Disease relevance of Chloromercuriphenylsulfonate

• Since p-chloromercuribenzoic acid and p-chloromercuriphenylsulfonic acid are able to cross the outer membrane of Escherichia coli, their failure to inhibit in vivo Enzyme IIglc must be due to their inability to cross the inner membrane of the bacteria [1].
• CO(2) entry into Synechococcus sp. PCC7942 cells was drastically inhibited by the water channel blocker p-chloromercuriphenylsulfonic acid suggesting that CO(2) uptake is, for the most part, passive via aquaporins with subsequent energy-dependent conversion to HCO3(-) [2].
• The oxidizing agent p-chloromercuribenzenesulfonic acid (pCMBS) had no effect on 3H-FDG uptake under normoxic conditions but counteracted the effect of hypoxia [3].
• Moreover, histidine-induced hemolysis can be prevented by 1 mm or lower PCMBS without a discernible effect on histidine influx suggesting a possible membrane lesion or damage at the outer surface of the cell [4].
• Ag+ or p-chloromercuribenzenesulfonic acid produced similar contractures to that induced by Hg2+ [5].

Psychiatry related information on Chloromercuriphenylsulfonate

• Colon water absorption was markedly decreased by the mercurial agent p-chloromercuribenzenesulfonic acid and was not affected by water deprivation [6].

High impact information on Chloromercuriphenylsulfonate

• It may be postulated that a decreased number of sulfhydryl sites or a mutation of proteins in the PCMBS-sensitive cation channels of the HS cell membrane result in this hyposensitivity to PCMBS [7].
• Most (> or =75%) of the bound zinc was released from baculovirus-expressed rat nNOS by p-chloromercuriphenylsulfonic acid (PMPS) [8].
• The sulfhydryl reagent p-chloromercuriphenylsulfonate (1 mM) abolished Pf of AQP3, whereas it did not affect Pgly [9].
• PI hydrolysis in the lysates was inhibited by sodium p-chloromercuriphenylsulfonate but unaffected by EGTA, consistent with the proposal that hydrolysis is due to GPI-PLC [10].
• PCMBS reacts with EmrE in an asymmetric and unique way [11].

Chemical compound and disease context of Chloromercuriphenylsulfonate

• The possible protective effects of 30 and 180 mM mannitol added to the extracellular medium were studied in Ehrlich ascites tumor cells (EATC) injured by the nonpenetrating mercurial p-chloromercuribenzenesulfonic acid (PCMBS) or by anoxia [12].

Biological context of Chloromercuriphenylsulfonate

• Disulfide bonds reduced by DTT could be reoxidized by washing with excess buffer or by addition of 0.02% H2O2 thereby restoring NMN transport. p-Chloromercuribenzenesulfonic acid reversibly inactivated NMN transport with an IC50 of 25 microM/mg of protein [13].
• Addition of p-chloromercuriphenylsulfonic acid to the culture medium, at a concentration totally inhibiting the plasma membrane NADH-ferricyanide reductase in vitro, leads to cell death of rho 0 but not of rho + cells [14].
• It exhibits identical substrate specificity as compared with the crude preparation, is active over a broad pH range (4.0-8.5), inhibited by the thiol-blocking agent p-chloromercuriphenylsulfonic acid and by 1,10-phenanthroline, and is partially heat-labile [15].
• Nonspecific protein binding can be determined equally effectively either by incubation with 3 mM PCMBS or by addition of a 100-fold molar excess of nonlabeled retinol.(ABSTRACT TRUNCATED AT 250 WORDS)[16]
• Here we investigate the effect of hydrogen peroxide, an oxidant found in the aqueous humor, and of p-chloromercuriphenylsulfonic acid (p-chloromecuribenzene-sulfonic acid) (PCMBS), a relatively impermeant sulfhydryl probe, on membrane SH groups and ion homeostasis in cultured lens epithelial cells [17].

Anatomical context of Chloromercuriphenylsulfonate

• Solubilization of the membranes in the presence of p-chloromercuriphenylsulfonic acid, elevated concentrations of KCl, or deoxyribonuclease I released receptors in parallel with actin [18].
• Dose-dependent inhibition of the high affinity transport system by p-chloromercuribenzenesulfonic acid is demonstrated for phenylalanine, similar to the known sensitivity of blood-brain barrier transport in vivo [19].
• Efficiency of the liposome-erythrocyte fusion was suppressed significantly when erythrocytes were pretreated with N-ethylmaleimide (N-EM), a membrane-permeable sulfhydryl agent, whereas rho-chloromercuriphenylsulfonic acid (PCMBS), a membrane-impermeable sulfhydryl agent, had no appreciable effect on the fusion efficiency [20].
• Treatment of blastocysts with p-chloromercuriphenylsulfonic acid (pCMPS, > or =100 microM) for 5 min significantly impaired (P < 0.05) volume recovery, indicating the involvement of AQPs in fluid transport across the TE [21].
• We used p-chloromercuribenzenesulfonic acid inhibition of apoplastic loading to distinguish between the two pathways in three species that have abundant minor vein plasmodesmata and are therefore putative symplastic loaders [22].

Associations of Chloromercuriphenylsulfonate with other chemical compounds

• Glucose transport activity was stereospecific, temperature-dependent, sensitive to inactivation by p-chloromercuriphenylsulfonate, and accompanied plasma membrane material during subcellular fractionation [23].
• Growth for 96 hours in the presence of both EGF and cholera toxin or another cyclic AMP elevating agent induced an ectoATPase activity which was more active with CaATP and resistant to inhibition by the sulfydryl reagent, p-chloromercuriphenylsulfonate (pCMPS) (Knowles: Arch. Biochem. Biophys., 263: 264-271, 1988) [24].
• The sulfhydryl reagents mersalyl, PCMBS, NEM, and DTNB also inhibited net uptake, suggesting that sulfhydryl groups may be involved in the activity of the carrier protein [25].
• Use of specific inhibitors, including L-trans-epoxysuccinyl-leucylamino-(4- guanidino)-butane (E-64), p-chloromercuriphenylsulfonic acid (PCMS), and oryzacystatin, indicated that nearly all of the proteinase activity against casein was contributed by cysteine proteinases [26].
• D-Aspartate, p-chloromercuriphenylsulfonate and GABA had comparable effects on isolated medial giant nerve fibers.These studies indicate that L-glutamate is taken up primarily by the periaxonal glia of crayfish central nerve fibers by a low-affinity, saturable, Na(+)-dependent transport system and is retained by the fibers primarily in that form [27].

Gene context of Chloromercuriphenylsulfonate

• Not like bivalent Hg2+, monovalent p-chloromercuribenzenesulfonic acid was incapable of activating c-Src kinase [28].
• We found that a cysteine-specific reagent, p-chloromercuriphenylsulfonic acid (PCMPS), irreversibly inhibited one of the isozymes (GalNAc-T1) [29].
• The sulfhydryl reagent p-chloromercuriphenylsulfonic acid, which increases binding to brain receptors, produced only minor changes except in the case of GluR2 flip [30].
• Simultaneous incubation of neutrophil or platelet membranes with radiolabeled PAF and N-ethylmaleimide (NEM), p-(chloromercuri)benzenesulfonic acid (PCMBS), or 5,5'-dithiobis(2-nitrobenzoic acid) (DTNB) resulted in a dose-dependent inhibition of PAF specific binding to the membranes [31].
• Quantitative analysis of the competition between p-chloromercuriphenylsulfonate and VAChT ligands was possible after defining second-order reaction conditions [32].

Analytical, diagnostic and therapeutic context of Chloromercuriphenylsulfonate

• In contrast, p-chloromercuriphenylsulfonic acid significantly (p < 0.05) enhanced baroreflex sensitivity (-2.14 +/- 0.09 vs. -3.08 +/- 0.18); subsequent ethanol microinjection reversed this enhancement (-2.90 +/- 0.21 vs. -1.86 +/- 0.24) [33].
• We found that fluorescamine, which reacts with amino groups, inhibits rosette formation, while p-chloromercuriphenylsulfonic acid, which binds to sulfydryl groups, increases the percentage of the rosette-forming lymphocytes [34].

References