AIM: To study the effect of catecholamic acid (CBMIDA) on detoxication
of NiCl2. METHODS: Mice and rats were injected sc or im CBMIDA immedi
ately after ip NiCl2. Each mouse was injected ip CBMIDA after iv (NiCl
2)-Ni-63 185 kBq, and radioactivities of various tissues were measured
with liquid scintillation counter at 24 h. The localization of Ni-63
was shown by the whole-body autoradiography. RESULTS: CBMIDA sc 0.5-1.
5 g.kg(-1) markedly reduced the mortality from acute poisoning of ip N
iCl2 500 mg.kg(-1). After ip NiCl2 in mice, the LD50 was 82.7 mg.kg(-1
). Mice were injected sc 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 im
0.5 g.kg(-1) after ip NiCl2, the LD50 was 332 mg.kg(-1). CBMIDA 1.5 g.
kg(-1) im after iv (NiCl2)-Ni-63, decreased the contents of Ni-63 in b
lood and lung of mice vs control mice at 24 h. The contents of Ni-63 i
n brain, heart, spleen, and kidney were similar to those of the contro
l mice. The content of Ni-63 in bone was more than the control. The ex
cretions of Ni-63 through urine and feces were not increased by CBMIDA
at 24 h. The whole-body autoradiograpy showed that the radioactivity
was highly localized in the kidney, lung, and Harder's gland. There wa
s a moderate level of Ni-63 in the liver, bone, skin, and blood. A pro
nounced accumulation occurred in the bone. Them was a marked reduction
of Ni-63 in the lung, skin, liver, and blood after ip CBMIDA. CONCLUS
ION: The CBMIDA markedly raised the survival rate of nickel-poisoned m
ice add rats, and decreased Ni-63 levels in lung and blood.