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PubMed1971

Nitrosamine-induced carcinogenesis. The alkylation of N-7 of guanine of nucleic acids of the rat by diethylnitrosamine, N-ethyl-N-nitrosourea and ethyl methanesulphonate.

1. The extent of ethylation of N-7 of guanine in the nucleic acids of rat tissue in vivo by diethylnitrosamine, N-ethyl-N-nitrosourea and ethyl methanesulphonate was measured. 2. All compounds produced measurable amounts of 7-ethyl-guanine. 3. A single dose of diethylnitrosamine or N-ethyl-N-nitrosourea produced tumours of the kidney in the rat. Three doses of ethyl methanesulphonate produced kidney tumours, but a single dose did not. 4. A single dose of diethylnitrosamine produced twice as much ethylation of N-7 of guanine in DNA of kidney as did N-ethyl-N-nitrosourea. A single dose of both compounds induced kidney tumours, although of a different histological type. 5. A single dose of ethyl methanesulphonate produced ten times as much ethylation of N-7 of guanine in kidney DNA as did N-ethyl-N-nitrosourea without producing tumours. 6. The relevance of these findings to the hypothesis that alkylation of a cellular component is the mechanism of induction of tumours by nitroso compounds is discussed.

Alkanes↗
PubMed1973

Malignant transformation of BHK21 clone 13 cells in vitro by nitrosamines--a conditional state.

All the BHK(21) Clone 13 cells transformed by dimethylnitrosamine or nitrosomethylurea, and a single "spontaneously" transformed clone obtained in our laboratory, exhibit a conditional state of the transformed phenotype. Upon growth at 38.5 degrees , they have a transformed phenotype (clonal morphology and the ability to plate in soft agar); when grown at 32 degrees , their phenotype is normal. The conditional state of these cells, however, does not extend to their growth characteristics; their plating efficiency at the two temperatures in liquid medium is similar. Conversion from the normal to the transformed phenotype and the reverse is possible by temperature shifts. A working hypothesis is proposed suggesting that this phenomenon may be caused by a temperature-sensitive mutation of a cellular gene whose product is responsible for maintaining the normal phenotype. The high temperature would then affect either the synthesis or the function of the protein carrying the temperature-sensitive alteration and, as a consequence, the transformed phenotype would be expressed.

Animals↗
PubMed1987

Macrophage synthesis of nitrite, nitrate, and N-nitrosamines: precursors and role of the respiratory burst.

The macrophage cell line RAW 264.7 when activated with Escherichia coli lipopolysaccharide and interferon-gamma synthesized nitrite (NO3-) and nitrate (NO3-). Medium change after the activation showed that L-arginine was the only amino acid essential for this synthesis. D-Arginine would not substitute for L-arginine. Other analogues that could replace L-arginine were L-homoarginine, L-arginine methyl ester, L-arginamide, and the peptide L-arginyl-L-aspartate. L-Argininic acid, L-agmatine, L-ornithine, urea, L-citrulline, and ammonia were among the nonprecursors, while L-canavanine inhibited this L-arginine-derived NO2-/NO3- synthesis. When morpholine was added to the culture medium of the activated RAW 264.7 macrophages, N-nitrosation took place, generating N-nitrosomorpholine. GC/MS experiments using L-[guanido-15N2]arginine established that the NO2-/NO3- and the nitrosyl group of N-nitrosomorpholine were derived exclusively from one or both of the terminal guanido nitrogens of arginine. Chromatographic analysis showed that the other product of the L-arginine synthesis of NO2-/NO3- was L-citrulline. The role of the respiratory burst in NO2-/NO3- synthesis was examined using the macrophage cell lines J774.16 and J774 C3C. Both cell lines synthesized similar amounts of NO2-/NO3-. However, J774 C3C cells do not produce superoxide and hence do not exhibit the respiratory burst. Additional experiments also ruled out the involvement of the respiratory burst in NO2-/NO3- synthesis.

Arginine↗
PubMed1987

Treatment of nitrosamine-induced pancreatic tumors in hamsters with analogs of somatostatin and luteinizing hormone-releasing hormone.

Pancreatic ductal adenocarcinoma was induced in female Syrian golden hamsters by injecting N-nitrosobis(2-oxopropyl)amine (BOP) once a week at a dose of 10 mg per kg of body weight for 18 weeks. Hamsters were then treated with somatostatin analog D-Phe-Cys-Tyr-D-Trp-Lys-Val-Cys-Trp-NH2 (RC-160) or with [6-D-tryptophan]luteinizing hormone-releasing hormone [( D-Trp6]LH-RH) delayed delivery systems. Microcapsules of somatostatin analog RC-160, designed to release a dose of 5 micrograms/day, were injected twice a month and microcapsules of [D-Trp6]LH-RH, calculated to liberate 25 micrograms per day, once a month. After 18 weeks of BOP administration, the hamsters were divided into three groups of 10-20 animals each. Group I consisted of untreated controls, group II was injected with RC-160, and group III was injected with [D-Trp6]LH-RH. A striking decrease in tumor weight and volume was obtained in animals treated with [D-Trp6]LH-RH or with the somatostatin analog RC-160. After 45 days of treatment with either analog, the survival rate was significantly higher in groups II and III (70%), as compared with the control group (35%). The studies, done by light microscopy, high-resolution microscopy, and electron microscopy, showed a decrease in the total number of cancer cells and changes in the epithelium, connective tissue, and cellular organelles in groups II and III treated with the hypothalamic analogs as compared to controls. These results in female hamsters with induced ductal pancreatic tumors confirm and extend our findings, obtained in male animals with transplanted tumors, that [D-Trp6]LH-RH and somatostatin analogs inhibit the growth of pancreatic cancers.

Adenocarcinoma↗
PubMed1978

interactions of ionizing radiation, nitrosamines, sulfonoxyalkanes and antioxidants as they affect carcinogenesis and survival in mice.

Butylated hydroxytoluene (BHT), pretreatment of 8-wk-old BALB/c mice for 28 days protected against 30-day lethality by X-rays, diethylnitrosamine (DEN), dimethylnitrosamine (DMN) and ethyl methanesulfonate (EMS) but not against methyl methanesulfonate (MMS). In X-ray survivors, neither mean survival nor leukemia incidences were affected by BHT. However, BHT (lifetime), given alone or with DEN (300 MG/KG BW in H2O) or 250 R X-rays, increased irradiated survivors at 18 months but not leukemia or tumor incidences. BHT + DEN treated females had increased survival and a decreased frequency of forestomach squamous carcinomas compared with DEN alone; no differences were seen in males or in pulmonary adenomas. In X-ray + DEN treated females, effect upon survival was additive, but the specific diseases causing this effect were not identified.

Animals↗
PubMedDate not supplied

Effect of water on nitrosamine formation in fried bacon.

Bacon was soaked in water before frying and the effect on the formation of N-nitrosodimethylamine and N-nitrosopyrrolidine was studied. Soaking for 5 minutes reduced N-nitrosopyrrolidine levels by as much as 52%, but had little effect on N-nitrosodimethylamine levels. Longer soaking periods, up to 17 hours, gave the same results.

Animals↗
PubMedDate not supplied

Effect of dietary fats on endogenous formation of N-nitrosamines from nitrate in germ-free and conventional rats and rats harbouring a human flora.

Urinary excretion of N-nitrosoproline (NPRO) was measured in groups of four germ-free (GF) and conventional (CV) rats given a purified diet with or without inclusion of 100 g butterfat, coconut oil or maize oil/kg, and drinking water containing 0.235 M-NaNO3. In the CV environment rats given the fat-supplemented diets excreted significantly less NPRO than those on the low-fat diet. No corresponding decrease in NPRO excretion occurred in the GF environment. Nitrate reductase activity was measured in stomach contents and homogenates of stomach tissue from GF and CV rats given the different diets. No activity was detected in any of the contents from GF rats. Nitrate reductase activity was significantly reduced in contents from all the CV rats given the fat-supplemented diets, the effect being most marked in those given butterfat. Activity was much lower in tissue homogenates from GF rats than in those from their CV counterparts, but was not affected by diet in either environment. Groups of four CV rats, or rats harbouring a human faecal flora (HF), were given the purified diet with or without addition of 100 g butterfat or maize oil/kg and drinking water containing 0.235 M-NaNO3. All groups given the fat-supplemented diet with the exception of the HF rats given butterfat. It is concluded that the reduced excretion of NPRO by rats given diets containing fat was mainly due to inhibition of microbial nitrate reductase activity in the foregut. The smaller effect of butterfat on the HF rats accords with earlier findings in human subjects.

Animals↗
PubMed1986

Oxidative destruction of hydrazines produces N-nitrosamines and other mutagenic species.

As part of the joint International Agency for Research on Cancer-National Cancer Institute program for the evaluation and development of methods for the degradation of chemical carcinogens, four oxidative techniques for the degradation of hydrazines were investigated. The oxidizing agents used were as follows: sodium hypochlorite, calcium hypochlorite, potassium iodate, and potassium permanganate in sulfuric acid. In each case, at least 99% of the hydrazine initially present was destroyed; however, the potential usefulness of these methods was compromised by the formation (in some reaction mixtures) of carcinogenic N-nitroso compounds and/or unknown mutagenic species. Oxidative degradation of hydrazines is recommended only for the decontamination of glassware and for the treatment of spills, for which reductive degradation methods are not suitable.

Animals↗
PubMed1991

Inhibition of nitrosamine formation by ascorbic acid.

Nitrosation occurs under a wide variety of conditions by reaction of most types of amines with any of a large number of nitrosating species. Nitrite can be formed in vivo via bacterial reduction of nitrate and by activated macrophages and endothelial cells. The mechanism of nitrite formation by mammalian cells is via enzymatic oxidation of arginine to NO followed by oxidation to N2O3 and N2O4. Nitrosatable amines are found in many foods and some, eg, dimethylamine, are synthesized in the body. Precursors of N-nitroso compounds are thus almost constantly present together under favorable reaction conditions in vivo and there is, consequently, considerable interest concerning possible human health risks arising from endogenous formation of this class of compounds. Among many nitrosation inhibitors, most attention has focused on ascorbic acid, which reacts with many nitrosating agents and which is virtually nontoxic. This presentation discusses the chemistry of ascorbic acid inhibition of nitrosation reactions.

Amines↗
PubMed1980

Fine structure of rat liver during chronic intoxication with two heterocyclic N-nitrosamines: N-nitrosopiperidine and the non-carcinogen, 2,2',6,6'-tetramethyl-N-nitrosopiperidine.

A comparative fine structural investigation was carried out on the long-term effects on rat liver of chronic exposure to the carcinogen, N-nitrosopiperidine (NPIP) and its non-carcinogenic derivative, 2,2',6,6'-tetramethyl-N-nitrosopiperidine. Some morphological alterations apparently related to drug metabolism and toxicity were common to both compounds. Others, notably that involving the rough ER, were specific to NPIP and resembled those that are induced by other hepatocarcinogens and are characteristic of hepatic cell tumour. It is suggested that the rough ER lesion is associated with initiation and provides a morphological "marker" for the induction of liver neoplasia.

Animals↗
PubMed1989

Increased urinary nitrosamine excretion in patients with urinary diversions.

Tumor development at the site of ureterointestinal anastomosis is a recognized complication in patients with continent urinary diversions. Aerobic cultures of rectal urine samples from 30 patients with urinary diversions (26 ureterosigmoidostomies, two colon conduits, one ileal conduit and a Gersuny bladder) showed a complex bacterial flora containing nitrate-reducing organisms (Escherichia coli, Proteus and Klebsiella spp.). In comparison to normal bladder urine samples from control volunteers (n = 20), rectal urine samples from ureterosigmoidostomy patients (n = 26) showed a significant decrease (P less than 0.0001) in urinary nitrate (0.93 +/- 0.39 versus 0.27 +/- 0.23 mmol/l), a significant increase (P less than 0.0001) in urinary nitrite (not detected versus 29.24 +/- 39.93 mumol/l) as well as a significant increase (P = 0.013) in urinary N-nitroso compound excretion (57.33 +/- 33.87 versus 93.96 +/- 65.76 nmol/l). Significant increases were also found for the urinary excretion of individual volatile and non-volatile N-nitroso compounds, clearly demonstrating a bacterially mediated in vivo formation of N-nitroso compounds in the 'colon' bladders of patients with urointestinal diversions that may be an important etiological risk factor for colon carcinogenesis in this patient group.

Bacteria↗