potassium-iodate and potassium-bromate

This study investigates the impact of the oxidants potassium bromate and potassium iodate (8, 16, 32, 64, and 128 micromol/g dry matter of egg white protein) on pound cake making. The impact of the oxidants on egg white characteristics was studied in a model system. Differential scanning calorimetry showed that the oxidants caused egg white to denature later. During heating in a rapid visco analyzer, the oxidants caused the free sulfhydryl (SH) group levels to decrease more intensively and over a smaller temperature range. The oxidants made the proteins more resistant to decreases in protein extractability in sodium dodecyl sulfate containing buffer during cake recipe mixing and less resistant to such decreases during cake baking. We assume that, during baking, the degree to which SH/disulfide exchange and SH oxidation can occur depends on the properties of the protein at the onset of the process. In our view, the prevention of extractability loss during mixing increased the availability of SH groups and caused more such loss during baking. During cooling, all cakes baked with added oxidants showed less collapse. On the basis of the presented data, we put forward that only those protein reactions that occur during baking contribute to the formation of a network that supports final cake structure and prevents collapse.

Topics: Bread; Bromates; Calorimetry, Differential Scanning; Cooking; Disulfides; Egg Proteins; Egg White; Food Handling; Hot Temperature; Iodates; Oxidants; Oxidation-Reduction; Potassium Compounds; Protein Denaturation

Protein from flour and doughs prepared at high temperature in presence and absence of oxidants (potassium bromate, potassium iodate and L-ascorbic acid) was fractionated according to solubility into water, salt, alcohol, acetic acid, soluble protein fractions and insoluble residue protein. All fractions were freeze-dried and subjected to scanning electron microscopy to observe visually the changes in protein structure. Acetic acid-soluble and insoluble residue protein are alike in structure, but the former was thermally denatured easily, while the latter was very stable to heat treatment. Salt and alcohol, soluble protein were not deformed, but the water soluble protein was deformed by heat treatment in the absence of oxidant. Oxidants generally promoted deformation of protein structure with the exception that bromate partly protected acetic acid-soluble protein from deformation.

Topics: Ascorbic Acid; Bread; Bromates; Cooking; Edible Grain; Hot Temperature; Iodates; Microscopy, Electron, Scanning; Oxidants; Plant Proteins; Potassium Compounds; Triticum; Zea mays

Iodine could be added to the diet of human population in the form of iodide or iodate but iodate had not been adequately tested for genotoxicity and carcinogenicity. In the present study, genotoxic effects of potassium iodate were evaluated in vitro using the alkaline comet assay and the cytokinesis-block micronucleus assay on CHO cells and compared to halogenate salt analogues potassium bromate and chlorate and also to their respective reduced forms (potassium iodide, bromide and chloride). The results showed that the comet assay failed to detect the presence of DNA damage after a treatment of cells by potassium iodate for concentrations up to 10 mM. This absence of primary DNA damage was confirmed in the cytokinesis-block micronucleus assay. In the same way, results showed that potassium chlorate as well as potassium iodide, bromide and chloride did not induced DNA damage in the alkaline comet assay for doses up to 10 mM. By contrast, potassium bromate exposure led to an increase in both DNA damage and frequency of micronucleated cells. The repair of bromate-induced DNA damage was incomplete 24 h after the end of treatment. These results seem to indicate that potassium bromate would induce DNA damage by several mechanisms besides oxidative stress.

Topics: Animals; Bromates; CHO Cells; Comet Assay; Cricetinae; Cricetulus; Female; Iodates; Micronucleus Tests; Potassium Compounds

Sulfur speciation in low molecular weight (LMW) subunits of glutenin after reoxidation with potassium iodate and potassium bromate at different pH values, aged subunits of glutenin as well as gluten, and gliadin have been investigated in situ by S K-edge X-ray absorption near-edge structure (XANES) spectroscopy. XANES spectra were analyzed quantitatively using a least-squares fitting routine to provide relative percentage contribution of different sulfur species occurring in the samples. Using potassium iodate and potassium bromate for reoxidation of reduced LMW subunits of glutenin led not only to disulfide states but also to higher oxidation states (sulfoxide state, sulfonic acid state). Strongest oxidation occurred at low pH values. Higher oxidation states were also predominantly detected in the aged subunits of glutenin, whereas the disulfide state was the main sulfur species in gluten and gliadin samples. The results showed that the oxidation state of sulfur prior to oxidation (thiol, disulfide) strongly influences sulfur speciation after oxidation. The choice of the oxidizing reagent seems to be of minor importance.

Topics: Bromates; Glutens; Hydrogen-Ion Concentration; Indicators and Reagents; Iodates; Molecular Weight; Oxidation-Reduction; Potassium Compounds; Spectrum Analysis; Sulfur; X-Rays

We have investigated the role of reduced glutathione (GSH) in the genetic toxicity of the rodent renal carcinogen potassium bromate (KBrO(3)). A statistically significant increase in the concentration of 8-oxodeoxyguanosine (8-oxodG) relative to deoxyguanosine was measured following incubation of calf thymus DNA with KBrO(3) and GSH or N-acetylcysteine (NACys). This was dependent on these thiols and was associated with the loss of GSH and production of oxidized glutathione. A short-lived (<6 min) intermediate was apparent which did not react with the spin trap dimethylpyrroline N-oxide. DNA oxidation was not evident when potassium chlorate (KClO(3)) or potassium iodate (KIO(3)) were used instead of KBrO(3), though GSH depletion also occurred with KIO(3), but not with KClO(3). Other reductants and thiols in combination with KBrO(3) did not cause a significant increase in DNA oxidation. DNA strand breakage was also induced by KBrO(3) in human white blood cells (5 mM) and rat kidney epithelial cells (NRK-52E, 1.5 mM). This was associated with an apparent small depletion of thiols in NRK-52E cells at 15 min and with an elevation of 8-oxodG at a delayed time of 24 h. Depletion of intra-cellular GSH by diethylmaleate in human lymphocytes decreased the amount of strand breakage induced by KBrO(3). Extracellular GSH, however, protected against DNA strand breakage by KBrO(3), possibly due to the inability of the reactive product to enter the cell. In contrast, membrane-permeant NACys enhanced KBrO(3)-induced DNA strand breakage in these cells. DNA damage by KBrO(3) is therefore largely dependent on access to intracellular GSH.

Topics: 8-Hydroxy-2'-Deoxyguanosine; Acetylcysteine; Animals; Bromates; Carcinogens; Cattle; Cell Line; Chlorates; Chromatography, High Pressure Liquid; Comet Assay; Deoxyguanosine; DNA; DNA Damage; Electron Spin Resonance Spectroscopy; Epithelial Cells; Free Radicals; Glutathione; Glutathione Disulfide; Humans; Iodates; Kidney; Leukocytes; Potassium Compounds; Rats; Sulfhydryl Compounds; Thymus Gland; Time Factors