Magos L, Sparrow S, Snowden R T
Br J Exp Pathol. 1984 Oct;65(5):567-75.
Male Porton-Wistar rats, 32 weeks old, were given i.p. one of the following doses of HgCl2; 0.5, 1.0 or 1.5 mg Hg/kg. In the preceding 4-week period and throughout the experiment the animals had free access to either tap water or 1.0% saline. The urinary excretion of alkaline phosphatase measured in urine samples, collected during the first 24 h after treatment with mercury, indicated that chronic saline loading significantly attenuated tubular damage caused by 0.5 mg or 1.0 mg Hg/kg, but not by 1.5 mg Hg/kg. Tubular necrosis 12 and 24 h after mercury was also less severe and extensive in saline than in tap water-drinking rats. This difference was still noticeable 4 days after mercury treatment in rats dosed with 0.5 mg Hg/kg, but death in the two higher dose groups prevented further pair-to-pair histological comparison. At the selected dose levels chronic saline loading did not decrease renal mercury content at 12 or 24 h and therefore protection was not associated with decrease in renal mercury uptake. The experiment indicates that chronic saline drinking, which at higher doses attenuates HgCl2-induced acute renal failure but not tubular necrosis, is able to moderate the severity of tubular necrosis when the dose of HgCl2 is as low as 0.5 mg Hg/kg. This protective effect diminishes as the dose is increased.
选用32周龄的雄性Porton-Wistar大鼠，腹腔注射下列剂量之一的氯化汞：0.5、1.0或1.5毫克汞/千克。在实验前的4周期间以及整个实验过程中，动物可自由饮用自来水或1.0%的盐水。在汞处理后的头24小时内收集的尿液样本中检测碱性磷酸酶的尿排泄量，结果表明，长期饮用盐水可显著减轻由0.5毫克或1.0毫克汞/千克引起的肾小管损伤，但对1.5毫克汞/千克引起的损伤无效。与饮用自来水的大鼠相比，饮用盐水的大鼠在汞处理后12小时和24小时的肾小管坏死也较轻且范围较小。在用0.5毫克汞/千克给药的大鼠中，汞处理4天后这种差异仍然明显，但两个高剂量组的大鼠死亡，无法进行进一步的逐对组织学比较。在选定的剂量水平下，长期饮用盐水在12小时或24小时时并未降低肾脏汞含量，因此这种保护作用与肾脏汞摄取量的减少无关。该实验表明，长期饮用盐水在较高剂量时可减轻氯化汞诱导的急性肾衰竭，但对肾小管坏死无效，而当氯化汞剂量低至0.5毫克汞/千克时，长期饮用盐水能够减轻肾小管坏死的严重程度。随着剂量增加，这种保护作用会减弱。
