DCCD

The Ca transport and Ca -stimulated ATPase activity of sarcoplasmic reticulum is inhibited by 10-30nmol dicyclohexylcarbodiimide per mg protein in a Ca free medium [372]. A23187 enhanced the sensitivity of the enzyme to DCCD, while Ca or Sr at micromolar concentrations prevented the inhibition. Since Ca -loaded vesicles retained their sensitivity to DCCD in a Ca -free medium, the reactivity of the enzyme with DCCD is controlled by the occupancy of the high-affinity Ca sites on the cytoplasmic surface of the membrane. 

Scofano et al. [375] observed that at low reagent to protein ratios (lOnmole/mg protein), DCCD selectively inhibited the phosphorylation of the enzyme by Pi and the... 

Renal brush border DCCD,EEDQ Amilioride, 20-24... 

Abbreviations DEPC, diethylpyrocarbonate DCCD, Af.iV -dicyclohexylcarbodiimide EEDQ, N-ethyoxycarbonyl-2-ethoxy-1,2-dihydroquinoline NEM, A-ethylmaleimide PAO, phenylarsine oxide NPM, IV-phenylmaleimide PLP, pyridoxal phosphate DIDS, diisothiocyanostilbene disulfonate PITC, phenylisothiocyanate. 

Further evidence that carboxyl groups are important for transport activity was provided by Igarashi and Aronson [22], Friedrich et al. [23], and Kinsella et al. [24] using the carboxyl group-specific reagent, A,A -dicyclohexylcarbodiimide (DCCD). DCCD irreversibly inactivated the brush border Na /H exchanger in rabbit and... 

Interestingly, Grinstein et al. [19] found that DCCD did not inhibit the Na /H" exchanger in thymic lymphocytes (sensitive-type) whereas Ganapathy et al. [18] found that the placental brush border Na /H exchanger, which is also a sensitive-type, was susceptible to DCCD, and amiloride protected from inhibition. Thus, there may be structural differences between sensitive-type exchangers from these two tissues. 

Abbreviations MIA, 5-(A-methyl-A-isobutyl)amiloride DCCD, JV,AT -dicycIohexylcarbodiimide Az-PZA, 4A-azidosalicyIic-5A/-piperazine-amiloride Br-EIPA, 5-(Af-ethyI-IV-isopropyl)-6-bromoamiIoride PrBCM, propylbenzilylcholine mustard. 

The transport of EDTA into a bacterial strain capable of its degradation has been examined (Witschel et al. 1997). Inhibition was observed with DCCD (ATPase inhibitor), nigericin (dissipates ApH), but not valinomycin (dissipates Av /), and was dependent on the stability constant of metal-EDTA complexes. 

Attention has been directed to the dechlorination of polychlorinated benzenes by strains that use them as an energy source by dehalorespiration. Investigations using Dahalococcoides sp. strain CBDBl have shown its ability to dechlorinate congeners with three or more chlorine substituents (Holscher et al. 2003). Although there are minor pathways, the major one for hexachlorobenzene was successive reductive dechlorination to pentachlorobenzene, 1,2,4,5-tetrachlorobenzene, 1,2,4-trichlorobenzene, and 1,4-dichlorobenzene (Jayachandran et al. 2003). The electron transport system has been examined by the use of specific inhibitors. lonophores had no effect on dechlorination, whereas the ATP-synthase inhibitor A,A -dicyclohexylcarbodiimide (DCCD) was strongly inhibitory (Jayachandran et al. 2004). 

CHjOCCCH COjH l.CDIorlmH/DCCD O (X OCCCH CONHCA... 

Uptake by FeoB is inhibited by the energy poisons 1 111 FCCP, DCCD, and vanadate. Both Fe3+ and Fe2+ serve equally well as iron sources, but Fe3+ provided as a citrate salt is immediately reduced to Fe2+, as demonstrated by the formation of the magenta-coloured Fe2+-ferrocine complex. 

DCCD and vanadate. This indicates an active process energised by ATP. Ferrozine inhibition of Fe2+ and Fe3+ uptake implied the concerted involvement of both a Fe3+ reductase and FeoB in the uptake of iron supplied as Fe3+. It is concluded that FeoB-mediated Fe2+ represents a major pathway for H. pylori iron sequestration [189], In addition, growth experiments on the human pathogen L. pneumophila using artificial media, as well as replication studies within iron-depleted Hartmannella vermiformis amoebae and human U937 cell macrophages, provided evidence that the FeoB transporter is important for extracellular growth and intracellular infectivity [190],... 

Figure 1. Representative polarographic traces that depict inhibition by energy transfer inhibitors and allelochemicals of ADP-stimulated electron transport in isolated spinach thylakoids and circumvention of the inhibition by an uncoupler (FCCP, 2 pM). Trace A chlorotributyltin (TBT, 1 pM) trace B phlorizin (400 pM) trace C DCCD (20 pM) trace D quercetin (200 pM) trace E naringenin (1 mM). Water served as electron donor and methyl viologen as electron acceptor. Rates of oxygen utilization, that resulted from the autooxidation of methyl viologen, expressed as pmol 0 consumed/mg Chi h, are indicated parenthet ically.

DCMU is 3-(3,4-dichlorophenyl)-l,l-dimethylurea DCCD, dicyclohexylcarbodiimide FCCR cyanide-p-trifluoromethoxyphenylhydrazone DNR 2,4-dinitrophenol. 

Mode of Action of Dicyclohexylcarbodiimide (DCCD) When DCCD is added to a suspension of tightly coupled, actively respiring mitochondria, the rate of electron transfer (measured by 02 consumption) and the rate of ATP production dramatically decrease. If a solution of 2,4-dinitro-phenol is now added to the preparation, 02 consumption returns to normal but ATP production remains inhibited. 

---