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兔体内碘酸盐视网膜毒性剂量处理的研究。

Studies on the handling of retinotoxic doses of iodate in rabbits.

作者信息

Olsen K J, Ehlers N, Schønheyder F

出版信息

Acta Pharmacol Toxicol (Copenh). 1979 Apr;44(4):241-50. doi: 10.1111/j.1600-0773.1979.tb02325.x.

Abstract

Accumulation of iodate in eye tissues and fluids as a possible explanation of the retinotoxic effect of iodate has been studied by intravenous injection of NaIO3(30 mg/kg), 125IO-3 and 131I- in rabbits. 125IO-3 was determined in fluids and tissue extracts by precipitation with BaCl2 after addition of KIO3. 125IO-3 was rapidly broken down in blood (T 1/2 = 14 min.). 125IO-3 was not present in aqueous humour, vitreous or extracts from retina, choroid + pigmentary epithelium or liver. Concentrations of 125I were comparable in blood, choroid + pigmentary epithelium and liver tissue while in vitreous and aqueous humour low concentrations of 125I were found which, however, increased gradually during 5 hrs after injection to reach levels comparable with blood levels of 125I. Retina had a low concentration of 125I. The ratio 125I/131I (R) in blood decreases during the first 60 min. after injection followed by a slow rise. R in retina, choroid + pigmentary epithelium and liver was the same as in blood at the same time after injection. During the first 80 min. after injection R was higher in vitreous than in blood while it was lower in aqueous humour than in blood. At longer times after injection R was identical in the three fluids. The investigation has been supplemented with whole body scintigraphy of rabbits injected with NaIO3(30 mg/kg) and 131IO-3 or 131I-. The reduction kinetics of IO-3 to I- by some body fluids, tissues, cystein and glutathione was also studied. It is concluded that the retinotoxic effect of iodate is not due to accumulation of IO-3 in eye tissues, but more likely to damage to biochemical mechanisms involved in the reduction of IO-3 to I-.

摘要

通过给兔子静脉注射碘酸钠(30毫克/千克)、125碘酸根离子和131碘离子,研究了眼组织和眼内液中碘酸盐的蓄积情况,以此作为碘酸盐视网膜毒性作用的一种可能解释。在添加碘酸钾后,通过用氯化钡沉淀法测定眼内液和组织提取物中的125碘酸根离子。125碘酸根离子在血液中迅速分解(半衰期=14分钟)。房水、玻璃体、视网膜、脉络膜+色素上皮或肝脏提取物中均未检测到125碘酸根离子。血液、脉络膜+色素上皮和肝脏组织中的125碘浓度相当,而在玻璃体和房水中发现的125碘浓度较低,但在注射后5小时内逐渐升高,达到与血液中125碘水平相当的水平。视网膜中的125碘浓度较低。注射后最初60分钟内,血液中125碘/131碘(R)的比值下降,随后缓慢上升。注射后同一时间,视网膜、脉络膜+色素上皮和肝脏中的R与血液中的相同。注射后最初80分钟内,玻璃体中的R高于血液中的,而房水中的R低于血液中的。注射后较长时间,三种眼内液中的R相同。对注射碘酸钠(30毫克/千克)和131碘酸根离子或131碘离子的兔子进行了全身闪烁扫描,以补充上述研究。还研究了某些体液、组织、半胱氨酸和谷胱甘肽将碘酸根离子还原为碘离子的动力学。得出的结论是,碘酸盐的视网膜毒性作用并非由于碘酸根离子在眼组织中的蓄积,而更可能是由于参与将碘酸根离子还原为碘离子的生化机制受到损害。

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