常值 末次给药后10周（40 mg/kg组）。 一些 OCT A处理的小鼠另外用200拉德全氟辛烷磺酸照射。 OCT A注射后10天和52天的身体照射。 辐射导致所有小鼠的CFU-C显著减少 但在接受了 以前的A。 骨髓祖细胞的延迟恢复 也反映在较低的外周白色血细胞计数后， 在40 mg/kg OCT A处理的小鼠中进行第二次照射， 未处理的辐照对照。 这表明， OCT A的骨髓效应使小鼠对 随后的辐射引起损伤。 这些结果被接受 发表在Toxicol上，1988年（印刷中）。

Ochratoxin A (OCT A) has the potential to cause myelotoxicity in addition to the well-know toxic effects on the liver and kidney. Experiments reported here were designed to determine whether mice would recover from the myelotoxic effects induced by OCT A injection and secondly whether mice previously injected to OCT A would be sensitive to radiation-induced myelotoxicity than vehicle controls. Six-week-old female B6C3F1 mice were injected intraperitoneally on alternate days over a week with a total dose of 0, 20 or 40 mg/kg of OCT A and bone marrow parameters monitored for up to 16 weeks. There was a suppression of marrow granulocyte- macrophage progenitors (CFU-C) in OCT A treated animals which returned to normal values by two weeks (20 mg/kg group) or by five weeks (40 mg/kg group) following the last treatment. Some of the OCT A treated mice were additionally irradiated with 200 rads whole body irradiation at 10 and 52 days following OCT A injections. Irradiation caused a significant reduction in CFU-C's in all mice but the effect were more pronounced in the mice that had received OCT A previously. The delayed recovery in bone marrow progenitors was also reflected in lower peripheral white blood counts after the second irradiation in 40 mg/kg OCT A treated mice as compared to the untreated irradiated controls. This indicated that residual bone marrow effect of OCT A makes the mice more sensitive to subsequent irradiation induced injury. These results were accepted for publication in Toxicol., 1988 (In press).