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PubMed2006

Efficient synthesis of achiral seco-cyclopropylbenz[2,3-e]indoline analogues: [4-amino-2-(5,6,7-trimethoxyindole-2-carboxamido)naphthalen-1-yl]ethyl chloride and [4-hydroxy-2-(5,6,7-trimethoxyindole-2-carboxamido)naphthalen-1-yl]ethyl chloride.

Achiral seco-aminocyclopropylbenz[2,3-e]indoline and seco-hydroxycyclopropylbenz[2,3-e]indoline (seco-CBI) analogues of the duocarmycins and CC-1065, e.g., 7 and 8, are potent anticancer agents. This paper describes significantly improved synthetic strategies for preparing these compounds. Starting from Martius acid (9), the new strategy gave a 13-fold increase in the overall yield of 7, and the use of di-tert-butyl malonate was economically beneficial. For compound 8, the new strategy employed an Emmons-Horner reaction, followed by a Stobbe condensation, and the overall yield was improved 15-fold.

Antineoplastic Agents↗
PubMed2001

Chloride concentration in endosomes measured using a ratioable fluorescent Cl- indicator: evidence for chloride accumulation during acidification.

A novel long wavelength fluorescent Cl(-) indicator was used to test whether endosomal Cl(-) conductance provides the principal electrical shunt to permit endosomal acidification. The green fluorescent Cl(-)-sensitive chromophore 10,10'-bis[3-carboxypropyl]-9,9'-biacridinium dinitrate (BAC) was conjugated to aminodextran together with the red fluorescent Cl(-)-insensitive chromophore tetramethylrhodamine (TMR). BAC fluorescence is pH-insensitive and quenched by Cl(-) with a Stern-Volmer constant of 36 m(-1). Endosomes in J774 and Chinese hamster ovary (CHO) cells were pulse-labeled with BAC-TMR-dextran by fluid-phase endocytosis. Endosomal [Cl(-)] increased over 45 min from 17 to 53 mm in J774 cells and from 28 to 73 mm in CHO cells, during which time endosomal pH decreased from 6.95 to 5.30 (J774) and 6.92 to 5.60 (CHO). The acidification and increased [Cl(-)] were blocked by bafilomycin. Together with ion substitution and buffer capacity measurements, we conclude that Cl(-) transport accounts quantitatively for the electrical shunt during vacuolar acidification. Measurements of relative endosomal volume by a novel ratio imaging method involving fluorescence self-quenching indicated a 2.5-fold increase in volume during early acidification and Cl(-) accumulation, which was blocked by bafilomycin. These experiments provide the first direct measurement of endosomal [Cl(-)] and indicate that endosomal acidification is accompanied by significant Cl(-) entry and volume increase.

Animals↗
PubMed1981

Physiological Control of Chloride Transport in Chara corallina: II. THE ROLE OF CHLORIDE AS A VACUOLAR OSMOTICUM.

The extent to which Cl(-) is replaceable as the major anionic constituent of the vacuole of Chara corallina was investigated. It was found that external Cl(-) is not essential in order for nongrowing cells to increase internal osmotic pressure. After growth of cells in low (9 micromolar) Cl(-), the vacuolar Cl(-) concentration is one-half that of cells grown at normal external Cl(-) concentration (850 micromolar). In contrast, both internal osmotic pressure and total concentration of the major cations, K(+) and Na(+), in the same cells were found to be only slightly sensitive to the external Cl(-) concentration. Thus, it is proposed that, at limiting external Cl(-) concentration, the cell is able to transport or synthesize another anion for vacuolar use rather than utilize a neutral solute.Although the total vacuolar (K(+) + Na(+)) concentration is relatively insensitive to low Cl(-) conditions, a large increase in K(+) was recorded. This increase in K(+) was offset by a correspondingly large fall in Na(+). This is unrelated to any mechanistic dependence of Na(+) on Cl(-) for entry into the cell but may indicate a control system acting on vacuolar sequestration of both Na(+) and Cl(-). Cells grown in low Cl(-) display an ability to take up Cl(-), at enhanced rates, from the medium. The enhancement of Cl(-) influx is maintained for several hours after external Cl(-) is raised to a high level and indicates the existence of a control on Cl(-) influx acting in addition to that of cytoplasmic Cl(-) concentration, which has a shorter decay time.The results are discussed in relation to similar work on higher plants.

Journal Article↗
PubMed2001

4-[3-Bromo-4-hydroxyphenyl)amino]-6,7-dimethoxyquinazolin-1-ium chloride methanol solvate and 4-[(3-hydroxyphenyl)amino]-6,7-dimethoxy-1-quinazolinium chloride.

The title compounds, C16H15BrN3(O3)(+).Cl(-).CH4O (WHI-P154) and C16H16N3(O3)(+).Cl(-) (WHI-P180), are potent inhibitors [WHI-P154 with IC50 = 5.6 microM and WHI-P180 with IC50 = 4.0 microM for epidermal growth factor receptor (EGFR) kinase inhibition] of the EGFR tyrosine kinase as well as Janus Kinase 3. The molecular structures of these compounds are very similar except for the dihedral angle between the anilino and quinazoline moieties which is 1.10 (5) degrees for WHI-P154, and 45.66 (6) and 25.29 (7) degrees for the two molecules of WHI-P180 in the asymmetric unit. The nitrogen at the N3 position is protonated in both structures and participates in hydrogen bonding with the chlorine anions.

Animals↗
PubMed1992

Structures of new DNA photocleaving agents: 3,6-bis(dimethylamino)-10- [6-(4-nitrobenzoyloxy)hexyl]acridinium chloride (I) and 9-([6-(4- nitrobenzoyloxy)-hexyl]amino)acridinium chloride monohydrate (II).

(I) C30H35N4O4+.Cl-, Mr = 551.07, triclinic, P1, a = 10.512 (2), b = 11.203 (2), c = 14.469 (2) A, alpha = 111.49 (1), beta = 105.74 (1), gamma = 95.82 (1) degrees, V = 1487.4 (4) A3, Z = 2, Dm = 1.23 (by flotation), Dx = 1.231 g cm-3, lambda(Cu K alpha) = 1.5418 A, mu = 14.68 cm-1, F(000) = 584, T = 296 K, R = 0.109 for 3100 unique reflections with I greater than 3 sigma(I). (II) C26H26N3O4+.Cl-.H2O, Mr = 497.98, triclinic, P1, a = 9.4810 (8), b = 14.495 (2), c = 9.255 (1) A, alpha = 95.48 (1), beta = 98.17 (1), gamma = 101.78 (1) degrees, V = 1222.3 (5) A3, Z = 2, Dm = 1.35 (by flotation), Dx = 1.353 g cm-3, lambda(Cu K alpha) = 1.5418 A, mu = 17.34 cm-1, F(000) = 524, T = 296 K, R = 0.052 for 3589 unique reflections with I greater than 3 sigma(I). The diffraction work confirmed the molecular structures of the newly synthesized DNA photocleaving compounds, in which the p-nitrophenyl group is nearly coplanar with the acridine moiety in (I), whereas the two planar groups form a dihedral angle of 98.7 degrees in (II). The flexibility of the methylene chain and the substantial stacking ability of the aromatic groups observed may be essential for binding to DNA and reaction with the deoxyribose H atoms.

Aminoacridines↗
PubMed1993

Nickel chloride and cobalt chloride, two common contact sensitizers, directly induce expression of intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule (ELAM-1) by endothelial cells.

Intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1), and endothelial leukocyte adhesion molecule-1 (ELAM-1, E-selectin) are endothelial surface molecules that play a role for leukocyte recruitment to sites of inflammation, e.g., during contact hypersensitivity. We studied the effects of sensitizing agents (2,4-dinitro-benzenesulfonic acid, metal salt haptens) and chemically related substances on endothelial adhesion molecule expression. Using flow cytometry and an enzyme-linked immunosorbent assay, NiCl2 and, to a lesser extent, CoCl2 were found to up-regulate ICAM-1, VCAM-1, and ELAM-1 expression on cultured human umbilical vein endothelium whereas the other substances tested showed no effects. Induction of adhesion molecules by NiCl2 required de novo mRNA and protein synthesis. Up-regulation could be blocked by kinase inhibitor H-7 but not staurosporine, suggesting involvement of phosphorylation events independent of protein kinase C activation. Concomitant application of NiCl2 and neutralizing antibodies to IL-1 did not block up-regulation by the hapten demonstrating that the latter did not act via an IL-1-dependent autocrine mechanism. Regarding ELAM-1 induction, pre-treatment for 24 h with NiCl2 produced hyporesponsiveness to IL-1 and TNF-alpha upon restimulation, suggesting that NiCl2 and these cytokines may partially share a common pathway of activation. In addition, analysis of cultured foreskin specimens revealed that NiCl2 may induce up-regulation of ELAM-1 on microvascular endothelium in vivo. Our data demonstrate that both Ni++ and Co++ to which simultaneous contact sensitivity is frequently observed have the ability to directly up-regulate endothelial adhesion molecules. This shared property may represent an adjuvant mechanism that promotes sensitization and elicitation events in contact hypersensitivity to these haptens.

Capillaries↗
PubMed1996

Effects of substrates and phosphate on INT (2-(4-iodophenyl)-3-(4-nitrophenyl)-5-phenyl tetrazolium chloride) and CTC (5-cyano-2,3-ditolyl tetrazolium chloride) reduction in Escherichia coli.

The effects of substrates of primary aerobic dehydrogenases, and inorganic phosphate on aerobic INT and CTC reduction in Escherichia coli were examined. In general, INT produced less formazan than CTC, but INT (+) cell counts remained near values of CTC (+) cells. INT and CTC (+) cell numbers were higher than plate counts on R2A medium using succinate, formate, lactate, casamino acids, glucose, glycerol (INT only) and no substrate. Formate resulted in the greatest amount of INT and CTC formazan. Reduction of both INT and CTC was inhibited above 10 mmol l-1 phosphate, and this appeared to be related to decreased rates of O2 consumption. Formation of fluorescent CTC (+), but not INT (+) cells was also inhibited in a concentration dependent manner by phosphate above 10 mmol l-1. From light microscopic observations it appeared CTC formed increasing amounts of poorly or non-fluorescent formazan with increasing phosphate. Therefore, use of phosphate buffer in excess of 10 mmol l-1 may not be appropriate in CTC and INT reduction assays.

Colony Count, Microbial↗
PubMed1976

The effects of dimercaptosuccinic acid on the excretion and distribution of mercury in rats and mice treated with mercuric chloride and methylmercury chloride.

1 All five rats in a group survived if dimercaptosuccinic acid (DMSA), a water soluble derivative of 2,3-dimercaptopropanol (BAL), was given in doses of 10-40 mg/kg intraperitoneally 30 min, 4 and 24 h after administration of 2.4 mg/kg Hg as HgCl2, whereas three out of a group of five died if DMSA was not given. DMSA 20 mg/kg increased urinary excretion and decreased the body burden significantly more than 10 mg/kg DMSA, but further doubling of the dose had only marginal effects. 2 DMSA was able to reduce body burden and increase urinary excretion of Hg when intraperitoneal treatment started eight days after the subcutaneous administration of HgCl2. 3 DMSA was effective in decreasing body burden and the brain concentration of Hg in rats dosed orally with methylmercury (MeHgCl) when intraperitoneal treatment started with 40 mg/kg DMSA 24 h after Hg. Increase in the urinary excretion of mercury was responsible for the decrease in body burden. 4 DMSA was effective when given in the drinking water of rats or mice both against inorganic Hg and MeHgCl. In mice treated intraperitoneally with MeHgCl, DMSA 19.5 mug/ml in the drinking water caused a significant decrease in the body burden and increase in the excretion of Hg. 5 DMSA was about four times more efficient than D-penicillamine in decreasing the body burden of Hg. As their toxicity is in the same range, the higher efficiency of DMSA offers a larger margin of safety for the mobilization of Hg.

Animals↗