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The study revealed the inhibitory effect of sodium selenite on induction of bladder cancer by butylbutanolnitrosamine in rats. The incidence of carcinoma in the control group was 87.5% whereas in the sodium selenite group--50% (P less than 0.01).
Non-toxic doses of dimethylnitrosamine and diethylnitrosamine inhibit the multiplication of herpes simplex virus type 1 and type 2 in HEp-2, Wi-38 and primary HEK cells. These results are somewhat unexpected, since both HEp-2 and Wi-38 cells lack detectable microsomal enzyme activity. The possible significance of the preliminary results is discussed.
It has been shown in vitro with human acidic gastric juice the nitrosomorpholine (NMOR) formation from small doses of precursors (sodium nitrite and morpholine) with a significant difference relative to the control. The presented data suggest the possibility of the nitrosation reaction in the human gastric juice under hypo- and anacidic conditions. The data obtained are one more experimental confirmation of the epidemiological evidence of the potential role of nitrates (nitrites) in the etiology of stomach and esophageal cancers.
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Data have been presented on carcinogenic N-nitrosoamines (NA) synthesis from precursors in the gastric juice and in the stomach of rats. It is shown that vegetable juices and milk produce an inhibitory effect with respect to NA synthesis in vitro and in vivo, however, food products with high content of fat intensify amine nitrosation.
Long-term exposure to diesel exhaust from a small diesel engine was carried out in order to elucidate the effects of exhaust on the development of lung tumors in F344 rats and newborn ICR and C57BL mice. The deposition of inhaled particles progressed in accordance with duration of exposure in both sets of the animals. No evidence of lung tumor formation was detected following exposure to diesel exhaust alone in rats. However, the combined treatment with DIPN and diesel exhaust led to an overadditive effect in the development of lung tumors. There was a tendency for the diesel-exposed mice to have higher incidences of lung tumors compared with non-exposed mice. The results obtained in the present study suggest that diesel exhaust may act as a factor relating to human respiratory carcinogenesis.
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The effects of administering similar doses of some simple alkylating agents to rats by different regimens have been compared. Two of the compounds were methylating agents, nitrosodimethylamine and azoxymethane; two were ethylating agents, nitrosodiethylamine and azoxyethane; and nitrosomethylethylamine was both a methylating and an ethylating agent. The treatments gave rise to tumors in almost all treated rats. The results indicate the importance of pharmacokinetics in determining which organs are the targets of the alkylating carcinogens.
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Lung and liver tumors were induced in female A/J mice after treatment for 7 weeks (3 times/week, i.p.) with either 4-(N-methyl-N-nitrosamino)-1-(3-pyridyl)-1-butanone (NNK) (50 mg/kg) or nitrosodimethylamine (NDMA) (3 mg/kg). Both compounds can be activated via alpha-hydroxylation to methylating agents, while NNK may also undergo hydroxylation at the N-methyl carbon to form a pyridyloxobutylated adduct. The purpose of these studies was to identify and characterize the activated oncogenes present in tumors induced by NDMA and NNK. Following transfection of high molecular weight DNA onto NIH/3T3 mouse fibroblasts, transforming genes were detected in 90% of both NNK- (10 of 11) and NDMA- (9 of 10) induced lung tumors. In contrast, transformation of NIH/3T3 fibroblasts was observed only in 40% (2 of 5) and 13% (1 of 8) of the liver tumors from NNK- and NDMA-treated mice, respectively. Southern blot analysis indicated that the transforming gene present in all lung tumors was an activated K-ras oncogene. Both rearranged bands and amplified signals were detected in the transfectants. The one transformant from the NDMA-induced liver tumor contained an activated K-ras gene. In contrast, the two liver transformants from NNK-induced tumors did not contain an activated ras or raf gene. Hybridization with oligonucleotide probes that were centered around either codon 12 or 61 of the K-ras gene were utilized to localize the mutations. Activation of this gene appeared to occur largely via a mutation in codon 12 (15 of 20 transformants) and was observed with a similar frequency in pulmonary tumors induced by either compound. The remaining mutations were found in codon 61. The specific mutation within these two codons was determined by amplifying the exon containing the base change, followed by direct sequencing. With one exception the mutation observed in codon 12 was a GC to AT transition (GGT to GAT). One transformant contained a GC to TA transversion. The activating mutation detected in codon 61 was always an AT to GC transition of the middle A (CAA to CGA). The GC to AT mutation observed in codon 12 is consistent with the formation of the O6-methylguanine adduct. Similar concentrations (23 to 32 pmol/mumol deoxyguanosine) of this promutagenic adduct were detected in lungs during treatment with either NNK or NDMA.(ABSTRACT TRUNCATED AT 400 WORDS)
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Rate enhancements of from 12 to 49-fold occurred when dihexylamine was nitrosated at pH 3.5 in the presence of bacteria and yeast cells at a concentration of 12 mg/ml. Rates were similar in the presence of either boiled or unheated cells. The magnitude of the rate enhancement for nitrosation of other amines depended on the alkyl chain length. A nonenzymatic mechanism involving hydrophobic interactions of the precursor amines and cellular constituents is proposed.
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In studies on nitrosating agent(s) formed in skin of mice exposed to nitrogen dioxide, we showed that: (i) N-nitrosomethylaniline was produced in skin of mice exposed to nitrogen dioxide and then painted with N-methylaniline; (ii) a nitrosating precursor in methyl linoleate is associated with peroxidation products; (iii) cholesterol is a major nitrosating precursor in mouse skin, probably because it produces the nitrosating agent, cholesteryl nitrite; (iv) cholesteryl nitrite enhances autoxidation of lipids in vivo and on mouse skin and, like sodium nitrite, catalyses the autoxidation of iodide; (v) N-nitrosomethylaniline was produced in mice injected intraperitoneally with methylaniline and gavaged with amyl nitrite; and (vi) nitrosating agents may occur normally in human skin lipids.