Tandon S K, Singh S, Prasad S, Mathur N
Chemical Toxicology, Industrial Toxicology Research Centre, P0 Box 80, -226001, Lucknow, India.
Food Chem Toxicol. 2001 Jun;39(6):571-7. doi: 10.1016/s0278-6915(00)00167-8.
The hepatic and the renal subcellular distribution of zinc, cadmium or mercury and induction of tissue metallothionein (MT) at 24, 48 and 72 h following an oral equimolar dose (15 micro;mol metal/kg) of zinc (II) chloride, cadmium (II) chloride or mercury (II) chloride in male albino mice were investigated. There was a moderate increase in hepatic and renal zinc levels mainly in their nuclear mitochondrial fraction (NMF) 24 h post zinc chloride administration. Subsequently, the hepatic zinc increased and the renal zinc declined with time. The zinc-induced hepatic MT level was maximum at 48 h, which decreased slightly thereafter, while there was no marked increase in renal MT level at any time interval. The cadmium was equally distributed in liver and kidney more in their supernatant cytosol fraction (SCF) than in their NMF at 24 h after a dose of cadmium chloride. The cadmium levels showed a decreasing trend in hepatic fractions and an increasing trend in renal fractions with time. The cadmium-induced hepatic and renal MT were substantial at 24 h post cadmium administration, the former decreased thereafter while the latter enhanced at 48 h before declining. The accumulation of mercury in kidney was 1.5 times that in liver, which was localised more in their SCF than in their NMF at 24 h in response to a dose of mercuric chloride. The mercury levels of hepatic and renal subcellular fractions started declining after 24 h and at 72 h they were significantly lower. The induction of hepatic and renal MT was maximum at 24 h after mercuric chloride administration, which declined thereafter concomitant with the decrease in their mercury levels. However, the MT levels in both the organs remained considerably higher than in normal animals at 72 h post exposure. The results show that the accumulation of metal in liver and kidney follows the order: Hg > Cd > Zn and the induction of MT follows Hg > Cd > Zn in liver and Cd > Hg > Zn in kidney. The alterations in zinc and copper homeostasis were more marked in liver than in kidney and follows the order: Hg > Cd > Zn.
研究了雄性白化小鼠口服等摩尔剂量（15微摩尔金属/千克）的氯化锌、氯化镉或氯化汞后24、48和72小时，锌、镉或汞在肝脏和肾脏的亚细胞分布以及组织金属硫蛋白（MT）的诱导情况。氯化锌给药后24小时，肝脏和肾脏中的锌水平适度升高，主要集中在其核线粒体部分（NMF）。随后，肝脏中的锌含量增加，而肾脏中的锌含量随时间下降。锌诱导的肝脏MT水平在48小时达到最高，此后略有下降，而在任何时间间隔内肾脏MT水平均无明显升高。给予氯化镉后24小时，镉在肝脏和肾脏中的分布较为均匀，更多地存在于其上清液胞质部分（SCF）而非NMF中。随着时间的推移，肝脏部分的镉含量呈下降趋势，而肾脏部分的镉含量呈上升趋势。镉给药后24小时，镉诱导的肝脏和肾脏MT水平显著升高，前者随后下降，而后者在48小时升高后下降。肾脏中汞的蓄积量是肝脏的1.5倍，给予氯化汞后24小时，汞更多地存在于其SCF而非NMF中。肝脏和肾脏亚细胞部分的汞含量在24小时后开始下降，72小时时显著降低。氯化汞给药后24小时，肝脏和肾脏MT的诱导水平最高，此后随着汞含量的下降而下降。然而，暴露后72小时，两个器官中的MT水平仍明显高于正常动物。结果表明，金属在肝脏和肾脏中的蓄积顺序为：Hg＞Cd＞Zn，肝脏中MT的诱导顺序为Hg＞Cd＞Zn，肾脏中为Cd＞Hg＞Zn。肝脏中锌和铜稳态的改变比肾脏更明显，顺序为：Hg＞Cd＞Zn。
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