Effect of catecholamic acid on detoxication and distribution of NiCl2 in mice and rats

AIM: To study the effect of catecholamic acid (CBMIDA) on detoxication of NiCl2. METHODS: Mice and rats were injected s.c. or i.m. CBMIDA immediately after i.p. NiCl2. Each mouse was injected i.p. CBMIDA after i.v. 63NiCl2 185 kBq, and radioactivities of various tissues were measured with liquid scintillation counter at 24 h. The localization of 63Ni was shown by the whole-body autoradiography. RESULTS: CBMIDA s.c. 0.5-1.5 g.kg-1 markedly reduced the mortality from acute poisoning of i.p. NiCl2 500 mg.kg-1. After i.p. NiCl2 in mice, the LD50 was 82.7 mg.kg-1. Mice were injected s.c. CBMIDA 1.5 or 2.5 g.kg-1 after Ni poisoning, the LD50 of NiCl2 were raised to 789 or 820 mg.kg-1, respectively. The LD50 of NiCl2 was 39 mg.kg-1 in rat. If CBMIDA was injected i.m. 0.5 g.kg-1 after i.p. NiCl2, the LD50 was 332 mg.kg-1. CBMIDA 1.5 g.kg-1 i.m. after i.v. 63NiCl2, decreased the contents of 63Ni in blood and lung of mice vs control mice at 24 h. The contents of 63Ni in brain, heart, spleen, and kidney were similar to those of the control mice. The content of 63Ni in bone was more than the control. The excretions of 63Ni through urine and feces were not increased by CBMIDA at 24 h. The whole-body autoradiography showed that the radioactivity was highly localized in the kidney, lung, and Harder's gland. There was a moderate level of 63Ni in the liver, bone, skin, and blood. A pronounced accumulation occurred in the bone. There was a marked reduction of 63Ni in the lung, skin, liver, and blood after i.p. CBMIDA.
CONCLUSION: The CBMIDA markedly raised the survival rate of nickel-poisoned mice and rats, and decreased 63Ni levels in lung and blood.