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小鼠腹腔注射氯化镍溶液（５ｍｇＮｉ／ｋｇ）染毒，观察了Ｎ苯甲基Ｄ葡糖氨基二硫代甲酸钠（ＢＧＤ）、二乙氨基二硫代甲酸钠（ＤＤＴＣ）、二羟乙氨基二硫代甲酸钠（ＤＨＥＤ）及ｍｅｓｏ２，３二巯基丁二酸钠（ＤＭＳＡ）等螯合剂对镍致小鼠胰脏毒性的解毒作用。镍染毒后引起小鼠胰脏胰蛋白酶活性升高和羧肽酶Ａ活性降低以及组织中镍、钙、锌浓度增加；镍染毒３０ｍｉｎ和２４ｈ后进行各螯合剂治疗（剂量均为４００μｍｏｌ／ｋｇ），ＢＧＤ、ＤＤＴＣ和ＤＭＳＡ可明显抑制上述变化，其中ＢＧＤ解镍毒效果最好、自身毒性最小、对镍致小鼠胰脏毒性有更好的解毒作用。
Mice were intraperitoneally injected with nickel chloride solution (5mgNi / kg), and the effects of N-benzyl-D-glucosamine dithiocarboxylate (BGD), diethyldithiocarbamate (DDTC) Chelating agents such as sodium ethyldithiocarbamate (DHED) and meso2,3dimercaptosuccinate (DMSA) were used to detoxify the toxicity induced by nickel in mice. After exposure to nickel, the pancreatic trypsin activity and carboxypeptidase A activity of mice were increased, and the concentrations of nickel, calcium and zinc in the tissues were increased. The chelators were administered at 30 and 24 h after nickel exposure (the dosage was 400 μmol / kg). BGD, DDTC and DMSA significantly inhibited the above changes. Among them, BGD had the best anti-nickel toxicity effect and its own toxicity was minimal, which had a better detoxification effect on nickel-induced mouse pancreatic toxicity.