Tandon S K, Magos L
Br J Ind Med. 1980 May;37(2):128-32. doi: 10.1136/oem.37.2.128.
ABSTRACT Mobilisation of mercury by thiol-complexing agents is the accepted treatment for chronic mercury intoxication. The success of such treatment is judged by the urinary excretion of mercury which might be modified by existing kidney damage caused either by the mercury itself or by other factors. In the present work the ability of three thiol-complexing agents, D-penicillamine, N-acetyl-D, L-penicillamine, and 2,3-dimercaptosuccinic acid (DMSA) to remove mercury from a damaged kidney and to increase the urinary excretion of mercury were studied. Kidney damage was induced by the injection of 20 mg/kg sodium chromate three days before the injection of 2·5 μmoles/kg HgCl or three and seven days before the administration of a similar dose of mercury complexed with D-penicillamine. It was shown that both renal uptake and urinary excretion of mercury were decreased in animals with damaged kidneys. This effect lessened with time between the induction of damage and the injection of mercury-penicillaminate. Each of the three chelating agents was given 48 and 54 hours after the administration of HgCl in equivalent (400 μmoles/kg) doses. All were able to remove mercury from the kidneys, but DMSA was far the most effective and only DMSA increased the urinary excretion of mercury. The amount of mercury removed from the kidneys by the chelators was less in animals with renal damage than in controls, but the difference was insignificant if renal mercury depletion was related to the initial renal mercury content.
摘要 硫醇络合剂促使汞排出是慢性汞中毒的公认治疗方法。这种治疗的成功与否通过汞的尿排泄来判断，而汞的尿排泄可能会因汞本身或其他因素导致的现有肾脏损害而改变。在本研究中，研究了三种硫醇络合剂，即D-青霉胺、N-乙酰-D,L-青霉胺和2,3-二巯基丁二酸（DMSA）从受损肾脏中清除汞并增加汞尿排泄的能力。在注射2.5微摩尔/千克氯化汞前三天，或在给予类似剂量的与D-青霉胺络合的汞之前三天和七天，通过注射20毫克/千克铬酸钠诱导肾脏损伤。结果表明，肾脏受损的动物体内汞的肾脏摄取和尿排泄均降低。这种影响在损伤诱导与注射汞-青霉胺之间的时间间隔内会减小。在给予氯化汞后48小时和54小时，以等效剂量（400微摩尔/千克）给予三种螯合剂中的每一种。所有螯合剂都能从肾脏中清除汞，但DMSA最为有效，且只有DMSA增加了汞的尿排泄。与对照组相比，肾脏受损动物中螯合剂从肾脏中清除的汞量较少，但如果肾脏汞消耗与初始肾脏汞含量相关，则差异不显著。
