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At least 19 recordsLinked to original sources
PubMed1979

Cyanide intoxication in sheep: enhancement of efficacy of sodium nitrite, sodium thiosulfate, and cobaltous chloride.

For treatment of cyanide intoxication of ruminants, the present recommended doses of sodium nitrite (5 mg/kg of body weight) and sodium thiosulfate (25 to 50 mg/kg) are smaller than those recommended for other animals; the decrease is partially attributed to the greater susceptibility of ruminants to the toxic effects of sodium nitrite. Based on the high tissue concentration and activity rate of rhodanese in ruminants, sulfur donors such as sodium thiosulfate could be utilized more efficaciously. Doses of sodium nitrite and sodium thiosulfate (up to 22 and 660 mg/kg, respectively) were evaluated in the present studies. Adjustment of the antidotal combination provided almost three times the protection afforded by the previously recommended doses. Moreover, under the conditions tested, the newly adjusted dose levels of sodium thiosulfate alone were more effective than the previously used antidotal combination of sodium nitrite and sodium thiosulfate and this protective effect was enhanced by cobaltous chloride (10.6 mg/kg) or sodium nitrite. The present recommended therapeutic approach to cyanide intoxication in sheep should be based primarily on administration of a much higher dose of sodium thiosulfate in combination with sodium nitrite or cobaltous chloride (or both).

Animals↗
PubMed1977

Induction of liver tumors in rats by sodium nitrite and methylguanidine.

The carcinogenicity of sodium nitrite and methylguanidine singly and together were examined in rats. A hepatocellular carcinoma, a hemangiosarcoma and a spindle cell sarcoma were found in 3 of 15 rats fed continuously on pellet diet containing 0.16% sodium nitrite and 0.16% methylguanidine. Hemangiomas and bile duct adenomas of the liver were also found in 6 and 8, respectively, of the 15 rats in this group. Hemangiomas and bile ducts adenomas of the liver were found in 2 and 3, respectively, of the 4 rats fed on pellet diet containing 0.16% sodium nitrite. Only 1 of 5 rats fed on pellet diet containing 0.16% methylguanidine developed a hemangioma. No tumor was found in the control group. All the tumors were found in rats that survived for over 12 months. No significant changes were detected in the esophagus or stomach.

Adenoma, Bile Duct↗
PubMed1979

Acquisition deficits induced by sodium nitrite in rats and mice.

Graded doses of sodium nitrite were administered shortly before or immediately after a single training trial in an inhibitory avoidance task. A retention test was given at 24 h (rats) or 72 h (mice) after training. The results indicate that sodium nitrite impairs acquisition of an inhibitory avoidance response in rats and mice. Retention was impaired with doses lower than those required for producing hypoxic effects, as measured by the EEG, methemoglobin levels in the blood, blood pressure, and heart rate. Since hypoxia was not involved, it is likely that the effects were mediated by some direct action of sodium nitrite on the CNS.

Amnesia↗
PubMed1979

Chronic toxicity of sodium nitrite in mice, with reference to its tumorigenicity.

Sodium nitrite has been widely used as one of the most effective food additives to tinge color on cured meat. However, it has been elucidated that this chemical is not merely a precursor of N-nitroso compounds, many of which are strongly carcinogenic, but also a mutagenic substance in biological tests. In order to ascertain the possible tumorigenicity of sodium nitrite itself, chronic toxicity of the agent in mice, by means of daily oral administration as drinking water for more than 18 months, in the concentration of 0.5 (maximum tolerated dose), 0.25, and 0.125%, was tested. As a result, development of various tumors, including thymic lymphoma, nonthymic lymphoid leukemia, pulmonary adenoma and carcinoma, and benign and malignant tumors in soft tissue, was seen in these mice. However, as to the incidence of tumors as well as the developmental time of each histologically classified tumor, no apparent difference was detected between those in the experimental groups and the control group.

Animals↗
PubMed1979

[Mutagenic activity of basfungin in its combined action with sodium nitrite].

The mutagenic activity of basfungin, when acting in combination with sodium nitrite, was studied in a subacute experiment, using the method of bone marrow cytogenetic analysis. The results were compared with those in groups in which basfungin and sodium nitrite were applied separately, as well as with the results of the parallel control. The mutagenic effect in the combined action group did not essentially differ from the effect of application of basfungin alone, both qualitatively and diaulitatively. Interesting results were obtained in the group receiving sodium nitrite alone - the percentage of cells with chromosomal aberrations was significantly than the control values.

Animals↗
PubMed1979

Comparison of studies on saccharin and sodium nitrite.

A review of long term animal studies of saccharin and sodium nitrite was undertaken to assess the effect of variability of selected protocol elements on the results obtained. These elements were divided into 4 general categories: design, including selection of test animals, basal diet, dosage form and doses of test substance, route of administration, and duration of exposure; observations, including gross observations during life and at necropsy, clinical tests, and histopathology; performance, including conduct of the test and animal husbandry; and analytical procedures, including chemical and statistical analyses. Because many of the protocol elements are not fully discussed in study reports, it was often impossible to determine what actually had been done. The review of various saccharin studies suggests that bladder tumors resulted following in utero exposure. In utero exposure with sodium nitrite did not appear to cause reticuloendothelial changes. The numerous variations in protocol elements in the nitrite studies precluded identification of a prime element responsible for the variation in reticuloendothelial changes observed. It can be concluded from this review that achievement of reproducibility in long term studies requires minimal variation of protocol elements for the new study.

Animals↗
PubMed1979

Effect of processing variables on the outgrowth of Clostridium sporogenes PA 3679 spores in comminuted meat cured with sorbic acid and sodium nitrite.

The effects of the initial pH and a "short pump" on the outgrowth of Clostridium sporogenes PA 3679 spores in comminuted cured pork were studied. Fresh ground pork was cured with salt, sugar, phosphate, ascorbate, and varying amounts of sodium nitrite and sorbic acid. The product was comminuted and inoculated with 1,000 spores of C. sporogenes per g. The meat was stuffed into 1-ounce (ca. 28.4-g) aluminum tubes, cooked to 58.5 degrees C, cooled, and incubated at 27 degrees C to observe for swells. Product cured with 0.2% sorbic acid in combination with 40 ppm sodium nitrite (40 microgram/g) had better clostridium inhibition than did product cured with 120 ppm nitrite within a pH range of 5.0 to 6.7. The sorbic acid-40 ppm nitrite combination also gave better clostridial protection than did the 120 ppm nitrite alone when reduced amounts of curing ingredients were present.

Animals↗
PubMed1976

Effect of sodium nitrite inhibition on intracellular thiol groups and on the activity of certain glycolytic enzymes in Clostridium perfringens.

Activities of glyceraldehyde-3-phosphate dehydrogenase (EC 1.2.1.12) (GAP-DH) and aldolase (EC 4.1.2.13) in cells of Clostridium perfringens that had been inhibited with sodium nitrite were investigated. A complete loss in GAP-DH activity and a 67% decrease in aldolase activity were observed when growth of C. perfringens was inhibited. There was also a 91% decrease in the concentration of free sulfhydryl groups of soluble cellular components. Dithiothreitol restored some activity to inactive GAP-DH from sodium nitrite-inhibited cells, indicating that a loss of reduced sulfhydryl groups was involved in the inactivation of the enzyme. The evidence presented suggests that sodium nitrite inhibition of C. perfringens may involve an interaction of sodium nitrite as nitrous acid with sulfhydryl-containing constituents of the bacterial cell.

Cell Wall↗
PubMed1978

Carcinogenicity of triethanolamine in mice and its mutagenicity after reaction with sodium nitrite in bacteria.

Mice fed a diet containing 0.3 or 0.03% triethanolamine developed malignant tumors. Females showed a high incidence of tumors in lymphoid tissues, while this type was absent in males. Tumors in other tissues were produced at a considerable rate in both sexes, but no hepatoma was found. Triethanolamine was not mutagenic to Bacillus subtilis by itself, but it became mutagenic after reacting with sodium nitrite under acidic conditions or when the mixture was heated. Although N-nitrosodiethanolamine, a known carcinogen and mutagen, was detected in the reaction mixture by thin-layer chromatography, it may not be the main mutagenic product, because the product was a stable and direct mutagen and its mutagenic activity was destroyed by liver enzymes, unlike N-nitrosodiethanolamine. The lethal and mutagenic DNA damages produced by this unidentified product were susceptible to some extent to the repair functions of the bacteria.

Animals↗
PubMed1978

Carcinogenic effect of a quanidine pesticide administered with sodium nitrite on adult mice and on the offspring after prenatal exposure.

Adult Swiss mice were treated intragastrically during the last week of pregnancy with the fungicide dodecylquanidine acetate (dodine, DGA) together with 0.05% sodium nitrite. The incidence of malignant lymphomas, lung adenomas and hepatomas was 30--70% in females. The first tumors appeared 4 months after delivery in the FO generation and at 6--7 months in the F1 generation. Among the untreated control mice the frequency of spontaneous tumors was 6%, and lymphomas developed, if at all, only after 10 months. The oncogenic activity of DGA with sodium nitrite in the offspring was dependent on the dose of DGA.A and C type RNA virus particles were demonstrated in lymphomas by electronmicroscopy. DGA alone had no effect on the cancer incidence.

Animals↗
PubMed1979

Effect of sodium nitrite on the alpha-chlorohydrin-induced lesion of the testis--epididymis complexin the rat.

Administration of vasodilator, sodium nitrite (20 mg/kg body weight), 30 min before alpha-chlorohydrin treatment (90 mg/kg body weight) prevented the chlorohydrin-induced lesion in rat testis--epididymis complex. However, administration of vasodilator 90 min after alpha-chlorohydrin treatment did not prevent the chlorohydrin-induced lesion in the testis--epididymis complex. These observations suggest that the testicular vasculature is involved in drug action.

Animals↗
PubMed1979

Transplacental mutagenesis of products formed in the stomach of golden hamsters given sodium nitrite and morpholine.

Hamster embryos were exposed in utero to the action of sodium nitrite (NaNO2) and morpholine (Mo) administered simultaneously by stomach tube to the mothers on the 11th or 12th day of pregnancy. Embryo cells were examined for chromosomal aberrations, micronuclear formation, morphological or malignant transformation and drug resistance mutations. For detection of induced mutations, the embryo cells were cultured in normal medium for 72 h and then transferred to medium containing 10 or 20 micrograms/ml of 8-azaguanine (8AG) or 1m7 ouabain (Oua). The number of 8AG-, Ouaresistant colonies was markedly increased after administration of NaNO2 and Mo. The embryonic fibroblasts also showed a markedly increased frequency of micronucleation and a slight increase in chromosome aberrations. This treatment also caused morphological or malignant transformation of fetal cells. After cultivation in vitro, cells from some transformed colonies produced tumors when inoculated into the cheek pouch of young golden hamsters. Orally administered N-nitroso-morpholine (N-Mo), as a positive control, had the same transplacental biological actions on embryonic fibroblasts. However, transplacentally Mo alone was ineffective. A single administration of 500 mg/kg NaNO2 had only slight biological effects. N-Mo was produced in the stomachs of animals treated simultaneously with NaNO2 and Mo. A small amount of a nitrosamine, N-nitrosodimethylamine (DMN), was detected in the stomach after a single dose of NaNO2.

Animals↗
PubMed1977

Nitrosation in vitro and in vivo by sodium nitrite, and mutagenicity of nitrogenous pesticides.

37 nitrogenous pesticides, belonging to the chemical groups of amides, carbamates and ureas, were nitrosated with sodium nitrite in vitro. The nitrosated compounds were tested for mutagenic activity in the bacterial spot test with Salmonella typhimurium his G 46. Those pesticides reacting positively in this test after nitrosation were then fed to mice in combination with sodium nitrite in order to assess the formation and mutagenicity of these nitroso compounds in vivo. With the already known exception of ethylenethiourea (ETU), no pesticide produced enhanced numbers of micronuclei in mouse bone-marrow erythrocytes when fed together with nitrite. Dose-response experiments with intraperitoneal injection of N-nitroso-ETU revealed an apparent no-effect level of about 15--18 mg/kg. The findings are correlated with the pesticide residues actually present in the environment.

Animals↗
PubMedDate not supplied

[Effect of nitroglycerin and sodium nitrite on myocardial mitochondrial respiration and oxidative phosphorylation normally and in coronarogenic ischemia].

The effect of nitroglycerin and sodium nitrite (2.10(-6), 2.10(-5) and 2.10(-4) g/ml) on respiration and oxidative phosphorylation of mitochondria of the normal and ischemized dog myocardium has been investigated in the presence of glutamate, succinate and alfaketoglutarate. The drugs inhibited ADP-activated oxygen consumption and ADP phosphorylation rate upon oxidation of succinic acid formed in mitochondria from exogenic glutamate, without changes in the phosphorylation coefficient and free oxidation rate (i. e. in the absence of ADP) in mitochondria of the healthy and ischemic heart. In the ischemic area one can also observe an inhibition of ADP-activated oxidation of endogenic succinate formed from exogenic glutamate.

Animals↗
PubMed1975

Inhibitor of Clostridium perfringens formed by heating sodium nitrite in a chemically defined medium.

An inhibitor of Clostridium perfringens formed when low levels of nitrite were autoclaved with a defined chemical medium. A systematic study of the medium revealed that only amino acids and mineral salts were involved in the production of this inhibitor, which was proven to be a toxic compound formed from cysteine, ferrous sulfate, and sodium nitrite. The inhibitor was compared to several known compounds. S-nitrosocysteine inhibited the test organism, but would not form in the test system in amounts large enough to explain the observed inhibition. Roussin red salt was unstable in the test system and therefore was not the inhibitor. Roussin black salt, which was also inhibitory, could form in sufficient amounts to explain the inhibition. A complex of cysteine, iron, and nitric oxide was detected in the autoclaved solution of cysteine, ferrous sulfate, and sodium nitrite; this cysteine complex did not appear to be inhibitory, however, at levels which could form in the autoclaved medium. The observed inhibition may have been due to the combined effects of sublethal concentrations of each compound.

Anti-Bacterial Agents↗
PubMed1976

Transplacental effects of ethylnitrosourea precursors ethylurea and sodium nitrite in hamsters.

Four simultaneous dosages of the ethylnitrosourea precursors, ethylurea and sodium nitrite, were administered intragastrically to pregnant hamsters at 100 mg/kg and 50 mg/kg respectively, from the 12-15th days of pregnancy. The treatment induced multiple neurogenic tumors of the peripheral nervous system in the offspring. Female progeny developed a greater incidence and multiplicity of peripheral nervous system tumors with significantly shorter latencies than males, thus establishing evidence that the tumors were age and sex dependent. The tumors presented varied morphological patterns and upon transplantation, grew regularly, exhibiting their malignant nature. The possible influence of estrogenic hormones on the development and growth of peripheral nervous system tumors and comparative aspects of the relationship between prenatal and postnatal carcinogenesis with regard to the ensuing tumor spectra as a consequence of exposure to the same chemical agent, are discussed.

Animals↗