Disease relevance of iodate

• Lavage of a mucinous cystadenoma of the pancreas with povidone iodate [1].
• Serum thyroid-stimulating autoantibodies (LATS and LATS protector) and thyrotropin (TSH) concentrations were measured in the serum of 30 patients with hyperthyroidism living in Tasmania who developed their disease following correction of iodine deficiency by addition of iodate to the bread [2].
• Damaging the RPE with sodium iodate caused the resorption time, for blebs made with an ionic solution (Hanks'), to decrease from 2-6 hours to only about 30 minutes [3].
• To determine the role of retinal pigment epithelium in the induction of S-antigen-induced uveitis by administration of sodium iodate (NaIO3) to selectively damage the retinal pigment epithelium [4].
• The studies do not meet current standards of toxicity testing, mostly because they lacked toxicokinetic data and did not separate iodate-specific effects from the effects of an overdose of any form of iodine [5].

High impact information on iodate

• Single-crystal X-ray diffraction experiments reveal that 1 possesses a corrugated layered structure constructed from molybdenum oxide chains that are bridged by iodate anions [6].
• Phosphate and iodate are both found to bind to the three metal ions in the protein molecule, suggesting that these ions are involved directly in the catalytic process and thereby identifying the active site [7].
• PURPOSE: To characterize chemoattractants expressed by the retinal pigment epithelium (RPE) after sodium iodate (NaIO3)-induced damage and to investigate whether ocular-committed stem cells preexist in the bone marrow (BM) and migrate in response to the chemoattractive signals expressed by the damaged RPE [8].
• RPE damage was also induced by sodium iodate injection (40 mg/kg) into wild-type or albino C57Bl/6 mice [9].
• The applicability of the proposed tITP-CE method could apparently be extended to the determination of other trace seawater anions (e.g., iodate) [10].

Chemical compound and disease context of iodate

• Blebs made with sucrose also absorbed much more quickly after iodate [3].
• The disappearance of fluorescein injected into the vitreous was significantly delayed in diabetic and sodium iodate-treated rats, whereas this rate was normal in hypertension animals [11].
• Fluorophotometry was used to evaluate the blood-ocular barrier in rats following streptozocin-induced diabetes, experimental systemic hypertension, sodium iodate treatment, diet-induced galactosemia, and aldose reductase inhibitors [11].
• While iodide (I-) and iodate (IO3-) have been studied, no studies concerned with the subchronic toxicity of iodine (I2) have been conducted in experimental animals [12].
• Outer retinal degenerations were induced by injecting intravenously either monoiodoacetic acid (IAA) or sodium iodate (NaIO3) [13].

Biological context of iodate

• The kinetics of the radioactive iodine exchange reaction for the preparation of [123I]HIDM is controlled by the pH, the temperature, and the presence of reductant (sodium bisulfite), and oxidant (sodium iodate) [14].
• By contrast, the oxidants periodate, iodate, and hydrogen peroxide (applied for the same time, but at higher concentrations) merely produced a parallel shift of the h infinity(E) curve to more negative values of membrane potential [15].
• Effects of intravenous iodoacetate (a glycolysis inhibitor) and iodate (a metabolism inhibitor selective to retinal pigment epithelium) on light-evoked alkalinizations and hypoxia-induced acidifications were studied in the dark-adapted cat retina, in vivo, to learn about pH regulation [16].
• Iodate (IO3-) inhibited the FSK, ISO, and VO3- activations of AC in ciliary process membranes (IC50, 0.3 mM) [17].
• The outward active transport and the inward permeability of the blood-retinal barrier were studied in the rabbit eye after i.v. administration of sodium iodate [18].

Anatomical context of iodate

• Sodium iodate was injected intravenously in some rabbits to damage the retinal pigment epithelium (RPE) [19].
• To alter the conditions in the subretinal space, the outer blood-retinal barrier was disrupted by compromising retinal pigment epithelial (RPE) cells with a systemic injection of sodium iodate [20].
• One month after iodate, patches of Bruch's membrane were devoid of RPE, which was replaced by scar tissue [21].
• Sucrose permeability of the blood-retinal and blood-brain barriers. Effects of diabetes, hypertonicity, and iodate [22].
• PURPOSE: To investigate the differentiation of rat neural stem cells (rNSCs) into cells of retinal pigment epithelial (RPE) lineage both in vitro and in vivo, after subretinal transplantation into normal rats and in a sodium iodate (NaIO(3)) model of RPE loss [23].

Associations of iodate with other chemical compounds

• The procedure for iodine, which is also applicable to individual tablet assay, consists of ashing the sample, coverting iodide to iodate, and analyzing by differential pulse polarography [24].
• Transient breakdown of the retinal pigment epithelium diffusion barrier after sodium iodate: a fluorescein angiographic and morphological study in the rabbit [25].
• The BRB was disrupted by injection of sodium iodate (i.v.) or lipopolysaccharide (LPS, i.v. or anterior chamber) [26].
• We produced breakdown of the blood-retinal barrier (BRB) in pigmented rabbits by several different mechanisms: retinal cryopexy, retinal laser, intravenous sodium iodate (30 mg/kg), or intravitreal injection of epinephrine (0.1 mL, 10(-3) M) [27].
• Sodium current inactivation was measured in TEA-Ringer solution and after treatment with Anemonia sulcata toxin II (5 microM), internal iodate (20/40 mM), glutaraldehyde (10 mM), chloramine-T (0.6 mM), and 2,4,6-trinitrophenol (1 mM) [28].

Gene context of iodate

• The oxidation of Sb(III) with iodate was measured in 0.5 mol L(-1) NaCl solutions as a function of pH at environmentally significant concentrations of antimony and iodate [29].
• Combined action of intraaxonal iodate and external sea anemone toxin ATX II on sodium channel inactivation of frog nerve fibres [30].
• The activation of bovine spleen NMT with thiol reducing compounds, and its inhibition by the oxidizing agent sodium iodate, suggest a role for oxidation/reduction in NMT regulation [31].
• Monomeric vanadate is a potent competitive inhibitor of phospholipase C from Bacillus cereus, much better than other oxyanions (e.g., phosphate or iodate) [32].

Analytical, diagnostic and therapeutic context of iodate

• After experimental destruction of the retinal pigment epithelium (RPE) by intravenous injection of sodium iodate, the rabbit choriocapillaris (CC) atrophies [33].
• In contrast, 24 hr after treatment of animals with iodate, the PS product for the BRB but not the BBB was increased [22].
• Pigmented rabbits were treated with intravenous sodium iodate 30 mg/kg, (a specific RPE cell poison), intravitreal N-ethylcarboxamidoadenosine (NECA) 10(-3) mol/l (which specifically disrupts the vascular BRB), or retinal diode laser photocoagulation [34].
• An animal model of retinal pigment epithelium regeneration--rabbits with sodium iodate induced retinopathy--was used [35].
• Alteration of the blood-retinal barrier by sodium iodate: kinetic vitreous fluorophotometry and horseradish peroxidase tracer studies [36].

References