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At least 343 records · Page 19Linked to original sources
PubMed1979

Effect of intestinal gamma-glutamyl transferase inhibitor on the amount of gamma-glutamyl metabolites in mouse.

Experimental mice fed a balanced rodent chow, called LSM fodder, had markedly lower gamma-glutamyl transferase activity in the epithelium of intestinal villi then control mice fed wheat. After oral administration of gamma-14C-glutamyglycine, oxidized 14C-glutathione or gamma-glutamyl-p-amino-benzoate the amounts of gamma-glutamyl substrates and their metabolites in intestines, livers and kidneys of experimental mice were significantly lower than those in control mice. L-serine simultaneously administered with gamma-14C-glutamylglycine reduced the radioactivity of gamma-glutamyl substances in organs of the control mice. No differences in organ radioactivity of experimental and control mice were observed when some uniformly labeled with 14C amino acids were given. The obtained results are not in aggreement with hypothesis on a role of gamma-glutamyl transferase in amino acid transport.

4-Aminobenzoic Acid↗
PubMed1981

[Splitting activity of gastrointestinal mucosa using paba-peptide as a substrate (author's transl)].

Splitting activity of gastrointestinal mucosa was investigated by using N-benzoyl-L-tyrosyl-p-aminobenzoicacid (PABA-peptide) in 24 surgical materials obtained from all parts of the human gastrointestinal section. The highest activity was found in the adult jejunum (2.92-4.72 mIE/cm2 intact mucosa). The splitting activity of homogenates, prepared from correspondingly sized mucosa, always was 3-5 times higher than that of the intact mucosa; it was totally inhibited by NCDC, a specific inhibitor for chymotrypsin. The solid linkage and probably also the accumulation of very stable chymotrypsin on the mucosa seem to be responsible for the low sensitivity of the Pabapeptide-test. It is possible that the specificity of this test is considerably influenced by the dependency of the linkage capacity on the morphological structure of the mucosa.

4-Aminobenzoic Acid↗
PubMed1984

[Effects of krestin and p-aminobenzoic-N-xyloside sodium salt on activities of drug-metabolizing enzymes and glutathione-related enzymes in rat liver].

Effects of krestin (PSK) and p-aminobenzoic-N-xyloside sodium salt (K-247) (both products of Kreha Chemical Co., Japan) on activities of drug-metabolizing enzymes and glutathione (GSH)-related enzymes were investigated in rat liver. When PSK was administered at a dose of 100 mg/kg body weight, ip every day for 7 or 14 days, the action of UDP-glucuronyltransferase (UDP-GT) on o-aminophenol (o-GT) and those of GSH S-transferase (GST) on both 1, 2-dichloro-4-nitrobenzene ( DCNB ) and 1-chloro-2, 4-dinitrobenzene (CDNB) slightly increased together with increased activities of GSH-peroxidase on both H2O2 and cumene hydroperoxide, were as GSH levels were decreased. When PSK or K-247 was administered at 1% in diet for 4 or 8 weeks, o-GT activity and GST activities with both substrates increased on K-247 feeding, while GST activity for CDNB decreased on PSK and K-247 feedings. These changes were statistically significant but very small. The content of P-450 and the activity of gamma-glutamyl transpeptidase changed little in any administration schedules mentioned above.

4-Aminobenzoic Acid↗
PubMed1981

[Diaplacental influence on the disseminated intravascular coagulation (DIC) in an asphyxia model. II. Influence on the vessel's content (author's transl)].

There is reported on the possibilities of diaplacental influencing on the DIC arising from the hypoxia we provoked with the help of an asphyxia model in rabbit fetuses. We could demonstrate the impossibility of influencing on the fetal vasal content by means of low molecular dextran, heparin or streptokinase. On the contrary, the possibility exists to influence on the fetal hemostasis by low molecular synthetic substances. The antifibrinolytic drug PAMBA causes in case of advanced acidosis diaplacental a definite growth of the intravascular coagulation, as well. But an inhibition of the fibrin sedimentation in the terminal vessels at the asphyctic shock can be achieved by applying the ethyl ester of the 4-amidinophenylpyruvic acid (APPA).

4-Aminobenzoic Acid↗
PubMed1981

[Animal experiments on direct drug effects on disseminated intravascular coagulation (DIC) in asphyxic shock].

In a total of 41 rabbit fetus it could be demonstrated in an asphyxia model to what extent disseminated intravascular coagulation may be influenced by directly applying drugs in the foetal circulation. Administration of heparin or streptokinase in the umbilical vessels led to a decrease of fibrin sediments in the areas of terminal coagulation, whereas an increase was caused by injecting noradrenalin or PAMBA.

4-Aminobenzoic Acid↗
PubMed1982

[Experimental studies on the diffusion of antifibrinolytic agents in fibrin thrombi. A contribution to intrathecal antifibrinolytic therapy in subarachnoid hemorrhages].

The diffusion behaviour and the diffusion coefficients of antifibrinolytics in fibrin thrombi were determined by in vitro incubating attempts with tritium marked compounds of PAMBA, AMCA, and ECA as well as by chromogenic substrate determination for contrykal. The great diffusion ability of PAMBA supports the usefulness of intrathecal therapy of subarachnoidal bleeding for blocking endogenous fibrinolysis, whereas the exogenous fibrinolysis of the fibrin thrombus closing aneurysm is inhibited by the intrathecal application.

4-Aminobenzoic Acid↗
PubMedDate not supplied

Inosiplex: metabolism and excretion of the dimethylaminoisopropanol and p-acetamidobenzoic acid components in rhesus monkeys.

The principal excretion products derived from radiolabeled N,N-dimethylaminoisopropanol (Dip) and p-acetamidobenzoic acid (PAcBA) components of inosiplex (Isoprinosine) were identified and quantified in urine following single iv and oral administration of the drug in rhesus monkeys. The major metabolite derived from [3H] PAcBA was identified as PAcBA-O-acylglucuronide by 1) positive naphthorescorcinol reaction for glucuronic acid and 2) hydrolysis of the metabolite to PAcBA and glucuronic acid, using either dilute base (but not acid) or beta-glucuronidase. This metabolite accounted for 50% of the administered dose in orally dosed animals and 31% in iv dosed animals. A minor metabolite, which constituted approximately 5% of the excreted 3H from either iv or orally dosed animals, was identified as the hippuric acid conjugate of PAcBA by co-chromatography with a commercial standard. A single metabolite derived from [14C]Dip was identified as Dip-N-oxide by co-chromatography with synthetic material in several chromatographic systems; this metabolite accounted for 17 to 18% of the administered 14C in either the iv or orally dosed animals.

4-Aminobenzoic Acid↗
PubMed1984

A possible explanation of mechanisms inducing inhibition of vascularization of tumours by antifibrinolytic drugs--the influence of migratory behaviour of endothelial cells.

The observation that administration of antifibrinolytic drugs results in tumour growth stasis, having possibly its origin in reduced vascularization of the tumour, led us to investigate the migratory behaviour of bovine endothelial cells under in vitro conditions in the presence of drugs known to influence the activity of fibrinolytic enzymes. The Boyden-technique and microcinematography were used for this analysis. It could be shown that aprotinin, an inhibitor of serine proteinases and para-methylaminobenzoic acid, a specific inhibitor of plasminogen activation and plasmin action greatly reduced the migratory rate of the cells. Streptokinase, a plasminogen activator, stimulated the cell migration in optimal concentrations. The authors hypothesize that tumour vascularization is initiated by immigration of endothelial cells into the tumour by fibrinolytic action following a fibrin gradient induced by the tumour themselves. Fibrinolytic inhibitors suppress this process.

4-Aminobenzoic Acid↗
PubMed1984

Inhibitors of poly(ADP-ribose) synthesis enhance X-ray killing of log-phase Chinese hamster cells.

Postirradiation incubation of V79 Chinese hamster cells with inhibitors of poly(ADP-ribose) synthesis was found to potentiate the killing of cells by X rays. Potentiation increased with incubation time and with concentration of the inhibitor. Preirradiation incubation had only a small effect. The enhanced response correlated well with the known extent of the inhibition of poly(ADP-ribose) synthesis. A radiation-sensitive line, V79- AL162 /S-10, was affected to a lesser extent than the normal cells. Cells repaired the radiation damage with which the inhibitors interacted within 1 hr, a process that has similar kinetics to what is observed when a postirradiation treatment with hypertonic buffer is used [H. Utsumi and M. M. Elkind , Radiat . Res. 77, 346-360 (1979)]. However, the sectors of damage affected by inhibitors of poly(ADP-ribose) synthesis and hypertonic buffer do not entirely overlap. The inhibitor nicotinamide enhanced the killing mainly of late S-phase cells and did not affect cells at the G1/S border. It is concluded that the repair process(es) involving poly(ADP-ribose) synthesis is important for cell survival in repair-competent cells and that the radiation-sensitive cells that were examined are partially deficient in a repair pathway in which poly(ADP-ribose) participates.

4-Aminobenzoic Acid↗