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At least 19 recordsLinked to original sources
PubMed1978

Urinary catecholamine excretion and blood sugar response during acute poisonings with dinitrobenzenes.

Rats were injected intraperitoneally with 0.015 mmol of p-dinitrobenzene/kg, 0.15 mmol of m-dinitrobenzene/kg and 0.45 mmol of o-dinitrobenzene/kg body wt. The dinitrobenzenes induced methaemoglobin concentrations of 86%, 60% and 49%, respectively, as well as increases of urinary catecholamine excretion and blood sugar concentration. Due to hyperglycaemia the glycolysis may be stimulated as mechanism for energy production in methaemoglobin-induced oxygen deficiency and as mechanism for reduction of methaemoglobin, that means as responses favouring survival after poisoning.

Animals↗
PubMed1992

Functional/metabolic modulation of the brain stem lesions caused by 1,3-dinitrobenzene in the rat.

To determine whether neuronal activity plays a role in the localisation of brain stem lesions in 1,3-dinitrobenzene intoxication we produced asymmetrical changes in auditory input by rupturing the left tympanic membrane in Fischer rats. This raised the auditory threshold on that side from 57-63 dB to 104-122 dB. It also decreased glucose utilisation in the ipsilateral cochlear nucleus and significantly increased utilisation in the contralateral nucleus, resulting in a relative deficit of 72 +/- 6%. Similarly, tympanic membrane rupture led to decreased glucose utilisation in the contralateral and increased utilisation in the ipsilateral inferior colliculus. Additional exposure to "white noise" prevented the decrease in glucose utilisation in the contralateral inferior colliculus. Dosing with dinitrobenzene (10 mg/kg in 4 doses over 48 hr) to otherwise normal rats produces symmetrical vasculonecrotic lesions in these regions, but in animals with left tympanic membrane rupture the severity of morphological changes in the ipsilateral cochlear nucleus and the contralateral inferior colliculus were substantially reduced. Additional exposure to "white noise" increased the degree of damage in the ipsilateral cochlear nucleus and contralateral inferior colliculus. These findings indicate that altered auditory function in rats, with its associated metabolic consequences exercises a significant role in the development of brain stem damage in auditory pathways following dinitrobenzene intoxication.

Acoustic Stimulation↗
PubMed1978

Two-step modification of aspartate aminotransferase with 1,5-difluoro-2,4-dinitrobenzene. Cross-link localization.

At pH 7, the apoenzyme of carboxymethylated and acylated aspartate aminotransferase reacts selectively with 1,5-difluoro-2,4-dinitrobenzene to form a single intramolecular covalent bond with the epsilon-amino group of the functional lysine residue located within the active centre. On shifting the pH to 9, the second fluorine atom of the bifunctional reagent is substituted with the sterically adjacent side groups of cysteine and tyrosine residues. The modified apoenzyme was subjected to partial proteolysis with pronase, and the digest was used to obtain and isolate the labeled products and to localize amino acid residues involved in the reaction. The established structures of several peptides containing Cys-2,4-dinitrobenzene-Lys and Tyr-2,4-dinitrobenzene-Lys allowed the identification of the amino acid residues involved in the reaction with the bifunctional reagent as Lys 258, Cys 390 and probably Tyr-70. The residues of Cys and Tyr are thus located at a distance of approximately 5 A (the length of the dinitrophenylene bridge) from the lysine residue forming an aldimine bond with pyridoxal 5'-phosphate in the active site.

Animals↗
PubMed1992

The metabolism of 1,3-dinitrobenzene by rat testicular subcellular fractions.

The metabolism of 1,3-dinitrobenzene by rat testicular subcellular fractions (microsomes, cytosol or 9000 x g supernatant (S-9)) was studied. The effects of NADPH, oxygen, glutathione (GSH) and carbon monoxide upon the rate of metabolism were determined. Three metabolites were identified, and characterised as 3-nitrosonitrobenzene, 3-nitrophenylhydroxylamine and 3-nitroaniline by co-chromatography with authentic standards. These findings indicate the presence of an inherent enzyme system capable of facilitating nitro-reduction in the testes. The implications of these findings to the mechanism of 1,3-DNB-induced testicular toxicity are discussed.

Animals↗
PubMed1976

The use of 1-fluoro-2,4-dinitrobenzene as an affinity label for the antigen receptor of delayed hypersensitivity.

The passive transfer of delayed contact sensitivity to dinitrophenyl can be specifically inhibited by brief treatment of lymph node cells (LNC) from sensitized guinea-pigs with 1-fluoro-2,4-dinitrobenzene (DNFB). Analysis of KC1 extracts of LNC previously treated with (3H)DNFB, using polyacrylamide gel electrophoresis, revealed a peak of radioactivity present in both sensitive and normal cell extracts as well as a peak found only in sensitive cell extracts. Cell-free extracts appeared capable of transmitting delayed-onset skin reactivity to non-sensitized recipients.

Affinity Labels↗
PubMed1975

Motor nerve conduction velocity after carbon monoxide or m-dinitrobenzene poisoning following elimination of the poisons.

24 hrs after acute carbon monoxide or m-dinitrobenzene poisoning (about 60% CO-Hb or Met-Hb) the sciatic motor conduction velocity of rats is significantly reduced by 33% and 16% respectively. Whereas 48 hrs after methemoglobinemia the nerve conduction is normal, a retardation is detectable even 4 weeks following carboxyhemoglobinemia. Also, 4 weeks after single carbon monoxide intoxication producing a mean CO-Hb content of 19%, the motor conduction velocity is significantly decreased. This effect may be useful for detection of carbon monoxide intoxication after elimination of the poison. The results show that there are carbon monoxide effects independent of blockade of hemoglobin.

Animals↗
PubMed1979

Normal-phase high-performance liquid chromatographic determination of neomycin sulfate derivatized with 1-fluoro-2,4-dinitrobenzene.

A high-performance liquid chromatographic (HPLC) assay method has been developed for quantifying neomycin sulfate powders and ointments containing neomycin. A dinitrobenzene derivative of neomycin is formed and then chromatographed isocratically on a normal-phase system. Neomycin B and C and be separated and quantified with a relative standard deviation of approximately 1%. When monitored at 350 nm, the method is sensitive to about 1 ng of neomycin base per column injected. Gradient elution and isocratic HPLC methods for the analysis of derivatized neamine have also been developed. The relative standard deviation is less than 1% for the isocratic method. The HPLC method is applicable to the analysis of other aminoglucoside antibiotics.

Chromatography, High Pressure Liquid↗
PubMed1977

H-2 restriction of suppressor T-cell induction by hapten-modified lymphoid cells in tolerance to 1-fluoro-2,4-dinitrobenzene contact sensitization.

Studies using hapten-modified lymphoid cells as tolerogens for 1-fluoro-2,4-dinitrobenzene contact sensitization have shown that BALB/c(H-2d) mice can be made phenotypically tolerant by dinitrophenyl (DNP) on either syngeneic or allogeneic mouse lymphoid cells (DNP-LC). However, suppressor T-cell induction (Ts) in these mice (as demonstrated by adoptive transfer to syngeneic recipients) was restricted to H-2 identity between the DNP-LC and the donor mouse. It was also shown that identity at the right end of the H-2 complex was sufficient for Ts induction. In addition, this restriction was also demostrated in CBA (H-2 K) mice and for tolerance in the 1-chloro-2,4,6-trinitrobenzene contact sensitivity system using trinitrophenyl-modified lymphoid cells.

Animals↗
PubMed1979

Active suppression of 1-fluoro-2,4-dinitrobenzene-immune T cells. Requirement of an auxiliary T cell induced by antigen.

We investigated T-T cell interactions in the suppression of contact sensitivity. Suppressor cells that block the efferent limb of sensitivity (Ts-eff) can inhibit the passive transfer of contact sensitivity mediated by 1-fluoro-2,4-dinitrobenzene immune cells (T DH). But, Ts-eff cannot block the passive transfer of TDH which comes from cyclophosphamide (Cy) pretreated sensitized mice. We interpret these results to indicate that lymph node cells from sensitized mice contain not only TDH but also another intermediate cell which is required for the suppression of TDH by Ts-eff. This intermediate cell is sensitive to cyclophosphamide and requires antigen activation for its development. It is sensitive to adult thymectomy and anti-brain associated theta serum and is therefore designated as an auxiliary T-suppressor cell (Ts-aux). It is not sensitive to splenectomy and it carries I-J determinants. Ts-aux are required for the activity of suppressors of the efferent limb (Ts-eff) but not of suppressors of the afferent limb (Ts-aff). Thus, in the feedback loops in contact sensitivity, the generation of Tdh is coordinated with the development of auxiliary Ts which are essential for the suppression of those TDH.

Animals↗
PubMed1978

Reaction of tRNAPhe from yeast with 1-fluoro-2,4-dinitrobenzene. Attachment sites of the potential antigenic-determining 2,4-dinitrophenyl residues.

The reaction of 1-fluoro-2,4-dinitrobenzene with tRNAPhe from yeast, for the introduction of antigenic-determining 2,4-dinitrophenyl residues into tRNA, took place only at adenosine residues in tRNAPhe. After reaction at pH 8.0 and 50 degrees C two kinds of products were detected: one was ribose-modified adenosine which was derived from the 3' terminus of tRNA, and the other was base-modified adenosine. The sites and extent of the modification of each particular adenosine residue of tRNAPhe were determined as follows: 5 (6% modified), 31 (2%), 35 (36%), 67 (5%), and 76 (51%). Thus mainly the terminal adenosine and one adenosine in the anticodon loop bear the 2,4-dinitrophenyl residue.

Base Sequence↗
PubMed1975

Subcellular fractions from dermis and epidermis in contact sensitization of guinea pigs to 1-chloro-2,4-dinitrobenzene.

Subcellular fractions were prepared from the epidermis of guinea pigs which had been painted with 1-chloro-2,4 dinitrobenzene 14 h previously. The microsomal fraction showed less activity than other fractions in the MIF test. Similarly, the microsomal fraction from the dermis of skin irritated with croton oil before DNCB painting was relatively inactive. However, the microsomal fractions from the epidermis and more especially from the dermis of skin painted with DNCB while undergoing allergic contact dermatitis from pentadecylcatechol showed significant MIF activities.

Alkanes↗
PubMed1978

[Mechanical characteristics of isotonic work and high-energy phosphates in frog ventricle after 1-fluoro-2,4-dinitrobenzene].

The blocking of the creatinphosphokinase by 1-fluoro-2,4-dinitrobenzene (FDNB) allows to investigate the relationship between ATP-supply, contractility and relaxability of the frog's myocardium. In isotonically working isolated ventricles of frogs the time of work, systolic and diastolic volume, velocity of contraction and relaxation as well as the levels of CP, ATP, ADP and AMP were measured at different intervals until termination of each experiment. CP shows a small variation, ATP decreases to 60% and ADP + AMP increase for the same amount under FDNB during the development of a slight inhibition of contractility and a continuously growing inhibition and retardation of relaxation until systolic arrest. ATP content and volume of relaxation correlated strictly. The contracture and the diminished contractility are caused by the decrease of ATP, producing a lack of substrate for Ca transport and actin-myosin-ATPase. This models the course of events during an insufficiency like in angina pectoris and in myocardial infarction.

Adenine Nucleotides↗
PubMed1978

Genetic restrictions for the induction of suppressor T cells by hapten-modified lymphoid cells in tolerance to 1-fluoro-2,4-dinitrobenzene contact sensitivity. Role of the H-2D region of the major histocompatibility complex.

Genetic restrictions governing the induction and expression of suppressor T cells (Ts) in tolerance to 1-fluoro-2,4-dinitrogenzene (DNFB) contract sensitivity were studied. Tolerance was induced by using 2,4-dinitrophenyl (DNP)-modified lymphoid cells (DNP-LC) as tolerogen. Two kinds of Ts were found-those produced by DNP-LC syngeneic to the donor of the Ts (syninduced Ts), and those produced by DNP-LC allogeneic to the donor of Ts (alloinduced Ts). Studies employing congenic resistant mouse strains indicated that recognition of DNP-modified-major histocompatibility region determinants on the tolerogenic DNP-LC was essential for the induction of both types of Ts. Non-H-2 genetic background was irrelevant to Ts induction. Mapping studies indicated that induction of both syninduced and alloinduced Ts was associated with recognition of DNP-modified-MHC region determinants which map to the right of the H-2G region (i.e., H-2D gene products). Tolerization of donor mice with DNP-LC which were H-2D region compatible, but not with H-2K or I region compatible DNP-LC, was both sufficient and required for the induction of hapten-specific syninduced Ts. Tolerization of donor mice with DNP-LC which were incompatible only at the H-2D region was sufficient for the induction of alloinduced Ts. These Ts were capable of suppressing recipient mice only if the recipients shared the H-2D region with the strain providing the DNP-LC tolerogen, and were not capable of suppressing recipients sharing all but the H-2D region with the tolerogen.

Animals↗
PubMedDate not supplied

Strikingly different effects of dinitrobenzene sulfonic and trinitrobenzene sulfonic acids on various subpopulations of murine lymphoid cells.

Different changes according to T- or B-cell origin occur in dinitrophenyl (DNP)- and trinitrophenyl (TNP)-modified lymphoid cells. The electrophoretic mobility (EPM) or nylon-wool adherent splenic cells (B cell-enriched) modified by TNP and DNP and that of nylon-wool non-adherent splenic cells (T cell-enriched) and thymic cells modified by TNP increase respectively as follows: +24%, +20%, + 6%, and +16%. A relation has been found between these EPM amounts and amino groups which are positively charged on cell surface. The EPM decreases in the case of nylon-wool non-adherent splenic cells (T cell-enriched, -9%) and thymic cells modified by DNP (-4%). The hydrophobic fluorescent probe 1-anilino-8-naphthalene sulphonate used to study conformational changes of cells revealed a slight fluorescence decrease for TNP-modified cells (-11% for thymic cells, -38% for T cells of spleen, and -66% for B cells of spleen), and a fluorescence increase for DNP-modified cells. This fluorescence increase is more important for spleen T cells (+130%) and thymic cells (+233%) than for spleen B cells (+30%).

Animals↗