Disease relevance of sodium chlorate

• Furthermore, BSC40 cells treated with sodium chlorate to produce undersulfated GAGs are more refractory to vaccinia virus infection [1].
• To investigate the potential regulation of FGF-2 mitogenic activity by heparan sulfate proteoglycans (HSPG), we have treated human breast cancer cells by glycosaminoglycan degrading enzymes or a metabolic inhibitor of proteoglycan sulfation: sodium chlorate [2].
• Inhibition experiments with heparin and sodium chlorate showed that heparan sulfates are necessary for HPV 16 VLPs to bind to DC but not to LC [3].
• Platelet derived growth factor demonstrated a growth stimulating effect on B6FS, whereas no effect was evident on HT1080 fibrosarcoma cells. beta-d-Xyloside had no effect on the basal level or the platelet derived growth factor-induced cell proliferation, whereas sodium chlorate severely reduced the basal level of proliferation in both cell lines [4].
• Undersulfation of glycosaminoglycans induced by sodium chlorate treatment affects the progression of C6 rat glioma, in-vivo [5].

High impact information on sodium chlorate

• Oncogenic Ras-induced proliferation is abolished by addition of an anti-FGF-2 blocking antibody, suramin, or treatment with either sodium chlorate or heparitinase, demonstrating an autocrine requirement for FGF-2 [6].
• Treatment of HeLa cells with sodium chlorate, a potent inhibitor of proteoglycan sulfation, reduced luciferase expression by 69% [7].
• Incubation of cells with sodium chlorate reduced glycosaminoglycan sulfation by > 95% without affecting cell growth [8].
• Treatment of whole kidneys with sodium chlorate to disrupt proteoglycan synthesis results in the loss of BMP7 expression in the mesenchyme whereas expression in the epithelial components of the kidney are unaffected [9].
• Addition of alpha2-macroglobulin as well as treatment with heparinase, chondroitinase ABC, and sodium chlorate did not decrease levels of VCAM-1 and E-selectin stimulated by Lp(a), suggesting that neither the low density lipoprotein receptor-related protein nor cell-surface proteoglycans are involved in Lp(a)-induced adhesion molecule production [10].

Chemical compound and disease context of sodium chlorate

• A 28-d experiment evaluated the growth, acute-phase response, and bacterial shedding patterns in pigs (n = 96; initially 6.8 +/- 1.3 kg) fed mannanoligosaccharides (MANNAN) and sodium chlorate (CHLORATE) before and after oral challenge with Salmonella enterica serotype Typhimurium (ST) [11].
• Eight chemicals, including glycerol monolaurate, hydrogen peroxide, acetic acid, lactic acid, sodium benzoate, sodium chlorate, sodium carbonate, and sodium hydroxide, were tested individually or in combination for their ability to inactivate Campylobacter jejuni at 4 degrees C in suspension [12].
• Chlorine (hypochlorite and hypochlorous acid), monochloramine, chlorine dioxide, sodium chlorite, and sodium chlorate were evaluated for induction of chromosomal aberrations and micronuclei in bone marrow of CD-1 mice, and for induction of sperm-head abnormalities in B6C3F1 mice [13].

Biological context of sodium chlorate

• Treatment of cells with sodium chlorate, which blocks sulfation of proteoglycans, reduced the binding of aFGF to its low and high affinity binding sites by 95 and 80%, respectively [14].
• This self-catalyzed cyclization reaction is inhibited by the intercalating dye methidiumpropyl.EDTA (MPE; R.P. Hertzberg and P.B. Dervan (1982) J. Am. Chem. Soc. 104, 313-315) [15].
• The affinity cleavage reagent methidiumpropyl-EDTA (MPE) [Hertzberg, R. P., & Dervan, P. B. (1982) J. Am. Chem. Soc. 104, 313-315] intercalates between base pairs in helical DNA and, when complexed with Fe(II), cleaves the DNA by oxidative degradation of the deoxyribose [16].
• Our data showed that both hairpin polyamides preferentially selected DNA sequences having consensus recognition sites as defined by the Dervan pairing rules [17].
• In contrast, sodium chlorate unexpectedly induced early expression of type II collagen and increased the number of cartilage nodules during chondrogenesis [18].

Anatomical context of sodium chlorate

• In our studies, Balb/c3T3 fibroblasts were treated with 50 mM sodium chlorate to completely inhibit (99%) sulfation of proteoglycans [19].
• To test further this hypothesis, the binding capacity of the plasma membrane for the lipase was decreased by inhibiting the sulfation of glycosaminoglycans with sodium chlorate, an inhibitor of sulfate adenyltransferase [20].
• In the present study, we have demonstrated that treatment of both astrocytic cell lines and primary astrocytes with inhibitors of proteoglycan synthesis, beta-D-xylosides and sodium chlorate, can strongly influence the axon growth promoting properties of both matrix and whole cells [21].
• Dorsal root ganglia grown on Neu7 cells treated with sodium chlorate extended 2 to 3 times the number of axons for approximately 300 mm longer distance than on control cultures [21].
• Heparinase digestion of the endothelial cell's glycocalyx or sodium chlorate inhibition of endothelial cell sulfated glycan synthesis significantly reduced the number of adherent H. somnus [22].

Associations of sodium chlorate with other chemical compounds

• The biological effect of bFGF is conveyed through its binding to the high-affinity receptor sites and the binding is dependent on the presence of cell surface heparin-like molecules, as treatment of cells with heparitinase or sodium chlorate abolishes high-affinity binding and growth inhibition [23].
• SR-BI-mediated LDL-CE-selective uptake was not inhibited by the proteoglycan synthesis inhibitor, p-nitrophenyl-beta-D-xylopyranoside or by the sulfation inhibitor sodium chlorate, indicating that SR-BI-mediated LDL-CE uptake occurs independently of LDL interaction with cell-surface proteoglycan [24].
• GGH(Hin139-190) binds sequence specifically to DNA at four 13 base pair sites (termed hixL and secondary) and, in the presence of Ni(OAc)2 and monoperoxyphthalic acid, reacts predominantly at a single deoxyribose position on one strand of each binding site [Mack, D.P., & Dervan, P.B. (1990) J. Am. Chem. Soc. 112, 4604] [25].
• Testosterone production by dibutryl-cAMP stimulated Leydig cells was also inhibited by sodium chlorate [26].
• In some experiments, chondrocyte cultures were treated with sodium chlorate (NaClO(3)) to inhibit GAG sulfation, or with chondroitinase ABC (ChABC) to digest chondroitin sulfate (CS) in the matrix [27].

Gene context of sodium chlorate

• Using a metabolic inhibitor of sulfation, sodium chlorate, we show that the interactions of the CS/DS chains of versican with L- and P-selectin and chemokines are sulfation-dependent but the interaction with CD44 is sulfation-independent [28].
• In addition, when the sulphation of glycosaminoglycans (GAGs) is prevented by growing the HepG2 cells in the presence of 30 mM sodium chlorate, TFPI binding is unaffected, whereas the binding of bovine lipoprotein lipase, a protein known to associate with cell-surface GAGs, falls to 50% of control levels [29].
• Finally, pretreatment of Sertoli cells with sodium chlorate, an inhibitor of cell surface proteoglycan sulfation, also retarded the decrease in recombinant IGFBP-3 [30].
• We show that altering endogenous gradients of HS sulfation with sodium chlorate or over-O-sulfated synthetic heparin in lung organ cultures dramatically decreases Fgf10 binding [31].
• The inhibitor of sulfation, sodium chlorate, vastly reduces PrPSc in ScN2a cells (Gabizon, R., Meiner, Z., Halimi, M., and Ben-Sasson, S. A. (1993) J. Cell. Physiol. 157, 319-325) [32].

Analytical, diagnostic and therapeutic context of sodium chlorate

• Addition of heparin or xylosides to cell cultures resulted in a pronounced accumulation of, heparanase in the culture medium, whereas sodium chlorate had no such effect [33].
• The crystallization of sodium chlorate (NaClO3) is a classic example of spontaneous chirality, since it is achiral in solution but adopts a chiral form in the solid state [34].
• Filtration times through polycarbonate sieves are increased by a factor of 40 after 2 h incubation with 30 mM sodium chlorate [35].
• Heparitinase I (hep I) and sodium chlorate prevented binding of HIV-1/IIIB to MT-4 cells as revealed by indirect immunofluorescence procedures, thereby inhibiting infection [36].

References