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PubMed1993

Internal vibrations of a molecule consisting of rigid segments. I. Non-interacting internal vibrations.

For molecular crystals, a procedure is proposed for interpreting experimentally determined atomic mean square anisotropic displacement parameters (ADPs) in terms of the overall molecular vibration together with internal vibrations with the assumption that the molecule consists of a set of linked rigid segments. The internal librations (molecular torsional or bending modes) are described using the variable internal coordinates of the segmented body. In paper I of this two-part report, it is assumed as a zero-order approximation that the internal vibrations about the linkage axes between pairs of segments are uncorrelated with each other and with the overall molecular rigid-body vibrations. As a first-order approximation, the possibility that each internal vibration can be correlated with the external vibrations is also considered. An important feature of this approach is that the internal librations are required to give zero contribution to the overall momentum of the molecule at all times, so the internal coordinates must be orthogonal to the external ones. Also, each of the internal librations involves the motion of all atoms in the molecule. The resulting internal vibrational parameters are invariant to the choice of reference segment. With this procedure, the experimental ADPs obtained from crystal structure determinations involving six small molecules (sym-trinitrobenzene, adenosine, tetra-cyanoquinodimethane, benzamide, alpha-cyanoacetic acid hydrazide and N-acetyl-L-tryptophan methylamide) have been analyzed. As a consequence, vibrational corrections to the bond lengths and angles of the molecule are calculated as well as the frequencies and force constants (with e.s.d.'s) for each internal torsional or bending vibration. Compared with other models used for describing internal vibrations, there are differences in how the total ADP is partitioned between the internal and overall molecular vibrations.

Adenosine↗

PubMed1984

Role of UVB-induced serum factor(s) in suppression of contact hypersensitivity in mice.

Ultraviolet, 280-320 nm (UVB), irradiation of the shaved dorsal skin of mice results in suppression of the development of contact hypersensitivity (CHS) to antigens applied subsequently to a distant nonirradiated skin site. Serum from BALB/cAnNCr mice exposed to a single dose of UVB radiation (8.6 X 10(4) J/m2) was evaluated for its ability to induce suppression of CHS to 2-chloro-1,3,5-trinitrobenzene (TNCB), a contact allergen, after transfer to normal recipients. Serum from UVB-irradiated donors was capable of inducing immunosuppression only when collected and transferred within a restricted time period, i.e., approximately 2-6 h post irradiation, and at least 400 microliters of serum per recipient was required. Serum from UVB-irradiated donors was sufficient to induce splenic suppressor cells in recipient mice.

Animals↗

PubMed1981

The role of epidermal cells in the induction and suppression of contact sensitivity.

Haptens, such as trinitrochlorobenzene (TNCB), bind to autologous skin proteins in the induction of allergic content sensitivity. In order to clarify the role of epidermal cells in the induction of allergic contact sensitivity in vivo, we used trinitrobenzene sulfonate (TNBS)-conjugated epidermal cells (TNP-EC) in attempts to sensitize syngeneic mice. Spleen cells conjugated with TNBS (TNP-SC) were used for comparison. Four to 28 days after injection (via various routes) of the haptenated cells, contact sensitivity was assessed by the application of the same hepaten to the ear. Sensitization regularly resulted from the subcutaneous infection of TNP-conjugated cells, and was longer lasting and was always stronger when TNP-EC were used rather than when TNP-SC were used. Neither TNP-EC nor TNP-SC injected intravenously resulted in allergic contact sensitivity, but both induced immunological hypo or unresponsiveness as assessed by subsequent painting with a sensitizing dose of TNCB. TNP-pvSC given intraperitoneally also did not sensitize and induced hyporesponsiveness which was in sharp contrast to the regular sensitization which resulted when TNP-EC were given intraperitoneally. Both similarities and differences in the abilities of haptenated epidermal cells and spleen cells to induce sensitization and tolerance are described and the results are discussed in relation to the role of antigen-presenting cells contained in the haptenated cell populations.

Animals↗

PubMed1977

Ion binding to lysine-modified derivatives of cytochrome c.

The effect of Cl- and K+ ions on the apparent equilibrium constant of the reaction between horse ferricytochrome c and potassium ferrocyanide was studied. Unmodified cytochrome was compared with two lysine-modified derivatives. One, guanidinated, had all lysyl groups converted to homoarginine (but retained the same positive charge); the other was trinitrophenylated at one lysine (measured spectrophotometrically). Both modified derivatives had a somewhat larger equilibrium constant in the reaction of the reduced protein with ferricyanide, but, unlike trifluoroacetylated cytochrome c (which has a negative charge), the redox properties were not dramatically different. The native protein and the lysine-modified cytochromes showed differential K+ binding in Tris-cacodylate buffer at constant ionic strength (0.003-0.005 M). More K+ was bound to ferrocytochrome c. This redox-linked binding, however, was unaffected by modification of lysine. All three derivatives also showed redox-linked differential Cl- ion binding (more Cl- ion was bount to ferricytochrome); however, in this case, the binding was reduced in the lysine-modified molecules. This was interpreted as loss of a single anion site. This anion site critically depends on one or a few lysines which are more reactive with trinitrobenzene sulfonate.

Binding Sites↗

PubMed2001

Toxicity of sediment-associated nitroaromatic and cyclonitramine compounds to benthic invertebrates.

The toxicity of nitroaromatic (2,4-diaminonitrotoluene [2,4-DANT] and 1,3,5-trinitrobenzene [TNB]) and 14C-labeled cyclonitramine compounds (hexahydro-1,3,5-trinitro-1,3,5-triazine [RDX] and octahydro-1,3,5,7-tetranitro-1,3,5,7-tetrazocine [HMX]) to the marine polychaete Neanthes arenaceodentata and the estuarine amphipod Leptocheirus plumulosus following 10- or 28-d exposures to spiked sediments was investigated. Organismal-level effects on survival, growth, and reproduction and cellular-level effects on apoptosis (programmed cell death) were evaluated. Because cyclonitramines have low affinity for sediment, overlying water was not exchanged in the RDX and HMX exposures. Nitroaromatics sorbed strongly to sediment, resulting in near complete resistance to solvent extraction. Cyclonitramines sorbed weakly to sediment, as more 14C-activity was found in the overlying water than in the sediment at exposure termination. No significant decrease in survival or growth was observed with cyclonitramines at initial sediment concentrations as high as 1,000 microg/g. Survival was significantly affected by nitroaromatics at nominal sediment concentrations as low as 200 microg/g, with L. plumulosus being more sensitive than N. arenaceodentata. Growth was significantly decreased at sublethal concentrations of 2,4-DANT for N. arenaceodentata. Reproduction, measured only with L. plumulosus, was significantly decreased only in the highest RDX treatment and also in the lower TNB treatment. However, no decrease was observed in higher concentrations of TNB. Body burden at exposure termination was below detection limit (1 microg/kg) for all compounds. Significant inhibition of apoptosis was not accompanied by significant decreases in growth or reproduction. Because of its critical function in many biological processes. alterations in this endpoint may result in adverse effects on the organism and could be used as an early indicator of toxicity.

Animals↗

PubMed1990

[Several methods for determining total titers of free alpha-amino acids in body fluids].

Comparisons were made among different variants of ninhydrin reaction to determine overall titres of free alpha amino acids in body fluids. Included were para-benzoquinone, 2,4,6-trinitrobenzene sulphonic acid, and 2,4-dinitro-1-fluorobenzene (DNFB). The best reproducibility of results was recorded from DNFB which can be used, as well, for analysis of milk or rumen juice.

Amino Acids↗

PubMed1988

Class II MHC-bearing keratinocytes induce antigen-specific unresponsiveness in hapten-specific Th1 clones.

Previous studies of Ia+ keratinocytes (KC) indicated that they functioned poorly or not at all when utilized as accessory cells for T cell activation. When Ia+ KC were modified with trinitrobenzene sulfonic acid, these cells did not induce a proliferative response in the TNP-specific, 1-Ek-restricted Th1 clone SE-4 (less than 5% of control). Analysis of supernatants generated from SE-4 cells incubated with these non-stimulatory accessory cells revealed low levels of IL-3 and IFN-gamma, but an absence of IL-2, when compared with supernatants generated from SE-4 cells stimulated with TNP-modified cultured Langerhans' cells that contain high levels of all of these lymphokines. Incubation of SE-4 cells with TNP-modified Ia+, but not Ia- KC or FITC-modified Ia+ KC, resulted in unresponsiveness to subsequent stimulation with TNP-modified functional accessory cells. Blocking studies with anti-class II MHC mAb revealed that the induction of unresponsiveness by hapten-modified Ia+ KC was restricted to the I-Ek molecule. Thus, the Ag and MHC specificities of unresponsiveness induced by TNP-modified Ia+ KC were identical to those observed for the proliferation of this clone in response to TNP-modified functional accessory cells. These data indicate the existence of a naturally occurring population of Ia+ cells that, after hapten-modification, induce an unresponsive state instead of proliferation of T cells.

Animals↗

PubMed1986

Induction of TNP-specific cytotoxic T lymphocyte memory in vivo in the absence of T helper cell activity.

The question of whether TH cells are required for the priming of CTL precursors (CTLp) in vivo was studied by using Txbm mice (Thymectomized, irradiated, and stem cell-reconstituted mice). In these mice, TNP-specific CTL could be induced in vitro with TNP-coupled spleen cells only if the cultures were supplemented with an IL 2-containing supernatant (ConAsup). In contrast to normal mice, TNP-specific Lyt-2-TH cells could not be induced by skin painting with trinitrochlorobenzene (TNCB) (as tested by the ability to help CTL formation from thymocyte or normal spleen precursors). These data confirm previous findings that Txbm mice possess CTLp but that their TH compartment is deficient. TNCB skin painting had, however, a clear priming effect on the CTLp population: spleen cells from TNCB-painted mice could give rise to specific CTL with a lower amount of ConAsup than spleen cells from unprimed mice. In addition to this, priming changed the CTLp so that stimulation with lightly coupled cells (0.1 mM trinitrobenzene sulfonic acid [TNBS] instead of 10 mM TNBS) became effective. These changes took place without a significant increase in the frequency of TNP-specific CTL precursors. The data obtained are consistent with the concept that at least with some antigens, CTLp proliferation (clonal expansion), which is probably caused by activated TH cells, is not required for the induction of immunologic memory in vivo.

Animals↗

PubMed1986

Membrane defects of the tolerant B cell. IV. Failure to accelerate antigen receptor loss.

Mechanisms of immunologic tolerance affecting antibody responses include conditions extrinsic to the B cell such as dominant suppression by T cells (1), regulation by anti-idiotype (2), and tolerance in T helper cell populations (3). But tolerance can also result from changes in the antigen-reactive B cells such as their deletion (4), or that mysterious process by which they become "intrinsically tolerant", i.e., refractory to stimulation (5). One approach to learning more about the mechanism of intrinsic tolerance at the level of cell physiology is to determine which of the activation events that normally follow antigen contact occur or fail to occur in such cells. An established model of intrinsic B cell tolerance previously exploited in such studies in the trinitrophenyl (TNP)-self-induced tolerance model of Fidler and Golub (6). Having established that BDF1 mice injected with 2,4,6-trinitrobenzene sulfonic acid (TNBS) become tolerant to TNP, they showed by appropriate transfer experiments that the tolerance could be not induce antibody to TNP in such mice (8). cells (7). They also showed that lipopolysaccharide could not induce antibody to TNP in such mice (8). Together, these data indicated that in this example, tolerance is intrinsic to the B cells. B cells with receptors for TNP remain in these mice (9), providing an opportunity to study activation events in intrinsically tolerant B cells. This paper is part of an ongoing series of studies of activation events in TNP-antibody-binding cells (ABC)2 using this tolerance model (9-11). It shows that a TNP-antigen that normally induces rapid loss of antigen receptors on TNP-ABC cannot do so in mice rendered tolerant to TNP.

Animals↗

PubMed1987

Signals provided in vivo by human rIL-2 and Con A can switch hapten-specific tolerance from unresponsiveness to responsiveness in the South African clawed toad.

Injection in vivo of trinitrobenzene sulphonic acid (TNBS) will conjugate trinitrophenyl (TNP) to the cells and proteins of rodents, and induce hapten-specific tolerance to this epitope. However, the induction of hapten-specific tolerance by this method in the South African clawed toad, Xenopus laevis, is restricted to its subsequent presentation on Ficoll or polyvinylpyrrolidone (PVP). This restricted tolerance depends on the stimulation of an N-methyl-N-nitrosourea (NMU)-insensitive, cyclophosphamide (CyP)-sensitive hapten-specific (suppressor) population that is functionally demonstrable in vitro. Unresponsiveness to TNP-Ficoll can be switched to responsiveness by injection in vivo of recombinant DNA-produced human IL-2 (rIL-2) or the plant-derived lectin, concanavalin A (Con A). Responsiveness to TNP-Ficoll requires thymic presence, although thymic extracts from rIL-2- or Con A-injected toads will suffice. Unresponsiveness to TNP-PVP can also be broken by these reagents, but thymic presence is not required with this immunogen. TNP-Ficoll responses are thymus requiring, while those to TNP-PVP are not, in the toad. Since TNBS failed to stimulate hapten-specific tolerance to a secondary challenge to TNP-Ficoll, we suggest that the suppressor function involved in the establishment of the unresponsive state may act on the differentiation, rather than on the function, of the relevant B cells.

Animals↗

PubMed1980

Mechanisms of regulation of cell-mediated immunity. VI. Antigen density dependence of the induction of genetically restricted suppressor cells.

We have investigated the relationship of antigen density on cell surfaces to the induction of genetically restricted suppressor T cells (Ts). It was found that Ts able to suppress the development of hapten-specific contact sensitivity were induced by the i.v. inoculation of trinitrobenzene sulfonate (TNBS) hapten-coupled cells. The Ts induced by this technique were found to be gentically unrestricted in terms of generation or expression when 10 mM TNBS were used to prepare the hapten-coupled cells. Transferable suppression could be obtained by 10 mM coupled allogeneic cells or, alternatively, TNP-coupled Ia- syngeneic erythrocytes or even H-2-negative syngeneic tumor cells. However, 1 mM TNBS-derivatized hapten-coupled cells induced Ts that were able to suppress only recipients syngeneic with the tolerogen. The significance of these findings to our understanding of the induction and expression of Ts and the triggering signals that are necessary for their activation are discussed.

Animals↗

PubMed1983

Allergic contact dermatitis induced by intratracheal administration of hapten.

It is known that the skin is the natural route for induction of allergic contact dermatitis (ACD). Because the lung is another potential portal of entry for sensitizing chemicals, studies were performed to evaluate immune responses to haptens deposited in the lung. As a result, a new method for inducing ACD was developed. Intratracheal (IT) inoculation of 2,4,6-trinitrobenzene sulfonic acid (TNBS) led to maximal ear swelling 24 hr after challenge on the ear with 2,4,6-trinitrochlorobenzene (TNCB) in carrier. This response was specific for immunizing hapten. Furthermore, it was equally possible to induce ACD by intratracheal inoculation of trinitrophenyl- (TNP) modified bronchoalveolar cells (BAC) or haptenated spleen cells. Adoptive transfer studies demonstrated that the hypersensitivity that resulted from IT inoculation of TNBS or TNP BAC could be transferred with cells. With a monoclonal anti-hamster Ia reagent, it was demonstrated that, like Langerhans cells, 80 to 90% of cells in the bronchial lavage fluid expressed Ia determinants on their membrane. These cells were morphologically indistinguishable from macrophages. Because an individual is capable of being sensitized when hapten is introduced by the pulmonary or epicutaneous routes, the possibility is raised that the alveolar macrophages in the lung possess a similar capability for antigen presentation of hapten in the induction of ACD as does the Langerhans cell.

Animals↗

PubMed1981

Cell-mediated lympholytic responses against autologous cells modified with haptenic sulfhydryl reagents. I. Effector cells can recognize two distinct classes of hapten-reactive self sites on cell surface proteins.

Mouse spleen cells were modified with a sulfhydryl-reactive reagent, N-iodoacetyl-N'-(5-sulfonic-1-naphthyl) ethylene diamine (I-AED) and used as stimulator cells in primary in vitro cultures with unmodified spleen cells of the same strain. CTL could be readily demonstrated when tested on hapten-modified syngeneic target cells. These CML responses were hapten specific and H-2 restricted. In the H-2b strain, effector cell populations were identified that recognized AED in association with K-end and D-end coded self MHC products. Functional modification of the target cells by I-AED can be effectively blocked by prereacting the cells with other SH-reagents, which is consistent with CTL recognition of the hapten on cysteine residues. Since these premodifications of the cell surface do not block the functional modification by trinitrobenzene sulfonate (TNBS), the sulfhydryl-reactive compounds and TNBS modify distinct classes of cell surface groups as determined by CTL function. The results of antibody inhibition experiments are also consistent with this interpretation. Using fluorescent labeled anti-hapten antibodies, FACS II analysis showed that there are approximately 20-fold fewer AED than TNP groups on the approximately 20-fold fewer AED than TNP groups on the cell surface when equivalent concentrations of I-AED and TNBS are compared. The possibility is discussed that these sulfhydryl-reactive compounds can be used together with the H-2Kb mutants for the localization of H-2 coded self determinants recognized in association with foreign antigens.

Animals↗

PubMedDate not supplied

Natural and reinforced immunity against hapten-modified cells in vivo: importance of serum-borne and cellular factors.

Chromium 51-labelled murine splenocytes were injected intravenously into syngeneic non-immune recipients. The percentages of radioactivity recovered in the spleens and the livers were determined, together with the liver/spleen (L/S) radioactivity ratios. It was found that using trinitrobenzene sulphonate (TNBS)-treated cells resulted in a diminution of splenic recovery, with a concomitant augmentation of the L/S ratio, which corresponded to figures found when non-treated xenogeneic lymphocytes were injected. When using splenocytes modified with trifluoromethyl-dinitrobenzene sulphonate (CF3-DNBS)--an analogue of TNBS--this sort of natural immunity was not observed. As cell modifications with TNBS and CF3-DNBS have previously been shown to cross-react in purely cellular immunity tests, the striking difference observed here was tentatively attributed to differential sensitivity to serum-borne factors which mediate this in vivo natural resistance. These factors are likely to be naturally occurring anti-trinitrophenyl antibodies. Contrastingly, if TNBS- and CF3-DNBS-modified splenocytes were injected into either anti-TNBS or anti-CF3-DNBS immunized mice, the modification of radioactivity recovery and L/S indexes (compared to those in non-immunized controls) was always greater in the case of the CF3-DNBS cells. It is concluded that, of these two cross-reacting cell surface modifying treatments, one (TNBS) is sensitive both to natural and reinforced immunity, whereas the second (CF3-DNBS) is sensitive only to reinforced immunity. As we have previously shown in vitro, that CF3-DNBS-modified cells do not seem to be sensitive to cytotoxic antibodies, we believe that the in vivo immune rejection observed is essentially a cell-mediated reaction, whereas the natural immunity is mainly a serum-dependent reaction.

Animals↗

PubMed1981

Suppression of contact hypersensitivity in mice by ultraviolet irradiation is associated with defective antigen presentation.

A single dose of radiation from FS40 sunlamps results in systemic depression of delayed-type hypersensitivity (DTH) to 2-chloro-1,3,5-trinitrobenzene (TNCB) and 1-fluoro-2,4-dinitrobenzene (DNFB). Immunosuppression is proportional to the log10 dose of radiation and exhibits a delayed time course. Animals sensitized one day after ultraviolet (u.v.) treatment respond normally, but sensitization 3-15 days after treatment results in about 70% suppression of the DTH response. The dose response of DTH in normal and u.v.-treated animals to 1,3,5-trinitrophenyl (TNP) conjugated adherent splenocytes from normal or u.v.-treated donors was investigated. When normal mice were immunized with TNP-conjugated adherent splenocytes from normal or u.v.-treated donors, a DTH response could be elicited in these animals by injection of TNP-conjugated splenocytes into the ear. However, u.v.-irradiated recipients could not be sensitized by TNP-conjugated adherent cells from u.v.-treated mice but were sensitized by such cells from normal mice. Lysed, TNP-conjugated, normal adherent splenocytes did not immunize u.v.-irradiated recipients, but did immunize normal recipients. These results confirmed that antigen presentation is deficient in u.v.-treated mice. The time of appearance of the antigen-presenting defect in the spleen cells of u.v.-treated mice was the same as for the depression of contact sensitivity, strengthening the evidence for a causal relationship between defective antigen presentation and depression of contact sensitivity.

Animals↗

PubMedDate not supplied

[Photophysics of complex formations between chlorophyll a and its analogs with pi acceptors].

Efficient quenching of fluorescence was shown to proceed in the complexes of chlorophyll a and its analogs with tetracyanochinodimethane (TCD), 1,3,5-trinitrobenzene (TNB), m-dinitrobenzene (DNB) and n-benzoquinone. In chlorophyll a--TCD and--DNB complexes quenching is characterized by the rate constant approximately greater than 5 x 10(10) s-1, and in chlorophyll a--n-benzoquinone greater approximately than 5 x 10(9) s-1. Possible ways of desactivation of singlet-excited state of chlorophyll a in the complexes with TCD and TNB were analysed. No triplet states of chlorophyll a complexes with TCD and TNB and no cation-radicals were recorded. It is suggested that efficient desactivation of the pigment singlet-excited state may be explained by a reversible phototransfer of the electron.

Benzoquinones↗

PubMed1981

The goldfish immune response. I. Characterization of the humoral response to particulate antigens.

Anti-red blood cells (RBC) and anti-hapten antibody synthesis were studied in the goldfish, Carassius auratus. Spontaneous haemagglutination titres were found against all the antigens tested. A weak secondary response was observed in RBC-primed fish boosted during the end-phase of the primary antibody production. However, when the second antigenic challenge was performed during the early exponential phase of a primary stimulation, an important amplified response was obtained. The antibody production and immunological memory can be dissociated: no antibody synthesis occurred in glutaraldehyde-fixed RBC (F-RBC) primed was obtained when untreated or F-RBC were given to F-RBC primed animals. The amplified response to sheep red blood cells (SRBC) was significantly inhibited when fish were primed with a mixture of SRBC and Xenopus red blood cells (XRBC), demonstrating an antigenic competition phenomenon. Studies on anti-trinitrobenzene responses confirm the efficiency of E. coli lipopolysaccharide as a carrier for fish anti-hapten immunization. The kinetics and regulation of antibody synthesis in fish are discussed in relation to the described results.

Animals↗

PubMed1994

Class pi glutathione S-transferase: Meisenheimer complex formation.

The enzyme-catalysed formation of the dead-end Meisenheimer complex, 1-(S-glutathionyl)-2,4,6-trinitrocyclohexadienate, between glutathione and 1,3,5-trinitrobenzene by two class pi glutathione S-transferases was studied under equilibrium conditions. The apparent formation constant of the complex at pH6.5, is 1.21 x 10(3) M-1 and 1.47 x 10(3) M-1 for isoenzyme pGSTP1-1 from porcine lung and hGSTP1-1 the human recombinant orthologue, respectively. These values are about 40- to 50-times larger than that determined for the nonenzymatic reaction in solution. Competitive inhibitors in the form of glutathione analogues that bind the G-site (glutathione sulphonate) or both the G-site and the H-site (S-hexylglutathione) regions of the active site markedly diminish complex formation. Comparison of kinetic data for glutathione S-transferase isoenzymes from the pi and mu gene classes suggests that the catalytic efficiencies for nucleophilic aromatic substitution reactions correspond with the ability of the enzyme's active site to stabilise the Meisenheimer complex. Formation of the red-coloured complex in orthorhombic crystals of pGSTP1-1 demonstrated that the crystallized protein retains its catalytically functional conformation in the crystal lattice.

Animals↗