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2,3-二巯基丙烷-1-磺酸盐即时和延迟治疗对小鼠以及胎儿和成年大鼠体内无机汞分布和毒性的影响。

The effect of immediate and delayed treatment with 2,3-dimercaptopropane-1-sulphonate on the distribution and toxicity of inorganic mercury in mice and in foetal and adult rats.

作者信息

Wannag A, Aaseth J

出版信息

Acta Pharmacol Toxicol (Copenh). 1980 Feb;46(2):81-8. doi: 10.1111/j.1600-0773.1980.tb02425.x.

Abstract

The distribution and excretion of mercury were studied in mice and rats given a single injection of HgCl2 combined with chelation treatment. BAL-sulph (2,3-dimercaptopropane-1-sulphonate) given intravenously (500 mumol SH/kg) to mice 24 hrs after the mercury injection (2.0 mumol Hg/kg) reduced the kidney Hg-level significantly, while NAPA (N-acetyl-DL-penicillamine) and BAL (2,3-dimercaptopropanol) did not. Severe kidney damage with oliguria was observed in pregnant as well as in non-pregnant rats after injection of 5 mumol/kg of HgCl2. The gross pathological changes could be avoided with immediate treatment with BAL-sulph (500 mumol SH/kg), and such treatment protect against the oliguric reaction. Treatment delayed for 24 hrs reduced the renal Hg-levels significantly, but was ineffective in preventing the kidney damage. This indicates that irreversible changes might have occurred in kidneys cells at this time. The Hg-levels in the brain were either unchanged or lowered in animals given BAL-sulph treatment. BAL-sulph is supposed to act by chelation Hg++, particularly in the extracellular space. The complexes formed appears to be rapidly excreted by healthy kidneys. Mercury poisoning with severe renal damage is, however, associated with a block in urinary Hg-excretion. The poisoned animals responded on the BAL-sulph treatment with a substantial raise of faecal mercury excretion.

摘要

研究了单次注射HgCl₂并结合螯合治疗后汞在小鼠和大鼠体内的分布与排泄情况。汞注射(2.0 μmol Hg/kg)24小时后给小鼠静脉注射BAL-磺酸盐(2,3-二巯基丙烷-1-磺酸盐,500 μmol SH/kg)可显著降低肾脏汞含量,而N-乙酰-DL-青霉胺(NAPA)和2,3-二巯基丙醇(BAL)则无此效果。给怀孕和未怀孕的大鼠注射5 μmol/kg HgCl₂后,观察到严重的肾损伤并伴有少尿。立即用BAL-磺酸盐(500 μmol SH/kg)治疗可避免大体病理变化,且这种治疗可预防少尿反应。延迟24小时治疗可显著降低肾脏汞含量,但对预防肾损伤无效。这表明此时肾细胞可能已发生不可逆变化。接受BAL-磺酸盐治疗的动物大脑中的汞含量要么未变,要么降低。BAL-磺酸盐被认为通过螯合Hg²⁺起作用,尤其是在细胞外空间。形成的复合物似乎能被健康的肾脏迅速排泄。然而,伴有严重肾损伤的汞中毒与尿汞排泄受阻有关。中毒动物对BAL-磺酸盐治疗的反应是粪便汞排泄大幅增加。

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