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EC number: 213-254-4
CAS number: 932-64-9
Based on in vivo toxicity studies, there is good evidence that the test substance is absorbed via the gastrointestinal tract and to a lesser extent via the skin. There is also evidence of systemic distribution to the liver in male and female rats and the testes. The liver may be a site of metabolism and the kidneys a possible route of excretion. In rat liver microsomes, the substance undergoes nitroreduction leading to the formation of ATO (5-amino-1,2,4-triazol-3-one), a primary amine . NTO also undergoes an oxidative denitrification, providing urazole and nitrite
The metabolism of NTO was investigated (Le Campion et al, 1998). 14C5-
14C3-labelled NTO 1 were synthesized to facilitate the
elucidation of its bacterial and mammalian metabolism. The metabolites
formed were characterised, and the degradative pathways compared. The Bacillus
licheniformis strain was isolated from
industrial waste containing high concentrations of the explosive (15
g/L). Microbial metabolism of NTO 1 proceeded
through an oxygen-insensitive nitroreduction leading to the primary
amine ATO (5-amino-1,2,4,-triazol-3-one) 2, followed
by cleavage of the triazolone ring. The maximum microbial nitroreduction
occurred at pH 6 in the presence of sucrose, while
the ring cleavage occurred at pH 8. A permanent control and adjustment
of the pH was required to achieve the complete
degradation of NTO by B. licheniformis. The triazolone ring
resulted from the hydrolysis of the ‘pseudo guanido’ group
(R–NH–C(NH2)=N–R'). Mammalian degradation of NTO was catalysed by
dexamethasone-induced murine hepatic
microsomes, and influenced by the presence of oxygen. Thus, under a
nitrogen atmosphere, NTO 1 is exclusively reduced to
the amine 2. In the presence of oxygen, besides a low amount of 2,
5-hydroxy-1,2,4-triazol-3-one urazole 3 is the major
metabolite formed. This compound is obtained through an oxidative
denitrification of NTO accompanied by simultaneous
formation of nitrite. Both nitroreduction and oxidative-denitrification
of NTO were NADPH-dependent and totally inhibited
by carbon monoxide. These observations suggest a possible implication of
cytochrome P-450, which was confirmed by
inhibition and induction experiments. No ring cleavage was observed in
the microsomal metabolism of NTO.
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