| Sodium cyanide was not mutagenic in Salmonella typhimurium strains TA100, TA1535, TA97, or TA98 with or without exogenous metabolic
activation (NTP, 1993). Potassium cyanide was not mutagenic in five strains
(TA1535, TA1537, TA1538, TA98, and TA100) of S. typhimurium with or without metabolic activation (De Flora, 1981). Hydrogen cyanide
induced mutations in S. typhimurium TA100 in the absence of S9 activation, but was not mutagenic to strain
TA98 with or without S9 activation (Kushi et al., 1983). ACH did not induce mutations in S. typhimurium strains TA1535, TA1537, TA1538, TA100, or TA98 in a plate incorporation
assay or at concentratons of 100-950 Κg/ml in a CHO/HGPRT assay (Monsanto
DNA repair tests in Escherichia coli WP67, CM871, and WP2 with potassium cyanide were negative (De Flora et al., 1984). Potassium cyanide induced both time- and dose-dependent DNA fragmentation
accompanied by cytotoxicity in rat thymocytes in vitro. Cyanide also induced DNA damage
in baby hamster kidney cells (BHK-21) in vitro, where, unlike thymocytes, internucleosome DNA fragmentation was not observed
(Bhattacharya & Rao, 1997). The cytotoxic mode of double strand breaks
in the pathogenesis of DNA fragmentation was studied by Vock et al. (1998), employing an A549 human epithelial-like lung carcinoma cell line
treated with potassium cyanide. Induction of double strand breaks by potassium
cyanide was observed only after cell viability was reduced to less than
60%, indicating that double strand breaks were the consequence of extragenomic
damage, as a secondary effect of high cytotoxicity in combination with
Sodium cyanide was a highly effective inducer of germline
aneuploidy in Drosophila (Osgood & Sterling, 1991).
No statistically significant increases in the frequency of
chromosomal aberrations or changes in mitotic index compared with control
values were found in bone marrow cells from four groups of 24 male and
24 female Sprague-Dawley rats administered a single dose of ACH by oral
gavage at levels of 0, 1.5, 5, or 15 mg/kg body weight with preparation
intervals of 6, 12, and 24 h post-administration (Monsanto Co., 1984b).
No testicular DNA synthesis inhibition was detected in mice
after a single oral potassium cyanide dose of 1 mg/kg body weight
(Friedman & Staub, 1976).
ENTP, 1993 NTP (1993): Sodium cyanide administered in drinking water toF344/N rats and B6C3F1 mice. Research Triangle Park, NC, National
Institutes of Health, National Toxicology Program (Toxicology Report Series No.
EDe Flora S (1981): Study of 106 organic and inorganic compounds in Salmonella/microsome test. Carcinogenesis, 2: 283-298.
EKushi A, Matsumoto T, Yoshida D (1983): Mutagen from gaseous phase of protein pyrolyzate. Agricultural and Biological Chemistry, 47: 1979-1982
EMonsanto Co. (1983b): In-vivo bone marrow chromosome study in rats. St.
Louis, MO, Monsanto Co. (Report HL-83-195; US EPA/OPTS Public Files No.
EMonsanto Co. (1983c): Salmonella typhimurium/mammalian microsome plate
incorporation assay with compound (ACH). St. Louis, MO, Monsanto Co. (Report
PK-83-204; US EPA/OPTS Public Files No. 878216403). EDe Flora S, Camoirano A, Zanacchi P, Bennicelli C (1984): Mutagenicity testing with TA97 and TA102 of 30 DNA-damaging compounds, negative with other Salmonella strains. Mutation Research, 134: 159-165.
EBhattacharya R, Rao PVL (1997): Cyanide induced DNA fragmentation in
mammalian cell cultures. Toxicology, 123:207?215.
EVock EH, Lutz WK, Hormes P, Hoffmann HD, Vamvakass A (1998): Discrimination
between genotoxicity and cytotoxicity in the induction of DNA double-strand
breaks in cells treated with etoposide, melphalan, cisplatin, potassium
cyanide, Triton X-100, and gamma-irradiation. Mutation Research, 413: 83-94.
EOsgood C, Sterling D (1991): Dichloroacetonitrile, a by-product of water chlorination, induces aneuploidy in Drosophila. Mutation Research, 261(2) 85-91.
EFriedman MA, Staub J (1976): Inhibition of mouse testicular DNA synthesis
by mutagens and carcinogens as a potential mammalian assay for mutagenesis.
Mutation Research, 37: 67-76.