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PubMed1981

The cellular uptake and covalent binding of nitroso-chloramphenicol.

A comparative study of the cellular transport of CAP and its nitroso derivative (NO-CAP) was carried out in Raji cells, a transformed human lymphoblastoid cell line. Both agents were concentrated by the cells by a factor of 3 (cellular/extracellular concentration ratio). The cellular uptake of NO-CAP, like that of CAP, was found to be rapid and temperature-independent. Thus the greater cytotoxicity of NO-CAP is apparently not due to an enhanced uptake of the nitroso derivative relative to CAP. In contrast to the similarity of uptake, NO-CAP becomes covalently bound to both Raji cells and freshly isolated human bone marrow cells to a much higher extent (15-fold). Also, cells previously loaded with CAP or NO-CAP retain three times as much of the nitroso compound during a 24 hr dialysis against a drug-free isotonic solution. The increased binding of NO-CAP to human hematopoietic cells attests to the greater reactivity of the p-substituted aromatic nitroso group and is consistent with the postulate that reduction products of the nitro group of CAP may be responsible for CAP-induced aplastic anemia.

Anemia, Aplastic↗
PubMed2004

Nitrosobenzene dimerizations as a model system for studying solid-state reaction mechanisms.

Thermal dimerization of nitroso compounds in the solid state was investigated by using para-substituted nitrosobenzenes as model compounds. A mechanism that includes the interplay of topochemical reaction trajectories and phase transfer was proposed on the basis of FT-IR spectroscopic kinetics, time-resolved powder diffraction, and low-temperature X-ray structure determination. From shapes of the kinetic curves analyzed on the basis of the Avrami model, it was found that phase transfer could be triggered by a dimerization reaction of para-substituted nitrosobenzene to azodioxide, which, in turn, can be caused by different packing factors such as disorder in the starting nitroso monomer crystals. Since the represented model can be extended to a broad series of compounds, we propose it as a general method for investigations of solid-state reaction mechanisms.

Journal Article↗
PubMed1991

Relevance of N-nitrosamines to oesophageal cancer in China.

Oesophageal cancer occurs at a very high frequency in certain areas of China, especially in Linxian county, Henan province. Previous studies suggested that N-nitroso compounds play a causative role. In order to study further the exposure of Linxian inhabitants, the intake of N-nitrosamines in the diet was determined. The total daily intake of volatile nitrosamines and of N-nitroso-N-methylbenzylamine (NMBzA) was higher in Linxian than in two other counties. NMBzA can induce cancer in animal and human oesophageal epithelium. Human fetal oesophageal epithelia were cultured with NMBzA for 4 h, and eight monkeys were treated with NMBzA. High-molecular-weight DNA extracted from explants and from the oesophageal epithelia of monkeys induced malignant transformation of NIH 3T3 cells. Alu and monkey-specific repeat sequences were present in transformed cells, and H-ras was found in the transforming DNA. Human fetal oesophageal epithelium cultured with NMBzA was transplanted into the mesentery of BALB/c nude mice. Tumours were found after eight months; and the Alu sequence was present in DNA extracted from tumours induced by NMBzA, showing that the tumours were of human origin. The results provide direct evidence that NMBzA is carcinogenic in human oesophageal epithelium and that N-nitrosamines are one of the causative factors of oesophageal cancer in Linxian county.

Animals↗
PubMed1992

Release of multiple endothelium-derived relaxing factors from porcine coronary arteries.

Using a chemiluminescence method in the present study, we measured nitric oxide and one-electron oxidation products of nitric oxide (NOX) released from porcine coronary artery segments in response to bradykinin, ADP, and the calcium ionophore A23187. Total NOX was compared with the bioactivity of endothelium-derived relaxing factors (EDRF) by a biodetector ring preparation before and after inhibition of L-arginine-dependent nitric oxide synthesis and in the presence of indomethacin. Under basal conditions, arterial segments released NOX and relaxed biodetector rings. Bradykinin, ADP, and A23187 elicited vasorelaxation greater than that observed basally; A23187, but not bradykinin or ADP, caused additional release of NOX greater than that measured basally. Hemoglobin completely reversed vasorelaxation elicited by all three agonists. We compared the amount of nitric oxide released under basal conditions and after stimulation with bradykinin, ADP, and A23187 with the amount of authentic nitric oxide necessary to elicit a bioequivalent response. Authentic nitric oxide did not account for the observed bioactivity as compared with the amount of nitric oxide actually measured in arterial segment effluent. To investigate whether a second non-nitric oxide-containing compound was responsible for the increased bioactivity and the discrepancy between the bioactivity and quantity of nitric oxide measured, we exposed arterial segments to omega-nitro-L-arginine methyl ester to inhibit L-arginine-dependent synthesis of nitroso compounds. The drug completely abolished the nitric oxide signal derived from both basally released and A23187-stimulated relaxing factor and completely reversed vasorelaxation. In contrast, omega-nitro-L-arginine methyl ester only partially reversed bradykinin-stimulated vasorelaxation.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Diphosphate↗
PubMed1987

Tricyclic drugs: potent mutagenicity of traces of a nitroarene formed in the reaction of opipramol with nitrite.

The tricyclic psychotropic drug opipramol (Insidon) reacts in vitro with sodium nitrite in acidic solution to form products including mutagens for Salmonella typhimurium TA98 and TA100. Two aspects are particularly noteworthy. The strong mutagenicity of the crude reaction mixture is almost exclusively due to a compound which is present only in trace quantities (less than 0.1%). This mutagen was identified as a nitroarene, 4-[3-(2-nitro-9-(10H)-acridinon-10-yl)propyl]-1-piperazine-ethanol . Hence, while the formation of carcinogenic N-nitroso compounds from the interaction of nitrogen-containing compounds with nitrite is well known, the present study demonstrates the formation of a highly mutagenic C-nitro compound in the presence of nitrite.

Acridines↗
PubMed1990

Hypoxia-selective antitumor agents. 3. Relationships between structure and cytotoxicity against cultured tumor cells for substituted N,N-bis(2-chloroethyl)anilines.

A series of aniline mustards with a wide range of electron-donating and -withdrawing substituents in the 3- and 4-positions has been synthesized and evaluated for cytotoxicity in cell culture to examine the potential of using nitro group deactivated nitrogen mustards for the design of novel hypoxia-selective anticancer drugs (Denny, W. A.; Wilson, W. R. J. Med. Chem. 1986, 29, 879). Hydrolytic half-lives in tissue culture media, determined by bioassay against a cell line (UV4) defective in the repair of DNA interstrand cross-links showed the expected dependence on the Hammett electronic parameter, sigma, varying from 0.13 h for the 4-amino analogue to greater than 100 h for analogues with strongly electron-withdrawing substituents. Cytotoxic potencies in aerobic UV4 cultures showed a similar dependence on sigma. This dependence predicted that the 4-nitroaniline mustard would be 7200-fold less potent than its potential six-electron reduction product, the 4-amino compound, in growth inhibition assays using a 1-h drug exposure. The measured differential was much lower (225-fold) because of the instability of the latter compound, but a differential of 17,500-fold was observed in the initial rate of killing by using a clonogenic assay. The potential for formation of reactive mustards by reduction to the amine or hydroxylamine was demonstrated by the 4-nitroso compound, which had an aerobic toxicity similar to that of the amine. Although these features confirmed the original rationale, the 3-nitro- and 4-nitroaniline mustards had only minimal hypoxic selectivity against UV cells. Toxicity to hypoxic cells appears to be limited by the low reduction potentials of these compounds and consequent lack of enzymatic nitroreduction. However, this study has demonstrated that nitro groups can be used to latentiate aromatic nitrogen mustards and indicates that examples with higher reduction potentials could provide useful hypoxia-selective therapeutic agents.

Alkylation↗
PubMed1988

Regeneration of O6-alkylguanine-DNA alkyltransferase in human lymphocytes after nitrosourea exposure.

Mitogen-stimulated human lymphocytes have an increased capacity to repair many forms of DNA damage caused by UV, ionizing radiation, and chemical carcinogens. Human lymphocytes rely on a particular DNA repair protein, O6-alkylguanine-DNA alkyltransferase (alkyltransferase) to repair efficiently O6-alkylguanine, an important mutagenic adduct formed by nitrosoureas and other N-nitroso compounds. The alkyltransferase is a "suicide" protein which becomes inactivated during the repair process. Thus, basal activity and the ability to synthesize new protein activity are important compounds of O6-alkylguanine repair. We compared basal and regenerated alkyltransferase activity in resting and mitogen-stimulated human lymphocytes. During stimulation with L-phytohemagglutinin, alkyltransferase activity increased by a mean of 70% over resting cells. Following exposure to N-nitroso-N-methylurea (MNU), alkyltransferase activity was consumed in a dose-dependent manner in both resting and L-phytohemagglutinin-stimulated cells by the repair of MNU-induced O6-methylguanine-DNA adducts. Recovery of alkyltransferase activity began within 1 day of MNU exposure in the L-phytohemagglutinin-stimulated lymphocytes but did not occur in resting cells. Enzyme induction was not observed. When the alkyltransferase was only partially inactivated by low dose MNU, resting lymphocytes still failed to recover alkyltransferase activity. The rate of recovery of alkyltransferase activity in proliferating cells was dependent on the basal level of activity, which varied about 3-fold among donors. These data indicate that mitogen-stimulated lymphocytes develop an increased capacity to repair nitrosourea-induced DNA damage and are able to regenerate activity following nitrosourea exposure. In contrast, resting lymphocytes do not rapidly synthesize new alkyltransferase molecules after nitrosourea exposure and appear susceptible to DNA damage caused by persistent O6-alkylguanine adducts. Thus, both basal alkyltransferase activity and the proliferative state of normal lymphocytes influence the response to nitrosourea exposure.

Cycloheximide↗
PubMed1997

Direct mutagenicity of the polycylic aromatic hydrocarbon-containing fraction of smoked and charcoal-broiled foods treated with nitrite in acid solution.

The polycyclic aromatic hydrocarbons (PAH) containing fractions of smoked and charcoal-broiled foods, namely, Sheat fish (Kytopterus apogon), Mimrow (Crossocheilus reba), Freshwater catfish (Clarias batrachus), chicken wings, rice pork sausage and pork, in addition to naphthalene, acenaphthene, anthracene, phenanthrene, fluoranthene, pyrene, benz[a]anthracene, naphthacene, benzo[a]pyrene, benzo[e]pyrene, 9,10-dimethyl-1,2-benzanthracene, dibenz[ah]anthracene, benzo[ghi]perylene and coronene, were evaluated for their mutagenic potential using Salmonella typhimurium strains TA98 and TA100 in the absence of metabolic activation after being treated with nitrite (500 mM) for 4 hr at 37 degrees C and in acid solution pH 3.0-3.5. The presence of N-nitroso compounds was also determined. Results showed that nitrite could convert most samples to direct-acting mutagens towards both strains except for fluoranthene and benzo[ghi]perylene, which exhibit mutagenicity only with TA98. It was demonstrated that treatment of PAHs with nitrite in acid solution produced some non-N-nitroso direct-acting mutagens, suggesting that they might belong to nitro-PAHs. Therefore, the consumption of charcoal-broiled and smoked foods simultaneously with nitrite is not recommended.

Animals↗
PubMed2003

[Determination of the optical purity of N-nitrosofenfluramine found in the Chinese slimming diet].

From 2001 to the summer of 2002, more than 800 cases of liver damage were reported in Japan among people taking Chinese diet aids. The Japanese Ministry of Health, Labor and Welfare has recently announced that N-nitrosofenfluramine was the hepatotoxic compound contained in the diet aids based on animal experiments performed by the National Institute of Health Sciences. Although N-nitrosofenfluramine is a derivative of fenfluramine, a previously used antiobesity drug, neither pharmacologic nor toxicologic properties have been reported for N-nitroso fenfluramine. It should be noted that N-nitrosofenfluramine has two optical isomers, although it is not yet known which isomer damages the liver and other organs. The Japanese Ministry of Health, Labor and Welfare has not commented on this point. Pursuing this question, 10 types of Chinese slimming aid samples including those obtained from patients with fulminating hepatitis were analyzed by NMR, GC/MS, and a newly established HPLC method using a chiral separation column. It was found that the N-nitrosofenfluramine in all of the toxic diet aids was the (S)-isomer form. No (R)-isomer was detected. These results strongly suggest that the nitroso-compound in the diets must be prepared from pharmacologically active (S)-fenfluramine (dexfenfluramine). Thus the pharmacologic and toxicologic properties of each isomer should be investigated.

Chromatography, High Pressure Liquid↗
PubMed1987

Demonstration of in vivo formation of the nitrosamine N-nitroso-N-methylaniline from amyl nitrite.

Kaposi's sarcoma is associated with Acquired Immune Deficiency Syndrome (AIDS) in U.S. homosexuals. A possible explanation is that butyl nitrite, inhaled as a drug of abuse, initiates the tumor via the in vivo formation of N-nitroso compounds. To demonstrate that such a process can occur, we injected mice i.p. with the amine N-methylaniline (250 mg/kg), gavaged them 30 min later with amyl nitrite (AmNO2, 40 mg/kg), killed the mice after another 30 or 60 min, and analyzed the carcasses for N-nitroso-N-methylaniline (NMA). We obtained 480 +/- 130 (mean +/- S.E. for 6 mice killed after 30 min) and 380 +/- 40 (for 6 mice killed after 60 min) nmol NMA/mouse. Much lower yields were obtained when AmNO2 was injected i.p. and methylaniline was gavaged. Hence, relatively large amounts of at least one nitrosamine can be produced in vivo from simple nitrite esters.

Amyl Nitrite↗
PubMed1998

Photoreactivity of nifedipine in vitro and in vivo.

Side effects of nitroaromatics used as drugs are often assumed to be caused by incomplete enzymatic reduction of the nitro group. However, photoactivation, although usually not considered as a cause of the toxic effects of nitroaromatics, can play a considerable role. Nifedipine, a nitroaromatic as well, is an important drug used in the treatment of myocardial ischaemia and hypertension. It is extremely sensitive to ultraviolet and visible light up to 450 nm and forms a nitroso derivative in vitro. In the present study it is shown that the nitroso compound is a short-lived intermediate in blood and plasma. It reacts with other constituents to form a stable lactam. In vivo, this lactam proves to be rapidly clear from the blood of rats and is excreted almost quantitatively via the bile. The first photoproduct of nifedipine, nitroso nifedipine, is shown to be converted into the lactam mentioned. Beside the lactam, two other products, which are considered to be derivatives of the lactam, are found. One of these two products is also found in the bile of a rat that was exposed to UVA light after intravenous nifedipine administration. This shows that in an in vivo situation, photoproducts can reach organs other than those exposed to the light. In vitro about 45 to 50% of the original amount of nifedipine is not recovered after exposure of nifedipine to UVA in the presence of bovine serum albumin or after incubation of nitroso nifedipine with bovine serum albumin in the dark. As complex binding of nifedipine of plasma proteins is high, the latter finding may have important implications for the situation in vivo.

Animals↗
PubMed1984

Formaldehyde as a possible mutagenic metabolite of N-nitrodimethylamine and of other agents which are suggested to yield non-alkylating species in vitro.

N-Nitramines are biologically active compounds of environmental significance. In this study the suggested bioactivation of N- nitrodimethylamine via oxidation at the methyl-group was confirmed, as was indicated by formaldehyde liberation. N- Nitrodimethylamine and formaldehyde as well as the suggested metabolites, N- nitrohydroxymethylmethylamine and N- nitromethylamine were tested for mutagenicity in histidine auxotrophic Salmonella typhimurium strains in a variety of conditions. N- Nitrodimethylamine was mutagenic only in S. typhimurium TA 100 after pre-incubation with bacteria and a complete metabolizing mixture containing 9000 g liver supernatant and NADPH-regenerating cofactors. N- Nitrohydroxymethylmethylamine and formaldehyde were approximately equally mutagenic without the metabolizing mixture in TA 100 and TA 98, but not in TA 1535. The addition of the 9000 g supernatant of homogenized liver increased the yield of his+ revertants induced by the two compounds. N- Nitromethylamine was not mutagenic with or without the metabolic activation system. The results suggest that formaldehyde is possibly the mutagenically active intermediate formed during in vitro metabolism of N- nitrodimethylamine . Furthermore the participation of formaldehyde as the mutagenic intermediate of other non-alkylating N-nitro and N-nitroso compounds is demonstrated.

Animals↗
PubMed1976

Comparative mutagenicity of N-nitrosamines in a semi-solid and in a liquid incubation system in the presence of rat or human tissue fractions.

The rat liver microsome-mediated mutagenicities of a series of N-nitrosodialkylamines and heterocyclic N-nitrosamines were determined in a liquid incubation system using Salmonella typhimurium TA1530. The influence on mutation frequency of the concentration of co-factors for mixed-function oxidase and composition and molarity of the buffer was investigated, using N-nitrosomorpholine as substrate. The mutagenicity of the N-nitroso compounds in the liquid incubation system under optimal reaction conditions at equimolar concentration was compared quantitatively with that obtained in a soft-agar incorporation assay. N-Nitrosodi-n-pentylamine and N-nitrosodi-n-butylamine showed no enzyme-mediated mutagenicity in the liquid incubation system, and metabolically activated N-nitroso-dimethylamine and N-nitroso-diethylamine showed negligible mutagenic activity in the soft-agar assays. In contrast with these results with the N-nitrosodialkylamines, the mutagenic effects of heterocyclic N-nitrosamines were similar in the liquid incubation system and in soft-agar incorporation assays. The heterocyclic N-nitrosamines showed rat-liver microsome-mediated mutagenicity in the following descending order: N-nitrosomorpholine greater than N-nitrosopyrrolidine greater than N-nitrosopiperidine greater than N-nitroso-N'-methylpiperazine. Seven human liver specimens converted all heterocyclic N-nitrosamines into mutagens; this activity was similar to that of rat liver, except that for N-nitroso-N'-methylpiperazine, fractions from three human liver biopsies were three to 30 times more active than those from untreated rats. The specific reversion of S. typhimurium TA1530 to histidine prototrophy provides experimental evidence that all the N-nitrosamines studied were converted by liver microsomal enzymes into monofunctional alkylating agents.

Animals↗
PubMed1987

In-vivo activation of N-nitrosodiethanolamine and other n-nitroso-2-hydroxyalkylamines by alcohol dehydrogenase and sulfotransferase.

Alcohol dehydrogenase (ADH) activates N-nitrosodiethanolamine (NDELA) to a potent mutagen in the Ames mammalian microsome mutagenicity assay. In vivo, NDELA, its metabolite N-nitroso-2-hydroxymorpholine (NHMOR) and other 2-hydroxylated N-nitrosoalkylamines induce single-strand breaks in rat liver after a single oral application. After competitive inhibition of ADH by pretreatment with ethanol, induction of single-strand breaks by NDELA and N-nitroso(2-hydroxyethyl)ethylamine (NHEEA) was completely suppressed, whereas breaks induced by NHMOR were only partially reduced. Ethanol also influences cytochrome P450-dependent monooxygenases. To investigate whether the observed effect depends on inhibition of ADH and/or of monooxygenases, rats were pretreated with the ADH inhibitor 3-butylthiolane-1-oxide; a considerable reduction in the single-strand-break-inducing potential of NDELA was seen. Moreover, DNA damage induced by NDELA, NHMOR and other hydroxylated N-nitroso compounds is strongly reduced by pretreatment with the sulfotransferase inhibitor, 2,6-dichloro-4-nitrophenol (DCNP). DCNP pretreatment completely suppressed the induction of single-strand breaks by NDELA, whereas the number induced by NHEEA was only partially reduced. Our data suggest that ADH and sulfotransferase are enzymes responsible for the in-vivo activation of N-nitroso-2-hydroxyalkylamines.

Alcohol Dehydrogenase↗
PubMed1981

Mutagenesis by chemical agents in V79 chinese hamster cells: a review and analysis of the literature. A report of the Gene-Tox Program.

The report reviews and evaluates the current literature (about 125 primary publications) on chemically induced specific locus mutations in the V79 Chinese hamster lung cell line. The V79 cell is convenient to use for mutagenesis studies since it has a rapid growth rate, high plating efficiency, and a stable karyotype. Mutation can be easily measured at either the hypoxanthine-guanine phosphoribosyl transferase or the Na+/K+ ATPase locus, both of which have been well characterized. Other less-studied markers are also described. We discuss the protocols for quantitative mutation studies including measurements of cytotoxicity, mutant expression times, mutant selection agents, cell densities during selection, and the stability and verification of mutant phenotypes. Mutations in the V79 cells by chemicals that require activation can be tested after their metabolism by cell homogenates or by intact cells, and the results with each type of activation are compared. For purposes of analysis, we classified a compound as mutagenic if it induced a mutation frequency that is at least 3 times higher than the spontaneous mutant frequency reported for that specific experiment. By this criterion two-thirds of the chemicals analyzed were mutagenic--; 11% with and 55% without metabolic activation. Of the 191 chemicals examined; 119 were polycyclic aromatic hydrocarbons; 25 were nitro or nitroso compounds, 9 were alkyl halides; 7 were purine or pyrimidine derivatives and the remaining 31 were from other chemical classes. We also defined mutagenic potency as the concentration of a compound that increases the mutant frequency by 10 times the spontaneous frequency. Mutagenic potencies of the compounds examined varied over a range of 5 X 10(6). We have also found large interlaboratory variations in the mutagenic potencies. Such variation in potency could be reduced by normalizing the results to a standard mutagen such as N-methyl-N'-nitro-N-nitrosoguanidine. The role of the V79 assay in mutagenicity and carcinogenicity testing is discussed and recommendations are suggested for future investigation.

Animals↗
PubMed1987

Induction of mutagenic activity of tetracycline by synergistic action with nitrite.

Synergistic mutagenicity of tetracycline(TC) and nitrite was investigated by the bacterial mutation test in the Salmonella/microsome system by using the reaction products obtained under neutral condition as well as under acidic condition (in simulated gastric juice). Results from tests using Salmonella typhimurium TA 100 disclosed a significant increase in the appearance of histidine (+) (his+) revertants by the reaction product between TC and nitrite in the presence of the rat liver-microsomal enzyme system (S9 mix), while the mutagenic potency of the reaction product of the two compounds in simulated gastric juice was extremely weak. In the process of the reaction of TC with and without nitrite in the presence of S9 mix, formaldehyde was detected, indicating the demethylation of TC by demethylase in S9. To explain the induction mechanism of the synergistic mutagenicity of TC and nitrite, it was suggested that the alkylating reaction of nitroso compound formed by nitrosation of the 4-demethylated intermediate of TC by the aid of microsomal metabolism is more important than the well known nitrosation mechanism under acidic condition such as in gastric juice in rats and in simulated gastric juice.

Animals↗
PubMed2001

A comparative study by electron paramagnetic resonance of free radical species in the mainstream and sidestream smoke of cigarettes with conventional acetate filters and 'bio-filters'.

Tobacco smoking is the most important extrinsic cause, after the diet, for increasing morbidity and mortality in humans. Unless current tobacco smoking patterns in industrialised and non-industrialised countries change, cigarettes will kill prematurely 10 million people a year by 2025. Greece is at the top of the list of European countries in cigarette consumption. In 1997, a Greek tobacco company introduced a new 'bio-filter' (BF) claiming that it reduces substantially the risks of smoking. In a recent publication [Deliconstantinos G, Villiotou V, Stavrides J. Scavenging effects of hemoglobin and related heme containing compounds on nitric oxide, reactive oxidants and carcinogenic volatile nitrosocompounds of cigarette smoke. A new method for protection against the dangerous cigarette constituents. Anticancer Res 1994; 14: 2717-2726] it was claimed that the new 'bio-filter' (activated carbon impregnated with dry hemoglobin) reduces certain toxic substances and oxidants (like NO, CO, NOx, H2O2, aldehydes, trace elements and nitroso-compounds) in the gas-phase of the mainstream smoke. We have investigated by electron paramagnetic resonance (EPR) the mainstream and sidestream smoke of the BF cigarette, in comparison with three other cigarettes with similar tar and nicotine contents, that have conventional acetate filters. We found that BF cigarette smoke has similar tar radical species with the same intensity EPR signals to those of the other cigarettes. The ability of the aqueous cigarette tar extracts to produce hydroxyl radicals (HO*), which were spin trapped by DMPO, was very similar to, or even higher than, the other 3 brands. The gas-phase of the mainstream smoke of the BF cigarette showed a 30-35% reduction in the production of oxygen-centered radicals (spin trapped with PBN). In the case of the sidestream smoke, BF cigarettes produced substantially higher concentrations of gas-phase radicals, compared to the other brands. These results suggest that BF is partially effective at removing some of the gas-phase oxidants but not effective in the reduction of tar and its radical species in the mainstream and sidestream smoke. It is well known from epidemiological studies that tar content is strongly associated with increasing risk to smokers of lung cancer. In our experiments, BF cigarettes produce a higher amount of tar and stable free radical species than the other 3 brands in the sidestream smoke (between puffs), thus potentially increasing risk to the smoker and passive smoker.

Acetates↗
PubMedDate not supplied

A review of the natural occurrence, synthetic production and use of carcinogenic hydrazines and related chemicals.

This writing details the natural occurrence, synthetic production and use of the carcinogenic hydrazines and related chemicals. Twenty-three such chemicals were found in nature in mushrooms, tobacco, bay leaves, antibiotics, soil and other sources. The synthetically-produced hydrazines and related chemicals include 61 compounds which were or are in use as pharmaceutical drugs, agricultural substances, industrial chemicals and fuels for military and space vehicles and rockets. Because there is an overlap between the naturally-occurring and synthetically-produced compounds, their total number is 76. Altogether, 98 hydrazines and related chemicals were studied for carcinogenic action thus far, of which 84 were found to be carcinogenic and the remaining 14 were inactive. This means that the human population is exposed in various degrees to a substantial number of these agents. Therefore, the hydrazine class, unlike the polycyclic aromatic hydrocarbons, N-nitroso compounds, and aromatic amines, poses a greater environmental risk to the human population. In view of these considerations, it appears reasonable to proceed with additional experimentation in this field of interest.

Agrochemicals↗