SEARCH · PubMed Health

Results for “SULFITES”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed2003

Final report on the safety assessment of sodium sulfite, potassium sulfite, ammonium sulfite, sodium bisulfite, ammonium bisulfite, sodium metabisulfite and potassium metabisulfite.

Sodium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Potassium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are inorganic salts that function as reducing agents in cosmetic formulations. All except Sodium Metabisulfite also function as hair-waving/straightening agents. In addition, Sodium Sulfite, Potassium Sulfite, Sodium Bisulfite, and Sodium Metabisulfite function as antioxidants. Although Ammonium Sulfite is not in current use, the others are widely used in hair care products. Sulfites that enter mammals via ingestion, inhalation, or injection are metabolized by sulfite oxidase to sulfate. In oral-dose animal toxicity studies, hyperplastic changes in the gastric mucosa were the most common findings at high doses. Ammonium Sulfite aerosol had an acute LC(50) of >400 mg/m(3) in guinea pigs. A single exposure to low concentrations of a Sodium Sulfite fine aerosol produced dose-related changes in the lung capacity parameters of guinea pigs. A 3-day exposure of rats to a Sodium Sulfite fine aerosol produced mild pulmonary edema and irritation of the tracheal epithelium. Severe epithelial changes were observed in dogs exposed for 290 days to 1 mg/m(3) of a Sodium Metabisulfite fine aerosol. These fine aerosols contained fine respirable particle sizes that are not found in cosmetic aerosols or pump sprays. None of the cosmetic product types, however, in which these ingredients are used are aerosolized. Sodium Bisulfite (tested at 38%) and Sodium Metabisulfite (undiluted) were not irritants to rabbits following occlusive exposures. Sodium Metabisulfite (tested at 50%) was irritating to guinea pigs following repeated exposure. In rats, Sodium Sulfite heptahydrate at large doses (up to 3.3 g/kg) produced fetal toxicity but not teratogenicity. Sodium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite were not teratogenic for mice, rats, hamsters, or rabbits at doses up to 160 mg/kg. Generally, Sodium Sulfite, Sodium Metabisulfite, and Potassium Metabisulfite were negative in mutagenicity studies. Sodium Bisulfite produced both positive and negative results. Clinical oral and ocular-exposure studies reported no adverse effects. Sodium Sulfite was not irritating or sensitizing in clinical tests. These ingredients, however, may produce positive reactions in dermatologic patients under patch test. In evaluating the positive genotoxicity data found with Sodium Bisulfite, the equilibrium chemistry of sulfurous acid, sulfur dioxide, bisulfite, sulfite, and metabisulfite was considered. This information, however, suggests that some bisulfite may have been present in genotoxicity tests involving the other ingredients and vice versa. On that basis, the genotoxicity data did not give a clear, consistent picture. In cosmetics, however, the bisulfite form is used at very low concentrations (0.03% to 0.7%) in most products except wave sets. In wave sets, the pH ranges from 8 to 9 where the sulfite form would predominate. Skin penetration would be low due to the highly charged nature of these particles and any sulfite that did penetrate would be converted to sulfate by the enzyme sulfate oxidase. As used in cosmetics, therefore, these ingredients would not present a genotoxicity risk. The Cosmetic Ingredient Review Expert Panel concluded that Sodium Sulfite, Potassium Sulfite, Ammonium Sulfite, Sodium Bisulfite, Ammonium Bisulfite, Sodium Metabisulfite, and Potassium Metabisulfite are safe as used in cosmetic formulations.

Animals↗

PubMed2005

Effect of sulfite on macrophage functions of normal and sulfite oxidase-deficient rats.

Sulfite has both an endogenous and an exogenous provenance in the mammalian tissues. The aim of the present study was to assess the effect of sulfite on macrophages functions in normal or sulfite oxidase deficient rats. Rats were divided into eight groups; (1) control group, (2) sulfite group (the rats received sodium meta bi-sulfite (25 mg/kg) in drinking water for 6 weeks), (3) vitamin E group (the rats received Vit E (50 mg/kg) by gavage for 6 weeks), (4) sulfite group+Vit E, (5)sulfite oxidase deficient group (the rats received high-W/Mo-deficient diet. The activity of sulfite oxidase was reduced in rats maintained on the high-W/Mo-deficient diet during the first 21 days of treatment. After the sulfite-oxidase deficiency, the rats continued to receive high-W/Mo-deficient diet for 6 weeks.), (6) sulfite+sulfite oxidase deficient group, (7) Vit E+sulfite oxidase deficient group, and (8) sulfite+Vit E+sulfite oxidase deficient group. Sulfite caused a significant increase in phagocytic and chemotactic activities of peritoneal macrophages. In sulfite-oxidase deficient rats, the increase in phagocytic and chemotactic activities in peritoneal macrophages after sulfite intake was found more than the control rats. Vit E supplementation prevented sulfite induced increase in macrophages functions. These results show that the macrophage functions are sensitive to sulfite intake. The effect of sulfite on macrophage functions may be related to reactive oxygen species. Because Vit E administration was able to modulate significantly sulfite-induced changes in the functions of peritoneal macrophages.

Animals↗

PubMed2005

Visual evoked potentials in normal and sulfite oxidase deficient rats exposed to ingested sulfite.

Sulfite oxidase (SOX) is an essential enzyme in the pathway of the oxidative degradation of sulfur amino acids, and protects cells from sulfite (SO(3)(2-)) toxicity. Rats do not mimic responses seen in human, because of their relatively high SOX activity levels. Therefore, the present study used SOX deficient rats since they are a more appropriate model for studying sulfite toxicity. The aim of the study was to investigate the effect of sulfite exposure on visual evoked potentials (VEPs) and thiobarbituric acid reactive substances (TBARS) in normal and sulfite oxidase deficient rats. Rats were assigned to six groups (n=10 rats/group) as follows; control (C), sulfite (S), sulfite+vitamin E (SE), deficient (D), deficient+sulfite (DS) and deficient+sulfite+vitamin E (DSE). Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding to their drinking water 200 ppm tungsten (W). Sulfite (25img/kg) was administered to the animals via their drinking water. At the end of the experimental period, flash visual evoked potentials were recorded, and TBARS, hepatic sulfite oxidase levels and plasma S-sulphonate concentrations were determined. Sulfite treatment caused a significant delay in P1, N1P2, and P3 components of VEPs in the S and DS groups compared with the C group. These prolonged mean latencies of VEP components were reversed by vitamin E treatment in SE and DSE groups. In addition, the mean latencies of P1 and P3 components were increased in SOX deficient groups compared with the C group. Lipid peroxidation was increased in the brain in S, D, DS and DSE groups compared with the control group. There were also significant increases in the retina TBARS levels of S and DS groups. Vitamin E caused a significant decrease in brain and retina TBARS levels of SE and DSE groups with respect to their corresponding controls. However, there were no important changes in amplitudes of other groups. In conclusion, our results showed that sulfite treatment caused an increase in the lipid peroxidation process that was accompanied by changes in VEPs. Furthermore, sulfite exposure resulted in greater lipid peroxidation and more electrophysiological alterations in the SOX deficient rats than in the control rats. Additionally, the reduction of all VEP latencies in the DSE group with respect to the DS group clearly indicated that vitamin E has the potential to prevent sulfite induced-VEP changes arising from dysfunction of the SOX enzyme.

Animals↗

PubMedDate not supplied

Effect of sulfite on cognitive function in normal and sulfite oxidase deficient rats.

Sulfites, which are commonly used as preservatives, are continuously formed in the body during metabolism of sulfur-containing amino acids. Sulfite is oxidized to sulfate ion by sulfite oxidase (SOX, EC. 1.8.3.1). The aim of this study was to investigate the possible toxic effects of sulfite on neurons by measuring active avoidance learning in normal and SOX-deficient rats. For this purpose, male albino rats used in this study were divided into eight groups such as control group (C), sulfite group (25 mg/kg) (S), vitamin E group (50 mg/kg) (E), sulfite (25 mg/kg)+vitamin E group (50 mg/kg) (SE), SOX-deficient group (D), deficient+vitamin E group (50 mg/kg) (DE), deficient+sulfite group (25 mg/kg) (DS) and deficient+sulfite (25 mg/kg)+vitamin E group (50 mg/kg) (DSE). Sulfite-induced impairment of active avoidance learning in SOX-deficient rats but not in normal rats. Sulfite had no effect on hippocampus TBARS levels in SOX normal groups. In SOX-deficient rats, TBARS levels were found to be significantly increased with sulfite exposure. Vitamin E reversed the observed detrimental effects of sulfite in the SOX-deficient rats on their hippocampal TBARS but not on their active avoidance learning. In conclusion, sulfite has neurotoxic effects in sulfite oxidase deficient rats, but this effect may not depend on oxidative stress.

Animals↗

PubMed1988

False positive and false negative reactions encountered in the use of sulfite test strips for the detection of sulfite-treated foods.

The reliability of a qualitative test for sulfites in foods (Sulfitest sulfite test strips) was evaluated by comparison of the results obtained from the analysis of 90 food and beverage samples to results obtained by the quantitative, modified Monier-Williams method (the preferred procedure for sulfite analysis in foods of the Food and Drug Administration). The results obtained with the sulfite test strips compared favorably to the results of the Monier-Williams procedure when the sulfite test strips were used on sulfite-treated lettuce and raw or cooked potatoes. However, the strips yielded many false negative and false positive results with other types of foods. False positive results (strips indicated a substantial amount of sulfite when sulfite was not detectable by the Monier-Williams method) were obtained with fin fish, red meats, and poultry. False negative results (strips indicated the absence of sulfites when sulfite was detected at levels greater than 10 ppm total sulfur dioxide by the Monier-Williams method) were obtained with dried fruits and wines under certain conditions of testing. The false negative responses with the test strips may result in the hazardous consumption of foods with high levels of sulfites, such as dried fruit or wine, by a sulfite-sensitive individual. The false positive responses would not be hazardous but could lead sensitive individuals to avoid foods that could be safely consumed. Although the strips may be useful for the detection of sulfites in certain foods, such as lettuce and potatoes, their use by sulfite-sensitive individuals cannot be recommended because of the confusion and potential hazards posed by the false negative and false positive responses.

False Negative Reactions↗

PubMed1985

Effect of sulfite on the energy metabolism of mammalian tissues in correlation to sulfite oxidase activity.

Mammalian tissues show significant differences in the activity of sulfite oxidase (EC 1.8.3.1) which detoxifies sulfite by oxidation to sulfate. Lung tissue and phagocytic cells such as alveolar macrophages, peritoneal macrophages, Kupffer cells and granulocytes show very low activities of sulfite oxidase. Liver tissue and hepatocytes, however, exhibit high activities of sulfite oxidase. Lung tissue and macrophages show an almost 100% decrease of the intracellular ATP levels when incubated with 1 mM sulfite at pH 6 for 30 min. In addition, the O2 consumption of lung tissue is inhibited by 1 mM sulfite at pH 6 by more than 80%. This sulfite-induced decrease of the ATP level and of the O2 consumption of lung tissue is enhanced between pH 6.0 and pH 7.4 with decreasing pH value of the incubation medium. In contrast, the ATP levels in liver tissue and hepatocytes are not affected by 1 mM sulfite at pH 6. The O2 consumption of liver tissue and hepatocytes is significantly increased by sulfite due to the high activities of sulfite oxidase. Therefore, the activity of the 'sulfite-detoxifying enzyme' sulfite oxidase and the sensitivity of the energy metabolism to sulfite show a reciprocal relationship in the tissues and cells studied.

Adenosine Triphosphate↗

PubMed2005

Determination of total sulfite in wine. Zone electrophoresis-isotachophoresis quantitation of sulfate on a chip after an in-sample oxidation of total sulfite.

This work deals with the determination of total sulfite in wine. The determination combines an in-sample hydrogen peroxide oxidation of total sulfite in alkalized wine to sulfate with the separation and quantitation of the latter anion by zone electrophoresis (ZE) on-line coupled with isotachophoresis (ITP) on a column-coupling chip. Sample clean up, integrated into the ITP-ZE separation, eliminated wine matrix in an extent comparable to that provided by a highly selective distillation isolation of sulfite. At the same time, conductivity detection, employed to the detection of sulfate in the ZE stage of the ITP-ZE combination, provided for sulfate the concentration limit of detection corresponding to a 90 microg/l concentration of sulfite in the loaded sample (0.9 microl). Such a detectability allowed a reproducible quantitation of total sulfite when its concentration in wine was 15 mg/l. Formaldehyde binding of free sulfite in wine, included into the pre-column sample preparation, prevented an uncontrolled oxidation of this sulfite form. This step contributed to an unbiased determination of sulfate present in the original wine sample (this determination corrected for the concentration of sulfate determined in the sample after the peroxide oxidation of sulfite to the value equivalent to the total sulfite). The 99-101% recoveries of sulfite, determined for appropriately spiked wine samples, indicate a very good accuracy of the present method. Such a statement also supports excellent agreements of the results of quantitation based on the in-sample peroxide oxidation of the total sulfite (bound sulfite released at a high pH) with those in which this analyte was isolated from wine by distillation (bound sulfite released at a very low pH).

Electrophoresis, Microchip↗

PubMed2006

Expressions of N-methyl-D-aspartate receptors NR2A and NR2B subunit proteins in normal and sulfite-oxidase deficient rat's hippocampus: effect of exogenous sulfite ingestion.

Sulfites whether ingested or produced through the sulfur-containing amino acids metabolism of the animal are very active molecules and can cause cellular toxicity. Sulfite oxidase (SOX), a heme- and molybdenum containing mitochondrial enzyme, prevents mammalian cells from adverse effects of sulfite toxicity by metabolizing sulfite to sulfate. The present study was aimed to investigate effect of sulfite on the N-methyl-D-aspartate (NMDA) receptor (NMDAR) NR2A and NR2B subunits in hippocampus of normal and SOX-deficient rats. Rats were divided into four groups; (1) control group, which was given rat chow and tap water ad libitum (C), (2) sulfite group, treated with sulfite (25 mg/kg) in drinking water and commercial rat chow ad libitum (S), (3) SOX-deficient group, maintained on high-W/Mo-deficient regimen to produce SOX deficiency (D), and (4) SOX-deficient + sulfite group (DS), prepared as those in the third group and were afterwards given sulfite (25 mg/kg) additionally. Whole treatment schedule were continued for 6 weeks. Sulfite treatment caused a decrease of NR2A and NR2B subunits of the NMDAR in hippocampus of rats in S and DS groups. Interestingly, similar decrement was observed in D group, probably due to increased endogenous sulfite production. In summary, the results indicated that feeding sulfite to the rats may cause down-regulation of NMDARs by degrading NR2A and NR2B subunits of it, which may be considered as a neuro-compensatory mechanism.

Animals↗

PubMed1989

Characterization of anaerobic sulfite reduction by Salmonella typhimurium and purification of the anaerobically induced sulfite reductase.

Mutants of Salmonella typhimurium that lack the biosynthetic sulfite reductase (cysI and cysJ mutants) retain the ability to reduce sulfite for growth under anaerobic conditions (E. L. Barrett and G. W. Chang, J. Gen. Microbiol., 115:513-516, 1979). Here we report studies of sulfite reduction by a cysI mutant of S. typhimurium and purification of the associated anaerobic sulfite reductase. Sulfite reduction for anaerobic growth did not require a reducing atmosphere but was prevented by an argon atmosphere contaminated with air (less than 0.33%). It was also prevented by the presence of 0.1 mM nitrate, which argues against a strictly biosynthetic role for anaerobic sulfite reduction. Anaerobic growth in liquid minimal medium, but not on agar, was found to require additions of trace amounts (10(-7)M) of cysteine. Spontaneous mutants that grew under the argon contaminated with air also lost the requirement for 10(-7)M cysteine for anaerobic growth in liquid. A role for sulfite reduction in anaerobic energy generation was contraindicated by the findings that sulfite reduction did not improve cell yields, and anaerobic sulfite reductase activity was greatest during the stationary phase of growth. Sulfite reductase was purified from the cytoplasmic fraction of the anaerobically grown cysI mutant and was purified 190-fold. The most effective donor in crude extracts was NADH. NADPH and methyl viologen were, respectively, 40 and 30% as effective as NADH. Oxygen reversibly inhibited the enzyme. Two high-molecular-weight proteins separated by gel filtration (Mr 360,000 and 490,000, respectively) were required for maximal activity with NADH. Indirect evidence, including in vitro complementation experiments with a cysG mutant extract, suggested that the 360,000-Mr component contains siroheme and is the terminal reductase. This component was further purified to near homogeneity and was found to consist of a single subunit of molecular weight 67,500. The anaerobic sulfite reductase showed some resemblance to the biosynthetic sulfite reductase, but apparently it has a unique, as yet unidentified function.

Anaerobiosis↗

PubMed1988

Sensitivity to sulfited foods among sulfite-sensitive subjects with asthma.

Eight individuals with asthma who had been diagnosed as sulfite sensitive on the basis of double-blind capsule-beverage challenges were subjected to challenges with various sulfited foods, including lettuce, shrimp, dried apricots, white grape juice, dehydrated potatoes (as mashed potatoes), and mushrooms. Four of these patients failed to respond to challenges with any of the sulfited foods. The other four patients experienced a decrease in pulmonary function on double-blind challenges with sulfited lettuce. Two of three of these patients reacted to challenges with dried apricots and white grape juice; the fourth patient has not yet been challenged with these products. Only one of these four patients reacted to challenges with dehydrated potatoes and mushrooms, and, in this case, the response to double-blind challenges with dehydrated potatoes was not consistent. None of the sulfite-sensitive subjects with asthma responded to challenges with sulfited shrimp. It is concluded that sulfite-sensitive subjects with asthma will not necessarily react after ingestion of sulfited foods. The likelihood of a reaction is dependent on the nature of the food, the level of residual sulfite, the sensitivity of the patient, and perhaps on the form of residual sulfite and the mechanism of the sulfite-induced reaction.

Adult↗

PubMed1987

Distribution, metabolism and toxicity of inhaled sulfur dioxide and endogenously generated sulfite in the respiratory tract of normal and sulfite oxidase-deficient rats.

We report on the distribution, metabolism, and toxicity of sulfite in the respiratory tract and other tissues of rats exposed to endogenously generated sulfite or to inhaled sulfur dioxide (SO2). Graded sulfite oxidase deficiency was induced in several groups of rats by manipulating their tungsten to molybdenum intake ratio. Endogenously generated sulfite and S-sulfonate compounds (a class of sulfite metabolite) accumulated in the respiratory tract tissues and in the plasma of these rats in inverse proportion to hepatic sulfite oxidase activity. In contrast to this systemic mode of exposure, sulfite exposure of normal, sulfite oxidase-competent rats via inhaled SO2 (10 and 30 ppm) was restricted to the airways. Minor pathological changes consisting of epithelial hyperplasia, mucoid degeneration, and desquamation of epithelium were observed only in the tracheas and bronchi of the rats inhaling SO2, even though the concentration of sulfite plus S-sulfonates in the tracheas and bronchi of these rats was considerably lower than that in the endogenously exposed rats. We attribute this histological damage to hydrogen ions stemming from inhaled SO2, not to the sulfite/bisulfite ions that are also a product of inhaled SO2. In addition to the lungs and trachea, all other tissues examined, except the testes, appeared to be refractory to high concentrations of endogenously generated sulfite. The testes of grossly sulfite oxidase-deficient rats were severely atrophied and devoid of spermatogenic cells.

Administration, Inhalation↗

PubMed2005

Effect of sulfite on red blood cell deformability ex vivo and in normal and sulfite oxidase-deficient rats in vivo.

The effect of sulfite, a widely used food additive, on red blood cell deformability ex vivo and in vivo was investigated. Ex vivo experiments were conducted in human blood exposed to sulfite (5, 10 and 20 mM). In vivo experiments were carried out in sulfite oxidase-competent (SOXC) and sulfite oxidase-deficient (SOXD) rats. In the in vivo experiments, sulfite was administered in the form of sodium metabisulfite (Na(2)S(2)O(5), 25 mg/kg/day) via drinking water. Vitamin E dissolved in olive oil at a dose of 50 mg/kg was administered by gastric gavages. Red blood cell (RBC) deformability was determined at various fluid shear stresses using an ektacytometer. Ex vivo sulfite exposure to RBC did not affect RBC deformability. In the in vivo experiments, although RBC deformability was not affected by sulfite treatment in SOXD rats, it was found to be significantly increased in SOXC rats. Vitamin E treatment in combination with sulfite caused impairment in RBC deformability in both SOXC and SOXD rats. We suggest that sulfite needs to be oxidized in order to improve RBC deformability.

Animals↗

PubMed1975

Biochemical studies on sulfate-reducing bacteria. XIV. Enzyme levels of adenylylsulfate reductase, inorganic pyrophosphatase, sulfite reductase, hydrogenase, and adenosine triphosphatase in cells grown on sulfate, sulfite, and thiosulfate.

Sulfate-reducing bacteria, Desulfovibrio vulgaris, strain Miyazaki, were grown on either sulfate, sulfite, or thiosulfate as the terminal electron acceptor. Better growth was observed on sulfite and less growth on thiosulfate than on sulfate. Enzyme levels of adenylylsulfate (APS) reductase [EC 1.8.99.2], reductant-activated inorganic pyrophosphatase [EC 3.6.1.1], sulfite reductase [EC 1.8.99.1] (desulfoviridin), hydrogenase [EC 1.12.2.1], and Mg2+-activated ATPase [EC 3.6.1.3] were compared in crude extracts of these cells at various stages of growth. 1) The specific activity of APS reductase in sulfite-grown cells was only one-fourth that in sulfate-grown cells throughout growth. Thiosulfate-grown cells had an activity intermediate between those of sulfate- and sulfite-grown cells. 2) Cells grown on sulfite had lower specific activity of reductant-activated inorganic pyrophosphatase than cells grown on sulfate or thiosulfate. 3) The specific activity of sulfite reductase (desulfoviridin) was highest in sulfite-grown cells. The sulfite medium gave the enzyme in high yield as well as with high specific activity. 4) The specific activities of hydrogenase and Mg2+-ATPase were not significantly altered by electron acceptors in the growth medium.

Adenosine Monophosphate↗

PubMed2006

I've recently developed an allergy to sulfites. I'm wondering if fruits and vegetables are coated with sulfites and, if so, will washing or peeling them get rid of the sulfites?

Explore the source record for details and available documents.

Fruit↗

PubMed2005

Stabilization of sulfide and sulfite and ion-pair chromatography of mixtures of sulfide, sulfite, sulfate and thiosulfate.

Ion chromatography of sulfide, sulfite, sulfate and thiosulfate in a mixture is often difficult because of instability of sulfide and sulfite, poor separation of sulfide from common anions such as bromide or nitrate and similar elution-times for sulfite and sulfate. An ion-pair chromatographic method for the determination of these sulfur anions has been established by stoichiometric conversion of sulfide and sulfite into stable thiocyanate and sulfate, respectively, prior to the chromatographic run. Sulfate, thiosulfate and thiocyanate were resolved on an octadecylsilica column with an acetonitrile-water mobile phase containing tetrapropylammonium salt (TPA) as an ion-paring reagent, and thiosulfate and thiocyanate in the effluent could be measured with a photometric detector (220 nm) and sulfate with a suppressed conductivity detector. When an acetonitrile-water (6:94, v/v) mobile phase (pH 5.0) containing 15 mM TPA and small amounts of acetic acid was used at a flow-rate of 0.6 ml min(-1), the three anions could be eluted within 32 min. Calibration plots of peak height versus concentration for sulfide (detected as thiocyanate) and thiosulfate gave straight lines up to 35 and 60 microM, respectively. The calibration plot for sulfide coincided with that obtained by using thiocyanate. A calibration plot for sulfite, measured as sulfate, was also linear up to 135 microM and was in accord with that of sulfate. Each calibration plot gave a correlation coefficient greater than 0.999. For six replicates obtained for a mixture of 30.0 microM sulfide, 50.0 microM sulfite, 50.0 microM sulfate and 20.0 microM thiosulfate, the proposed method gave a mean value of 30.1 microM with a standard deviation (SD) of 0.77 microM and a relative standard deviation (RSD) of 2.6% for sulfide, 101 microM (SD = 3.5 microM, RSD = 3.5%) for the total of sulfite and sulfate and 20.1 microM (SD = 0.44 microM, RSD = 2.2%) for thiosulfate. Recoveries for sulfide, sulfite plus sulfate, and thiosulfate in hot-spring water samples using the proposed method were found to be quantitative.

Anions↗

PubMed1994

Enhanced generation of hydroxyl radical and sulfur trioxide anion radical from oxidation of sodium sulfite, nickel(II) sulfite, and nickel subsulfide in the presence of nickel(II) complexes.

Electron spin resonance (ESR) spin trapping was utilized to investigate the generation of free radicals from oxidation of sodium sulfite, nickel(II) sulfite, and nickel subsulfide (Ni3S2) by ambient oxygen or H2O2 at pH 7.4. The spin trap used was 5,5-dimethyl-1-pyrroline-N-oxide (DMPO). Under ambient oxygen, a solution of sodium sulfite alone generated predominantly sulfur trioxide anion radical (.SO3-) due to the autoxidation of sulfite. Addition of nickel(II) chloride [Ni(II)] enhanced the .SO3- yield about 4-fold. Incubation of sulfite with Ni(II) in the presence of chelators such as tetraglycine, histidine, beta-alanyl-3-methyl-L-histidine (anserine), beta--L-histidine (carnosine), gamma-aminobutyryl-L-histidine (homocarnosine), glutathione, and penicillamine did not have any significant effect on that enhancement. In contrast, albumin, and especially glycylglycylhistidine (GlyGlyHis), augmented the enhancing effect of Ni(II) by factors of 1.4 and 4, respectively. Computer simulation analysis of the spin-adduct spectrum and formate scavenging experiment showed that the mixture of sodium sulfite, Ni(II), and GlyGlyHis generated both hydroxyl (.OH) radical and .SO3- radical, in the ratio of approximately 1:2. The free-radical spin adduct intensity reached its saturation level in about 5 min. The yield of the radical adducts could be slightly reduced by deferoxamine and very strongly reduced by diethylenetriaminepentaacetic acid (DTPA). Aqueous suspensions of sparingly soluble nickel(II) sulfite in the presence of air and GlyGlyHis generated surface-located .SO3- and .OH radicals. The same radicals were generated in Ni3S2 suspension in the presence of GlyGlyHis and H2O2, indicating sulfite production by oxidation of the sulfide moiety of this compound.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed2002

[Colorimetric determination of sulfite in "kanpyo" (dried gourd shavings) and "konnyakuseiko" (devil's-tongue fine powder) using sulfite oxidase and catalase].

A simple and convenient method for colorimetric determination of sulfite in foods based on its conversion to formaldehyde with sulfite oxidase and catalase was developed. Sulfite in a sample was extracted with water and then diluted with methanol. One mL of sample solution containing about 5-10 micrograms of sulfite was taken into a test tube with a ground-glass stopper, and 3 mL of 0.04 mol/L borate buffer (pH 8.7), 1 mL of 0.4% 3-methyl-2-benzothiazolinone hydrazone (MBTH) solution, 2,000 units of catalase solution and 1.0 units of sulfite oxidase were added. The mixture was incubated for 35 minutes at 37 degrees C. Then 0.15 mL of 1 mol/L hydrochloric acid and 5 mL of 0.2% iron(III) nitrate solution were added. The reaction mixture was transferred to a measuring flask after standing for 5 minutes at room temperature, and diluted to 20 mL with methanol. The absorbance of this solution was measured using a spectrophotometer at the wavelength of 635 nm. The calibration curve prepared with sodium sulfite showed linearity between 0 to 16 micrograms/mL as sulfur dioxide. The recoveries of sulfite in "Kanpyo" (dried gourd shavings) and "Konnyaku-seiko" (devil's-tongue fine powder) by the proposed method were 97-104%, and the coefficients of variation were below 6%. The sulfite values in these foods determined by the proposed method were reasonably consistent with those obtained by the bubbling distillation-alkaline titration method.

Aprotinin↗

PubMed1993

Sulfite sensitivity and sulfite oxidase activity in Drosophila melanogaster.

The relationship between sulfite oxidase (SO) and sulfite sensitivity in Drosophila melanogaster is addressed. Significant improvements to the SO assay have provided an investigative tool which can be applied to further studies of this molybdoenzyme. Using the second-instar larval stage of D, melanogaster, we have shown a direct relationship between measured levels of sulfite oxidase activity and the organism's ability to withstand a sulfite challenge. Implementation of a sulfite-testing procedure confirmed the documented instability of sulfite in solution and may explain some of the conflicting results reported in the SO literature. Results of the tungstate-addition experiments confirm that Drosophila SO is a molybdoenzyme and its activity was shown to be governed by three of the four loci known to affect more than one molybdoenzyme. The ability of D. melanogaster to withstand the application of exogenous sulfites is shown to be dependent on sulfite oxidase activity.

Animals↗