Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Iodates”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

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

At least 91 records · Page 5Linked to original sources

Simultaneous determination of iodate and periodate by capillary zone electrophoresis: application to carbohydrate analysis.

Iodate and periodate were rapidly (in 11 min) separated from each other with high column efficiency by capillary zone electrophoresis, using a fused silica tube (50 microns i.d., 80 cm) and 100 mM acetate buffer, pH 4.5, as carrier. On-column uv detection at 222 nm allowed sensitive detection down to the picomole level, and measurement of relative peak area to that of pyromellitic acid (internal standard) enabled reproducible determination of these ions. This method was proved useful for periodate oxidation analysis of various carbohydrates.

Carbohydrates↗

Oxidative stress of human erythrocytes by iodate and periodate. Reversible formation of aqueous membrane pores due to SH-group oxidation.

Human erythrocytes were exposed to oxidative stress by iodate and periodate. Oxidation causes a time- and concentration-dependent increase in membrane permeability for hydrophilic molecules and ions. The induced leak discriminates nonelectrolytes on the basis of molecular size and exhibits a very low activation energy (Ea = 1-4 kcal.mol-1). These results are reconcilable with the formation of aqueous pores. The pore size was approximated to be between 0.45 and 0.6 nm. This increase in permeability is reversible upon treatment with dithioerythritol. Blocking of membrane thiol groups with N-ethylmaleimide protects the membranes against leak formation. The oxidation causes dithioerythritol-reversible modification of membrane proteins as indicated by the gel electrophoretic behavior. These modifications can also be suppressed by blocking the membrane thiol groups with N-ethylmaleimide. About half of the membrane methionine is oxidized to acid hydrolysis-stable derivatives. A fast saturating increase in diene conjugation was observed in whole cells but not in isolated membranes, with only minor degradation of fatty acid chains. The oxidation of cell membrane lipids as well as oxidation of cell surface carbohydrates are not involved in leak formation. Taken together with earlier data (Deuticke, B., Poser, B., Lütkemeier, P. and Haest, C.W.M. (1983) Biochim. Biophys. Acta 731, 196-210), these findings indicate that formation of disulfide bonds by different oxidative mechanisms results in leaks with similar properties.

Carbohydrates↗

Interaction of vanadate and iodate oxyanions with adenylyl cyclase of ciliary processes.

Vanadate (VO3-) was found to activate adenylyl cyclase (AC) in ocular ciliary process membrane. This response was additive to that of isoproterenol (ISO) and vasoactive intestinal peptide (VIP), but it was potentiative with forskolin (FSK) and also with Ca2+/calmodulin activation of AC activity. The potentiated response of FSK in the presence of VO3- was due to an increase in Vmax without a change in the apparent affinity of FSK or VO3-, and therefore differs from the potentiated response of activated G-protein (Gs) and FSK, where the affinity of FSK was increased by 1-2 orders of magnitude. Potentiation occurred at low Mg2+ and was not observed at free [Mg2+] > 3 mM. Iodate (IO3-) inhibited the FSK, ISO, and VO3- activations of AC in ciliary process membranes (IC50, 0.3 mM). In vivo topical treatment of the rabbit eye with 50 microL of 5% NaIO3 had no effect alone but completely blocked the intraocular pressure response to a 50-microL topical dose of 1% FSK and partially blocked the response to a 50-microL dose of 0.001% ISO. These findings indicate that some AC enzymes may have a binding site for oxyanions which can directly regulate enzyme activity.

Adenylyl Cyclase Inhibitors↗

Ion chromatographic determination of trace iodate, chlorite, chlorate, bromide, bromate and nitrite in drinking water using suppressed conductivity detection and visible detection.

An ion chromatography method for the simultaneous determination of trace iodate, chlorite, chlorate, bromide, bromate and nitrite in drinking water has been developed using an anion-exchange column and the suppressed conductivity detector, followed by post-column addition of reagent to enhance visible absorbance detection of ions. A high capacity anion exchange Ion Pac9-HC column (250 mm x 4 mm I.D.) was used. Eight millimole per liter sodium carbonate was used as eluent, an auto-suppression external water mode was selected, 0.5 g/l o-dianisidine.2HCl (ODA)+4.5 g/l KBr+25% methanel+5.6% nitric acid was used as post-column reagent. The post-column reaction (PCR) temperature was at 60 degrees C, and the visible absorbance detected wavelength at 450 nm. The sample's pH and coexist anions had no influence on determination. The method enjoyed a wide linear range and a good linear correlation coefficient (r>0.999). The method detection limits were between 0.023 and 2.0 microg/l. The average recoveries ranged from 87.5 to 110.0%, and the relative standard deviations (RSD) were in the range of 1.1-4.6%. The analytical results by the method of post-column addition of reagent to enhance visible absorbance detection of anions was compared with that of the suppressed conductivity detection, and the former was proved to be better in sensitivity and selectivity. The results showed that this method was accurate, sensitive and might be good for application and suitable for trace analysis at the level of mug/l.

Anions↗

Behavioral and anatomical abnormalities in a sodium iodate-induced model of retinal pigment epithelium degeneration.

We characterized changes in the visual behavior of mice in which a loss of the retinal pigment epithelium (RPE) was experimentally induced with intravenous (i.v.) administration of sodium iodate (NaIO3). We compared and correlated these changes with alterations in neural retinal structure and function. RPE loss was induced in 4-6 week old male C57BL/6 mice with an i.v. injection of 1% NaIO3 at three concentrations: 35, 50, or 70 mg/kg. At 1, 3, 7, 14, 21, and 28 days (d) as well as 6 months post injection (PI) a behavioral test was performed in previously trained mice to evaluate visual function. Eye morphology was then assessed for changes in both the RPE and neural retina. NaIO3-induced RPE degeneration was both dose and PI time dependent. Our low dose showed no effects, while our high dose caused the most damage, as did longer PI times at our intermediate dose. Using the intermediate dose, no changes were detectable in either visual behavior or retinal morphology at 1 d PI. However, at 3 d PI visual behavior became abnormal and patchy RPE cell loss was observed. From 7 d PI onward, changes in retinal morphology and visual behavior became more severe. At 6 months PI, no recovery was seen in any of these measures in mice administered the intermediate dose. These results show that NaIO3 dosage and/or time PI can be varied to produce different, yet permanent deficits in retinal morphology and visual function. Thus, this approach should provide a unique system in which the onset and severity of RPE damage, and its consequences can be manipulated. As such, it should be useful in the assessment of rescue or mitigating effects of retinal or stem cell transplantation on visual function.

Animals↗

Simultaneous spectrophotometric and volumetric determinations of amoxycillin, ampicillin and cloxacillin in drug formulations: reaction mechanism in the base catalysed hydrolysis followed by oxidation with iodate in dilute acid solution.

A method for the analysis of degraded products of amoxycillin, ampicillin and cloxacillin in drug formulations, obtained as a result of their base hydrolysis is described. Simultaneous spectrophotometric and volumetric determinations of the antibiotic is based on the neutralization of the degraded product by dilute hydrochloric acid to get a pH approximately 2 to be conducive for redox titration using potassium iodate as titrant. A red purple colour is developed in carbon tetrachloride at the end point. Spectrophotometry is done after separating the organic layer and measuring the absorbance of red-purple colour at lambda(max) 520 nm. The pathways of different degraded products and their oxidation mechanism is described on IR, TLC and UV spectroscopic studies.

Acids↗

Retinal degeneration is delayed by tissue factor pathway inhibitor-2 in RCS rats and a sodium-iodate-induced model in rabbits.

PURPOSE: To investigate the in vivo effects of tissue factor pathway inhibitor 2 (TFPI-2), which stimulates proliferation of retinal pigment epithelial cells, but not the proliferation of fibroblast and vascular endothelial cells in vitro, on retinal degeneration using a sodium-iodate (SI)-induced model in rabbits and Royal Collage of Surgeons (RCS) rats. METHODS: 79 microg of recombinant TFPI-2 (rTFPI-2) or vehicle alone was injected intravitreously to 18 eyes of 12 pigmented rabbits a day after 20 mg/kg of SI was intravenously administered. Retinal function was assessed 4, 7, 14, and 21 days after the injection by analysing amplitudes of the c-wave of a bright flash electroretinogram. Additionally, 10 microg of rTFPI-2 or vehicle alone was injected intravitreously to 11 eyes of RCS rats at both 3 and 4 weeks old, then the retina was examined histologically at 5 weeks old. RESULTS: The rTFPI-2-treated eyes in rabbits showed a significantly less decrease in the relative amplitude of the c-wave than control eyes on days 4 and 7. The thickness of the outer nuclear layer was significantly thicker and the vacuole in the photoreceptor layer was less frequently observed in the rTFPI-2-treated RCS rats than the controls. CONCLUSIONS: Intravitreal injection of TFPI-2 rescues SI-induced retinal degeneration in rabbits and naturally occurring retinal degeneration in RCS rats at least partly. These results may suggest that this compound can be utilized in the treatment of retinal degeneration.

Animals↗

Morphologic characteristics of retinal degeneration induced by sodium iodate in mice.

PURPOSE: Retinal degeneration induced by sodium iodate (NaIO( 3)) in mice was evaluated morphologically. METHODS: Male and female ICR and C57BL mice were intraperitoneally administered 100 mg/kg NaIO(3) at 7 weeks of age, and were killed 6, 12, 24 hrs, and 3, 7 and 28 days after the treatment. Retinas were examined histologically, ultrastructurally, immunohistochemically, and by the TUNEL method. RESULTS: Retinal degeneration was evoked in all NaIO(3)-treated mice. The primary site of damage appeared in the retinal pigment epithelial (RPE) cells followed by photoreceptor cell degeneration. Initially, the RPE cells showed necrosis starting 6 hrs post-NaIO(3), followed by photoreceptor outer segment disruption and photoreceptor cell apoptosis at 24 hrs; photoreceptor cell apoptosis peaked at day 3 and was completed by day 7. At day 3, Müller cell proliferation, macrophage migration within the retina, and regeneration of damaged RPE cells occurred. Finally at day 7 and day 28, the retina showed a mosaic pattern of relatively normal retina and areas lacking RPE cells and photoreceptor cells. CONCLUSIONS: RPE cell necrosis followed by photoreceptor cell apoptosis and the resulting mosaic pattern of the retina phenotypically resembles gyrate atrophy of the choroid and retina.

Animals↗

Third-order neuronal responses contribute to shaping the negative electroretinogram in sodium iodate-treated rats.

PURPOSE: To determine possible mechanisms that shape the negative electroretinograms (ERGs) in rats with photoreceptor degeneration induced by destruction of the retinal pigment epithelium. METHODS: Sprague-Dawley rats (n = 48) were injected intravenously with 60 mg/kg of sodium iodate (NaIO(3)). Full-field ERGs were elicited by different stimulus intensities with a maximum luminance of 1.23 log cd-s/m(2) and recorded at 6 hr and on days 7, 14, and 28 after the NaIO(3) injections. DL-2-amino-4-phosphonobutyric acid (APB, 1 mM) or N-methyl-L-aspartic acid (NMDA, 5 mM) was injected into the vitreous cavity to isolate photoreceptor (PIII), second-order, and third-order neuronal responses. After recording the ERGs, animals were sacrificed for histological analysis. RESULTS: Negative ERGs were recorded under scotopic conditions on day 7 after the NaIO(3) injection. An intravitreal injection of NMDA eliminated most of the a-wave, resulting in the abolition of the negative ERG. On days 14 and 28, the a-wave amplitudes were reduced compared to those on day 7 with the loss of the negative ERGs. The mean amplitudes of the PIII and second-order neuronal responses were progressively reduced until day 7. In contrast, the mean amplitude of the third-order neuronal responses were relatively well-preserved until day 7 and then were decreased between days 7 and 14. As a result, the amplitude of the third-order neuronal response dominated over the second-order neuronal response on day 7. There was no significant difference in the middle and inner retinal morphology at each time point. CONCLUSIONS: NaIO(3) produced negative ERGs transiently, and the third-order neuronal responses were the main contributors to the negative ERG. The relative preservation of the third-order neuronal response plays a role in shaping the negative ERGs in this model.

Animals↗

Protective effect of hepatocyte growth factor against degeneration of the retinal pigment epithelium and photoreceptor in sodium iodate-injected rats.

PURPOSE: To investigate the possible protective effect of hepatocyte growth factor (HGF) against degeneration of photoreceptors and retinal pigment epithelium (RPE) in vivo. METHODS: Sprague-Dawley (SD) rats received an intravitreal injection of HGF in the right eye. The left eye was injected with vehicle as a control. Two days after the intravitreal injections, rats were administered 40 mg/kg of sodium iodate (NaIO3) intravenously. Scotopic ERGs were elicited by different stimulus intensities with a maximum luminance of 0.84 log cds/m2. To evaluate RPE function, the azide response was evoked by intravenous injection of 0.1 mg sodium azide. These electrophysiological measurements were conducted on days 4, 7, 14, and 28 after the NaIO3 injections. After recording ERGs or azide response, animals were sacrificed for quantification of the histological change and immunohistochemical analysis using antibodies against RPE 65. RESULTS: The threshold for the scotopic b-wave was significantly lower in HGF-treated eyes than in untreated control eyes (p < 0.005), and maximum b-wave amplitudes (Vbmax) were significantly larger in HGF-treated eyes (p < 0.05) across all experimental time points after NaIO3 injection. Azide response amplitudes were significantly larger in the HGF-treated eyes than in the untreated eyes (p < 0.05). The structure of the outer retina was preserved to a greater degree in the HGF-treated eyes than in the untreated eyes (p < 0.05). Immunohistochemical analysis demonstrated that irregular alignment of the outer nuclear layer was confined to the retinal area that was not stained with RPE 65. CONCLUSIONS: Our results indicated that an intravitreal injection of HGF provided significant protection against degeneration of the photoreceptor and RPE induced by systemic administration of NaIO3. This suggests that HGF could be used as a therapeutic agent for degeneration of photoreceptors as well as RPE.

Animals↗

Potassium iodate and its comparison to potassium iodide as a blocker of 131I uptake by the thyroid in rats.

Potassium iodide is the preferred thyroid blocker for personnel handling radioiodine and is recommended as a prophylaxis for the population in the near-field of a nuclear reactor which would be likely to be exposed to radioiodine in an accidental breach of containment. However, in hot and humid climates, this hygroscopic chemical has a poor shelf life due to hydrolytic loss of iodine vapors. On the other hand, another iodine-rich salt, potassium iodate (KIO3), is quite stable and has a much longer shelf life. The present study compares potassium iodide and KIO3 as thyroid blockers and examines the appropriate time at which they should be administered in case of radioiodine exposure. Either of the two were given in recommended dosage (100 mg stable iodine per 70 kg body weight) at -2, 0, +2, +4, +6, and +8 h after administration of tracer quantities of radioiodine (131I) to age-, weight-, and sex-matched rats. 131I uptake in thyroid was measured 24 h after its administration in the experimental animals and compared with placebo administered controls. Results suggest that KIO3 is as effective a thyroid blocking agent as potassium iodide. In comparison to controls, 24-h thyroid uptake of 131I can be substantially reduced if potassium iodide or KIO3 is given to the animals within 2-4 h after exposure to 131I. Another noteworthy observation is that KIO3 is effective even at 8 h when administered at twice the usual dosage in comparison to the single dose, which does not show appreciable thyroid blocking properties after 8 h.

Animals↗

Calcium iodate-another effective blocker of radioiodine uptake by the thyroid gland.

KI and KIO3 are the commonly used prophylactic drugs for the protection of thyroid glands against radioiodine. In this study, we have demonstrated the use of another iodine containing salt, calcium iodate [Ca(IO3)2], as an effective blocker of radioiodine uptake by the thyroid gland in rats. Ca(IO3)2 is permitted by the FDA as a food additive and is "generally regarded as safe" (GRAS, CFR No.1206). We have also compared the efficacy of Ca(IO3)2 with KIO3 in blocking thyroidal uptake of radioiodine, which could be important considering the better shelf life of Ca(IO3)2. Laboratory rats were administered 131I and stable iodide in the form of KIO3 or Ca(IO3)2 was given orally, 2 h after the administration of 131I. All the animals were monitored for whole body retention (WBR) of 131I, at 24 h and further for 14 d. The results of the present study provide us with evidence that Ca(IO3)2 can serve as another promising radioiodine blocker, and is as equipotent as KI/KIO3 in protecting the thyroid gland. We have not found any studies that examined the property of Ca(IO3)2 in blocking radioiodine uptake by the thyroid gland and the present study is an attempt in this direction.

Administration, Oral↗

Changes in ultrastructure and function of the sheep pigment epithelium and retina induced by sodium iodate. I. The ultrastructure of the normal pigment epithelium of the sheep.

The normal ultrastructure of the sheep pigment epithelial cells is described as a basis for the interpretation of toxic (sodium iodate) effects on these cells dealt with in two following papers. The morphological features of the different cell membranes and cell organelles, particularly the phagosomes and the lipid droplets, are discussed in relation to renewal of the photoreceptor outer segment, pigment epithelial and retinal metabolism, barrier mechanisms and electrical properties.

Animals↗

Early effects of sodium iodate on the directly recorded standing potential of the eye and on the c-wave of the DC registered electroretinogram in albino rabbits.

The early effects of intravenously administered sodium iodate (NaIO3) on the directly recorded standing potential (SP) of the eye and on the c- and b-waves of the DC registered ERG were studied in 8 anaesthetized albino rabbits. In 5 of 6 animals obtaining 40 mg NaIO3/kg bwt. the SP decreased immediately following the injection, and had attained a level 3.5 - 4 mV below the original one after 1 h. The c-wave declined rapidly and 6 min after the injection it was replaced by a large cornea-negative potential. The b-wave was relatively unchanged except in one animal. In 2 rabbits treated with 30 mg NaIO3/kg btw. and in the 6th animal obtaining 40 mg NaIO3/kg bwt. an SP increase instead of a decrease was seen, and the c-wave was more slowly (about 22 min after the injection) replaced by the cornea-negative potential. The b-wave was somewhat increases. These results demonstrate the dose-related and inter-individual variability in the SP reaction to NaIO3 and are in good agreement with the well-known ultrastructural pigment epithelial injury and c-wave changes produced by this substance.

Animals↗

Early effects of sodium iodate on the slow off-effects, particularly the h-wave, and on the c-wave of the DC recorded electroretinogram in rabbit.

The early effects of intravenously administered sodium iodate (NaIO3) on the slow, negative 'off-effect', the h-wave, and on the slow, positive 'on-effect', the c-wave, of the DC recorded electroretinogram were studied in 8 rabbits. Both the h- and c-waves disappeared gradually after NaIO3 administration and were replaced by potentials of opposite polarity. These results strongly support the assumption that the h-wave originates in the pigment epithelium and represents the reversal of events underlying the c-wave. The slow, positive 'off-effect', the g-wave, elicited by 'dark flashes' was seen to pass into the potential replacing the h-wave after NaIO3 treatment.

Animals↗

Paradoxical enhancement of the ERG c-wave by a small dose of sodium iodate.

The early effects of sodium iodate (NaIO3) on the ERG c- and b-waves were studied in rabbits. When 30 mg NaIO3/kg body weight was administered intravenously, the c-wave amplitude decreased and was replaced by a potential of opposite polarity. However, the administration of 20 mg/kg of NaIO3 enhanced the c-wave remarkably. Twenty min after administration, the mean c-wave amplitude significantly increased (P less than 0.001) to 211 +/- 6.2% of the pre-administration amplitude, whereas that of the control was 108 +/- 13.0%. The b-wave amplitude showed no significant changes. When 10 mg/kg of NaIO3 was administered, the enhancement of the c-wave was not remarkable. These effects were similar in both pigmented and albino rabbits. A lower blood concentration of NaIO3 applied to the basal side of the retinal pigment epithelium (RPE) may initially affect only the basal membrane of the RPE resulting in the decrease in the basal membrane resistance (Rba). This would explain the transient increase in the c-wave amplitude with 20 mg NaIO3/kg.

Animals↗

Effects of sodium iodate on experimental subretinal neovascularization in the primate.

We investigated the role of the retinal pigment epithelium (RPE) in the development of subretinal neovascularization (SRN) induced by bilateral laser photocoagulation of the retinas in monkeys. RPE function was affected by a unilateral carotid injection of sodium iodate, a selective RPE toxin, before laser photocoagulation. This caused severe RPE damage in the ipsilateral eye, but did not affect the contralateral eye. After laser photocoagulation no SRN was demonstrable clinically or histopathologically in the ipsilateral eye; in contrast, active SRN showing extensive fluorescein leakage was found in the contralateral eye. These results suggest that RPE may play a role in the development of laser-induced SRN.

Animals↗

Effects of iodate on intraretinal b and c waves of the cat electroretinogram.

In 12 cats, the intravenous and intravitreal administrations of sodium iodate (SI) were performed to examine the effects on b and c waves of electroretinogram in the dark-adapted retina. The intravitreal SI (0.5-3.5 mM) produced the complete suppression of intraretinal b waves without remarkable changes of slow PIII and light-evoked [K+]o decrease in the subretinal space. Intravenous SI (30 mg/kg) also showed the suppression of intraretinal b waves. SI not only acted as a poison to the retinal pigment epithelium but also might block the post-synaptic response.

Animals↗