Disease relevance of CCRIS 1952

• Exposure of E. coli to nitrosocimetidine induces the adaptive response to alkylating agents [1].
• Comparison of the acute toxicity of N-nitrosocimetidine with three structurally related carcinogens in the rat [2].

High impact information on CCRIS 1952

• Cimetidine (CM), a drug widely prescribed for ulcers, readily undergoes nitrosation to form nitrosocimetidine (NCM), a genotoxic agent [3].
• Methylation of DNA by nitrosocimetidine in vitro [4].
• Rat liver microsomal enzymes have been found to be capable of catalyzing the denitrosation of MNNG, NC and an NC analog, 1,3-dimethyl-2-cyano-1-nitrosoguanidine (CyanoDMNG) in an NADPH-dependent reaction [5].
• N-nitrosocimetidine as an initiator of murine skin tumors with associated H-ras oncogene activation [6].
• Induction of sister-chromatid exchanges by N-nitrosocimetidine in cultured human lymphocytes and its inhibition by chemical compounds [7].

Chemical compound and disease context of CCRIS 1952

• By this method, the acute toxicities of N-nitrosocimetidine and the parent drug cimetidine were virtually identical for each of the three routes of administration [2].

Biological context of CCRIS 1952

• Cellular DNA damage by nitrosocimetidine: a comparison with N-methyl-N'-nitroso-nitrosoguanidine and x-irradiation [8].
• N-Nitrosocimetidine (NC) induces significant numbers of sister chromatid exchanges (SCE) and chromosome aberrations in cultured Chinese hamster ovary (CHO) cells even at a concentration of 1.2 x 10(-7) M [9].
• DNA-methylation by nitrosocimetidine and N-methyl-N-nitro-N-nitrosoguanidine in the intact rat [10].

Anatomical context of CCRIS 1952

• Voltammetric determination of nitrosocimetidine in simulated gastric juice [11].
• Permanently proliferating lymphoblastoid cell lines (LCLs) and normal unstimulated peripheral blood leukocytes have been used to study the effects of nitrosocimetidine (NC) on cultured human lymphoid cells [8].

Analytical, diagnostic and therapeutic context of CCRIS 1952

• The degradation of nitrosocimetidine (NC) and its mechanism were found to be strongly dependent upon pH by monitoring NC and its degradation products by high-performance liquid chromatography (HPLC) [12].
• Radio-labelled nitrosocimetidine (NC) was shown to methylate DNA in a variety of tissues in the rat after oral administration [10].

References