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EC number: 206-114-9 | CAS number: 302-01-2
Specific investigations: other studies
Administrative data
Link to relevant study record(s)
Description of key information
There are several publications discussing the mechanism of action of hydrazine in rat and mouse suggesting that treatment with hydrazine disturb the balance of methylation and demethylation on N-7 and O-6 of guanine resulting in liver toxicity. Therefore, It is plausible that liver tumours after long-term high dose exposure to hydrazine are secondary to liver toxicity.
Additional information
There are several publications discussing the mechanism of action of hydrazine in rat and mouse suggesting a dose-dependent increase in liver DNA methylation after single and repeated oral administration. In this context it is discussed that treatment with hydrazine disturb the balance of methylation and demethylation on N-7 and O-6 of guanine by inhibiting the demethylation which would result in accumulation of the methylated purines in the liver DNA (see also DFG 1989). Dose-response studies in rats revealed a single oral dose of 0.1 mg/kg as a starting dose for effects on liver DNA methylation (borderline effect, clear effects with 10 mg/kg; van Delft 1997; clear effect at 30 mg/kg; Becker et al. 1981). After the third of four oral doses of 3 mg/kg increase of 7-methylguanine was observed as trace and readily detectable after 4 treatments (Becker et al. 1981). Evidence of liver toxicity was shown at 2.5 mg/kg (exposure for 1-10 days; decrease of GSH, increase of triglycerides; Jenner & Timbrell 1992) and 3 mg/kg (3-4 doses; Becker et al. 1981). Therefore it is plausible that the liver tumours after long-term high dose exposure are secondary to liver toxicity and alteration of the balance of methylation and demethylation
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