In Korea where night soil used as fertilizer for crops and vegetables they may be contaminated simultaneously with infective stage of ascaris, hookworm and other helminthes. In this circumstance, the ascaris eggs and hookworm larvae may adhere to certain kinds of leafy vegetables(Chyu, 1957) and may remain viable even after pickling in brine or in other substances (Han and Ko, 1952; Soh, 1960). It has been shown that Heliogen(Thitasut, 1961) will kill the parasite eggs and larvae, and Sodium nitrite (Kozai, 1960; Kim and Soh 1964) and Thiabendazole (Kutsmi, 1964 and 1965; Kim et al., 1966) also had ovicidal action. The present study has been planned to study the ovicidal and larvicidal actions of several chemicals in Korean pickle juice(Kimchi) and the results are summarized as follows: Heliogen solution(iodine 100 ppm) did not destroy the ascaris and hookworm eggs within 30 minutes at the temperature of 15-30 C, but the hookworm larvae were killed within 3 minutes under the same conditions. Sodium nitrite which was added to pickle juice at the rate of 0.1 percent destroyed more than 90 percent of ascaris fresh eggs within 10 days and the embryonated eggs were destroyed within 2 days. Hookworm eggs were destroyed within 3 days and larvae were killed within 7 hours. Thiabendazole which was added to pickle juice at the rate of 0.1-0.025 percent inhibited the infectivity of ascaris embryonated eggs within 24 hours and hookworm eggs were destroyed in the same concentrations of the reagent. Hydrogen ion concentration of pickle juice which was mixed with Sodium nitrite (0.1 percent) was not changed for 10 days. 1.5 mg of Sodium nitrite or Thiabendazole produced no toxicity in kidney and intestine of mice but slight pathological changes in the liver of the same animal.
parasitology-helminth-nematoda ; Ascaris lumbricoides ; thiabendazole ; mouse ; sodium nitrite ; iodine

Although sodium nitroprusside (SNP) is often used in pediatric intensive care units, cyanide toxicity can occur after SNP treatment. To treat SNP-induced cyanide poisoning, antidotes such as amyl nitrite, sodium nitrite, sodium thiosulfate, and hydroxycobalamin should be administered immediately after diagnosis. Here, we report the first case of a very young infant whose SNP-induced cyanide poisoning was successfully treated by exchange transfusion. The success of this alternative method may be related to the fact that exchange transfusion not only removes the cyanide from the blood but also activates detoxification systems by supplying sulfur-rich plasma. Moreover, exchange transfusion replaces cyanide-contaminated erythrocytes with fresh erythrocytes, thereby improving the blood's oxygen carrying capacity more rapidly than antidote therapy. Therefore, we believe that exchange transfusion might be an effective therapeutic modality for critical cases of cyanide poisoning.
Amyl Nitrite ; Antidotes ; Natural Resources ; Cyanides ; Erythrocytes ; Humans ; Hydroxocobalamin ; Infant ; Intensive Care Units, Pediatric ; Nitroprusside ; Oxygen ; Plasma ; Sodium ; Sodium Nitrite ; Thiosulfates

Cyanide poisoning can occur from industrial disasters, smoke inhalation from fire, food, and multiple other sources. Cyanide inhibits mitochondrial oxidative phosphorylation by blocking mitochondrial cytochrome oxidase, which in turn results in anaerobic metabolism and depletion of adenosine triphosphate in cells. Rapid administration of antidote is crucial for life saving in severe cyanide poisoning. Multiple antidotes are available for cyanide poisoning. The action mechanism of cyanide antidotes include formation of methemoglobin, production of less or no toxic complex, and sulfane sulfur supplementation. At present, the available antidotes are amyl nitrite, sodium nitrite, sodium thiosulfate, hydroxocobalamin, 4-dimethylaminophenol, and dicobalt edetate. Amyl nitrite, sodium nitrite, and 4-dimethylaminophenol induce the formation of methemoglobin. Sodium thiosulfate supplies the sulfane sulfur molecule to rhodanese, allowing formation of thiocyanate and regeneration of native enzymes. Hydroxocobalamin binds cyanide rapidly and irreversibly to form cyanocobalamin. Dicobalt edetate acts as a chelator of cyanide, forming a stable complex. Based on the best evidence available, a treatment regimen of 100% oxygen and hydroxocobalamin, with or without sodium thiosulfate, is recommended for cyanide poisoning. Amyl nitrite and sodium nitrite, which induce methemoglobin, should be avoided in victims of smoke inhalation because of serious adverse effects.
Adenosine Triphosphate ; Aminophenols ; Amyl Nitrite ; Antidotes* ; Disasters ; Edetic Acid ; Electron Transport Complex IV ; Equipment and Supplies ; Fires ; Hydroxocobalamin ; Inhalation ; Metabolism ; Methemoglobin ; Oxidative Phosphorylation ; Oxygen ; Poisoning ; Polyphosphates ; Regeneration ; Smoke ; Sodium ; Sodium Nitrite ; Sulfur ; Thiocyanates ; Thiosulfate Sulfurtransferase ; Thiosulfates ; Vitamin B 12

Objective: To investigate the effects of different prescription compositions of traditional Chinese medicine and its different extraction methods of compound formula extracts on hypoxia tolerance in mice, in order to preferably select their prescription compositions and preparation extraction methods. Methods: Male BALB/c mice were randomly divided into 6 groups: blank control group, compound danshen group, compound Rhodiola Rosea alcohol-water extract group (Rhodiola rosea, Astragali Radix, Polygonati Rhizoma, Lycii Fructus), compound Rhodiola Rosea water extract group, compound Astragalus alcohol-water extract group (Astragali Radix, Polygonati Rhizoma, Lycii Fructus) and compound Astragalus water extract group, 30 mice in each group. Each group was administered continuously by gavage for 10 d. The blank group was gavaged with sterilized injection water. The mice in the other groups were treated with 0.15 g/kg of compound danshen, 3 g/kg of compound Rhodiola Rosea alcohol-water extract or water extract, and 1.7 g/kg of compound Astragalus alcohol-water extract or water extract, respectively. Each group was subjected to normobaric hypoxia tolerance test, sodium nitrite toxicity survival test and acute cerebral ischemia-hypoxia test 1 h after the last gavage, and the mice brain tissues were used to determine the activity of antioxidant enzymes and metabolites related to oxidative stress. Results: Compared with the blank control group, in normobaric hypoxia tolerance test, the survival time of mice in the compound danshen group and the compound Astragalus alcohol-water extract group and water extraction group was prolonged significantly (P＜0.01), and the number of open-mouth gasping after cerebral ischemia and hypoxia was increased significantly (P＜0.05). There was no statistical difference in survival time after sodium nitrite injection in each group. Compared with the blank control group, the activities of T-AOC, SOD, GSH and CAT were increased significantly (P＜0.05, P＜0.01) and the content of MDA was decreased significantly (P＜0.01) in the compound Astragalus water extract group. Compared with the compound danshen group, the activities of SOD, CAT and GSH were increased significantly (P＜0.01, P＜0.05) and the content of MDA was decreased significantly (P＜0.05). Conclusion: Compound Astragalus water extraction has the best effect of hypoxia tolerance, compound Rhodiola Rosea can eliminate Rhodiola rosea and consists of Astragali Radix, Polygonati Rhizoma, Lycii Fructus and its extraction method is water extraction.
Animals ; Astragalus Plant ; Ethanol ; Hypoxia ; Male ; Mice ; Plant Extracts/pharmacology* ; Rhodiola ; Sodium Nitrite ; Superoxide Dismutase/metabolism* ; Water

Sodium nitrite is commercially used as a coloring agent, food preservative, and corrosion inhibitor. Accidental poisoning with sodium nitrite from contaminated food and water causes gastrointestinal irritation, vasodilatation, and methemoglobinemia with subsequent tissue hypoxia. We describe an outbreak case of sodium nitrite-induced methemoglobinemia following the ingestion of noodles contaminated with industrial antifreeze. The eEight patients involved initially complained that their noodles tasted 'unpleasant' and soon afterwards experienced nausea, vomiting, dizziness, and fatigue. Some of them noted cyanosis on their lips and fingers. Subsequent investigations demonstrated a high methemoglobin concentration which was corrected by the intravenous administration of methylene blue three hours after the onset of symptoms. The patients made a prompt, uncomplicated recovery and were discharged home 4 four days later. Industrial antifreeze contains sodium nitrite and calcium nitrite. Because an accidental poisoning of industrial antifreeze causes fatal methemoglobinemia, emergency physicians should promptly identify its symptoms and institute treatment with methylene blue promptly. In addition, industrial agencies must caution construction businesses against such contamination events.
Administration, Intravenous ; Anoxia ; Calcium ; Commerce ; Corrosion ; Cyanosis ; Dizziness ; Eating ; Emergencies ; Fatigue ; Fingers ; Humans ; Lip ; Methemoglobin ; Methemoglobinemia ; Methylene Blue ; Nausea ; Sodium ; Sodium Nitrite ; Vasodilation ; Vomiting

AIMTo study the sodium nitrite induced DNA mutation by convolution spectrometry (CS).

METHODSThe spectra of sodium nitrite-induced mutative calf thymus DNA was compared with ego criteria based on Spectra of the primary DNA within the wavelength range from 200 to 340 nm. Distilled water served as blank and normal saline served as negative control. Any difference was quantitatively expressed by differential value (delta) of convolution spectra. Near-infrared spectroscopy was employed as the reference method.

RESULTSThe differential value was positively correlated with the increasing time and concentration of sodium nitrite. delta values increased to 1.37%, 2.41% and 5.44% respectively within 2-hour's reaction between calf thymus DNA and 0.5, 0.05 and 0.005 microgram.mL-1 sodium nitrite, while on the contrary, changes could be hardly observed on the corresponding UV absorption spectra. The results were also confirmed by their corresponding near-infrared spectra.

CONCLUSIONThe delta values can be used to represent the compound's strength of mutagenesis. Every convolution procedure takes less than one minute, so CS provides a fast, simple and inexpensive alternative method to determine chemical or medicinal DNA mutation.

Animals ; Cattle ; DNA ; chemistry ; drug effects ; In Vitro Techniques ; Mutation ; drug effects ; Sodium Nitrite ; pharmacology ; Spectrum Analysis ; methods ; Thymus Gland ; chemistry ; drug effects

To investigate the potential ability of the nitrite to induce neuronal differentiation of PC12 cells, cultured PC12 cells planted on matrigel in the presence or absence of sodium nitrite were employed as model, nerve growth factor (NGF) served as a positive control. After 48 h, sodium nitrite enhanced cell viability and vascular endothelial growth factor (VEGF) secretion. Same as the effect of NGF, sodium nitrite (1.4 mmol x L(-1)) treated cultures contained a greater proportion of cells bearing neurites and neurites were much longer than those found in negative control cultures (P < 0.05). Compared with the negative control, sodium nitrite (1.4 mmol x L(-1)) also upregulated the expression of VEGF mRNA (P < 0.05) and hypoxia inducible factor 1 alpha (HIF-1 alpha) or VEGF protein expression (P < 0.05) in cultures of PC12 cells. On the other hand, these effects of the sodium nitrite were likely mediated by HIF-1alpha, since their effects were antagonized by addition of HIF-1alpha inhibitor YC-1. Taken together, these results suggest that low doses of sodium nitrite could induce neurite outgrowth in PC12 cells by activating the HIF-1alpha-VEGF pathway.
Animals ; Cell Differentiation ; drug effects ; Cell Survival ; drug effects ; Food Preservatives ; pharmacology ; Hypoxia-Inducible Factor 1, alpha Subunit ; genetics ; metabolism ; Neurites ; drug effects ; PC12 Cells ; RNA, Messenger ; metabolism ; Rats ; Sodium Nitrite ; pharmacology ; Up-Regulation ; Vascular Endothelial Growth Factor A ; genetics ; secretion

The present study was aimed to explore the effect of sodium nitrite on cytoskeletal protein phosphorylation and spatial learning and memory in rats. Rats were served with drinking water containing sodium nitrite (100 mg/kg) for 60 days, then, the ability of spatial learning and memory of the rats was measured by Morris water maze. Phosphorylation level of tau and neurofilament, and the expression of protein phosphatase 2A (PP2A) catalytic subunit in the hippocampus were detected by immunohistochemistry and Western blot. In comparison with the rats served with normal tap water, the rats served with sodium nitrite water showed significantly longer latency to find the hidden platform in Morris water maze (P < 0.05), elevated phosphorylation level of tau and neurofilament, and decreased expression of PP2A catalytic subunit (P < 0.05). These results indicated that administration of sodium nitrite could impair the spatial learning and memory of the rats, and the hyperphosphorylation of cytoskeletal proteins and the down-regulation of PP2A might be underlying mechanisms for the impairment.
Animals ; Cytoskeletal Proteins ; metabolism ; Down-Regulation ; Hippocampus ; metabolism ; Maze Learning ; Memory ; drug effects ; Neurofilament Proteins ; metabolism ; Phosphorylation ; Protein Phosphatase 2 ; metabolism ; Rats ; Rats, Sprague-Dawley ; Sodium Nitrite ; pharmacology ; Spatial Learning ; drug effects ; tau Proteins ; metabolism

Recent data have revealed that inhibiting autophagy exacerbates lipid accumulation in hepatocytes and nitrite treatment reduces total triglyceride levels in the high-fat diet mice. Therefore, the present study aimed to determine the effects of nitrite on simple hepatic steatosis and the possible role of autophagy. Firstly, steatotic L-02 cells were induced by incubating L-02 cells with 1.2 mmol · L(-1) oleic acid (OA) for 24 h. Secondly, steatotic L-02 cells were treated with 0.2 mmol · L(-1) sodium nitrite (SN) plus 3-methyladenine (3-MA), or chloroquine (CQ) for 24 h, and then lipid accumulation was measured with oil red O staining and triglyceride quantification. The notable steatosis could be observed in L-02 cells following exposure to 1.2 mmol · L(-1) OA for 24 h. Treatment with 0.2 mmol · L(-1) sodium nitrite reduced lipid accumulation in steatotic L-02 cells. 3-MA weakened the ability of sodium nitrite to ameliorate hepatic steatosis. Additionally, the sodium nitrite increased number of LC3-II immunostaining puncta and LC3-II protein expression was confirmed by immunofluorescence or Western blot analysis, and the effects were enhanced by CQ treatment. The number of increased cytoplasm vacuoles and lysosomes increased was confirmed by phase contrast and fluorescence microscope respectively. The increased autolysosome was detected by electron microscopy, this phenomenon could be reversed by CQ treatment. These data demonstrated that sodium nitrite enhanced the autophagic flux and decomposition of triglycerides in steatotic L-02 cells.
Adenine ; analogs & derivatives ; Autophagy ; Blotting, Western ; Cells, Cultured ; Chloroquine ; Cytoplasm ; Fatty Liver ; Hepatocytes ; drug effects ; Humans ; Lipid Metabolism ; drug effects ; Microscopy, Fluorescence ; Microtubule-Associated Proteins ; metabolism ; Oleic Acid ; Sodium Nitrite ; pharmacology ; Triglycerides

Nitrites play multiple characteristic functions in invasion and metastasis of hepatic cancer cells, but the exact mechanism is not yet known. Cancer cells can maintain the malignant characteristics via clearance of excess mitochondria by mitophagy. The purpose of this article was to determine the roles of nitrite, reactive oxygen species (ROS) and hypoxia inducing factor 1 alpha (HIF-1 α) in mitophagy of hepatic cancer cells. After exposure of human hepatocellular carcinoma SMMC-7721 cells to a serial concentrations of sodium nitrite for 24 h under normal oxygen, the maximal cell vitality was increased by 16 mg x (-1) sodium nitrite. In addition, the potentials of migration and invasion for SMMC-7721 cells were increased significantly at the same time. Furthermore, sodium nitrite exposure displayed an increase of stress fibers, lamellipodum and perinuclear mitochondrial distribution by cell staining with Actin-Tracker Green and Mito-Tracker Red, which was reversed by N-acetylcysteine (NAC, a reactive oxygen scavenger). DCFH-DA staining with fluorescent microscopy showed that the intracellular level of ROS concentration was increased by the sodium nitrite treatment. LC3 immunostaining and Western blot results showed that sodium nitrite enhanced cell autophagy flux. Under the transmission electron microscopy (TEM), more autolysosomes formed after sodium nitrite treatment and NAC could prevent autophagosome degradation. RT-PCR results indicated that the expression levels of COX I and COXIV mRNA were decreased significantly after sodium nitrite treatment. Meanwhile, laser scanning confocal microscopy showed that sodium nitrite significantly reduced mitochondrial mass detected by Mito-Tracker Green staining. The expression levels of HIF-1α, Beclin-1 and Bnip3 (mitophagy marker molecular) increased remarkably after sodium nitrite treatment, which were reversed by NAC. Our results demonstrated that sodium nitrite (16 mg x L(-1)) increased the potentials of invasion and migration of hepatic cancer SMMC-7721 cells through induction of ROS and HIF-1α mediated mitophagy.
Acetylcysteine ; pharmacology ; Autophagy ; Carcinoma, Hepatocellular ; pathology ; Cell Line, Tumor ; Cell Movement ; Humans ; Hypoxia-Inducible Factor 1, alpha Subunit ; metabolism ; Liver Neoplasms ; pathology ; Mitochondrial Degradation ; Neoplasm Invasiveness ; Nitrites ; metabolism ; Reactive Oxygen Species ; metabolism ; Sodium Nitrite ; pharmacology