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Biomedical subjects

G Tóth

Publications and source records attributed to G Tóth.

At least 163 records · Page 9Linked to original sources
PubMed1985

Neocortical cytopathology in focal aminopyridine seizures as related to the intracortical diffusion of [3H] 4-aminopyridine. Electrophysiologic and light-microscopic studies.

Focal seizure was induced in rat and cat neocortex by the topical application of aminopyridines. The epileptic character of the focal events was followed by surface and intracellular recordings of seizure activity. The pathologic alterations in the neurons, the glial cells, and the protein permeability of the neocortical blood vessels were investigated by means of light microscopy, using standard histological stainings and immunohistochemical detection of endogenous serum albumin. Diffusion of [3H] 4-aminopyridine in the neocortex was studied by light-microscopic autoradiography. The spreading of the neuropathologic changes strictly followed the diffusion of the tritiated compound, suggesting the gradual involvement of neocortical layers in the seizure process.

4-Aminopyridine↗
PubMed1985

Characterization of rat brain opioid receptors by [Tyr-3,5-3H]1, D-Ala2, Leu5-enkephalin binding.

[Tyr-3,5-3H]1, D-Ala2, Leu5-enkephalin [( 3H]DALA) was used for labeling the opioid receptors of rat brain plasma membranes. The labeled ligand was prepared from [Tyr-3,5-diiodo]1, D-Ala2, Leu5-enkephalin by catalytic reductive dehalogenation in the presence of Pd catalyst. The resulting [Tyr-3,5-3H]1, D-Ala2, Leu5-enkephalin had a specific activity of 37.3 Ci/mmol. In the binding experiments steady-state level was reached at 24 degrees C within 45 min. The pseudo first order association rate constant was 0.1 min-1. The dissociation of the receptor-ligand complex was biphasic with k-1-s of 0.009 and 0.025 min-1. The existence of two binding sites was proved by equilibrium studies. The high affinity site showed a KD = 0.7 nM and Bmax = 60 fmol/mg protein; the low affinity site had a KD = 5 nM and Bmax = 160 fmol/mg protein. A series of opioid peptides inhibited [3H]DALA binding more efficiently than morphine-like drugs suggesting that labeled ligand binds preferentially to the delta subtype of opioid receptors. Modification of the original peptides either at the C or N terminal ends of the molecules resulted in a decrease in their affinity.

Animals↗
PubMed1985

[Stimulatory effect of vitamin A on T and B lymphocytes in experimental ascariasis in pigs].

The nonspecific, stimulative effect of vitamin A, applied per os, was studied on the T and B cell population in the course of post-invasive, migratory phase of experimental ascariasis of swine. The vitamin under study was found to exert an activating influence on the level of both immunocompetent cells already in the early phase of invasive process, with the maximum on the 9th, and/or 12th day after invasion. The protective effect of vitamin A, i. e. the effect on the reduction of migrating larvae of ascarids in the lungs, was 50%. This phenomenon is in accord with the present knowledge on the role of this vitamin in immunity.

Animals↗
PubMed1984

Further analysis of the effects of cholecystokinin octapeptides on avoidance behaviour in rats.

Experiments were performed to examine the acute effects of cholecystokinin octapeptides and fragments on the active and passive avoidance behaviour of rats following peripheral and central administration. Both the sulphated (CCK-8-SE) and non-sulphated cholecystokinin octapeptide (CCK-8-NS) and also the COOH-terminal tetra-, penta-, hexa- and heptapeptides of cholecystokinin octapeptide facilitated the extinction of active avoidance behaviour and retention of passive avoidance behaviour. This latter effect of cholecystokinin octapeptides was reversed by anxiolytic chlordiazepoxide pretreatment, showing that in these test situations cholecystokinin octapeptides are able to modify fear-motivation or arousal of the animals; their effect is at least partly similar to that of the neuroleptic substance haloperidol. Subcutaneous treatment with CCK-8-SE or CCK-8-NS appeared to be 3-10 times more effective than intraperitoneal treatment. Following intracerebroventricular administration, 100-300 times lower doses were needed to cause a behavioural effect similar to that after subcutaneous injection. Microinjection of CCK-8-SE or CCK-8-NS in the fmol dose range into the nucleus accumbens facilitated the extinction of active avoidance behaviour and attenuated the retention of passive avoidance behaviour, while microinjection of these peptides into the central amygdaloid nucleus caused opposite effects on these behavioural tests. It seems that the neuroleptic-like effects of cholecystokinin octapeptides are mediated through the nucleus accumbens, and the opposite action (non neuroleptic-like) through the central amygdaloid nucleus.

Amygdala↗
PubMed1984

Interrelationships between the membrane-bound ATP-dependent energy systems of the gastric mucosa and the gastric cytoprotective effect of beta-carotene on the development of gastric mucosal damage produced by 0.6 M HCl in rats.

The effects of different doses (0.01-0.1-1.0-10.0/mg/kg-1) of beta-carotene were studied on gastric secretory responses of 4 hr pylorus-ligated rats: development of gastric mucosal damage (as assessed by number and severity of lesions) produced by intragastric administration of 0.6 M HCl; tissue level of adenosine triphosphate (ATP), adenosine diphosphate (ADP), adenosine monophosphate (AMP), adenylate pool (ATP + ADP + AMP), ratio of ATP X ADP-1, "energy charge" (ATP + 0.5 ADP X X (ATP + ADP + AMP)-1) (during the development of gastric mucosal damage by 0.6 M HCl and of gastric cytoprotection by beta-carotene. It was found that beta-carotene did not decrease the gastric secretory responses of 4 hr pylorus-ligated rats; The development of gastric mucosal damage could be decreased dose-dependently by the administration of beta-carotene; the ATP transformation could be decreased by beta-carotene; the tissue levels of cAMP and AMP could be increased significantly and dose-dependently by beta-carotene; the ratio of ATP X ADP-1 could be increased significantly and dose-dependently by beta-carotene; the values of adenylate pool and "energy charge" remained unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphate↗
PubMed1984

Interrelationships between the gastric cytoprotective effects of vitamin A and beta-carotene and the gastric mucosal superoxide dismutase activity in rats.

Gastric mucosal damage was produced in rats by the intragastric administration of 96% ethanol or 0.6 M HCl, according to the method of Robert et al. Vitamin A or beta-carotene, in doses of 10 mg/kg, given intragastrically 30 min before the administration of the necrotizing agents. The animals were killed 1 hr after the administration of the necrotizing agents. The following experimental parameters were studied, without and with application of vitamin A and beta-carotene; number of gastric lesions (ulcers); severity of gastric mucosal lesions (ulcers); gastric mucosal superoxide dismutase (SOD) activity. It was found that; vitamin A and beta-carotene, in doses of 10 mg/kg, are able to prevent significantly both the number and severity of gastric mucosal lesions (ulcers) produced by the application of 96% ethanol or 0.6 M HCl; the significant increase of ethanol-induced gastric mucosal SOD activity can be inhibited by the application of vitamin A and beta-carotene; vitamin A and beta-carotene are capable of preventing the development of gastric mucosal lesions (ulcers) produced by the intragastric administration of 0.6 M HCl, while these agents fail to compensate for the HCl-induced decrease of gastric mucosal SOD activity. It has been suggested that; vitamin A and beta-carotene are gastric cytoprotective agents; the ulcer preventive effects of vitamin A and beta-carotene are partly dependent on their scavanger behaviour.

Animals↗
PubMed1984

Determination of vitamin A, vitamin A precursors and cytoprotective carotenoids in animal and human blood.

In the past few years, considerable progress has been made in the investigation of the function of retinoids and carotenoids in higher animals and human including their role in cytoprotection. This has resulted in a considerable development in the analytical methods in the field of carotenoids and retinoids in biological materials. We have developed a method for the qualitative and quantitative determination of retinol and carotenoids in animal and human blood, using straight-phase liquid chromatography. Details of this work are presented jointly with a brief review of other analytical methods of these compounds.

Animals↗
PubMed1983

[1,6-alpha-aminosuberic acid, 3-(p-azidophenylalanine), 8-arginine] vasopressin: a new photoaffinity label for hydroosmotic hormone receptors. Characterization of the ligand and irreversible stimulation of hydroosmotic water flow in toad bladder by photoaffinity labeling.

The photoreactive analog of vasopressin [1,6-alpha-aminosuberic acid, 3-(p-azidophenylalanine), 8-arginine] vasopressin [( Asu1,6, Phe (p-N3)3]AVP) has been synthesized. This analog retains a high binding affinity for the vasopressin receptor in plasma membranes from bovine kidney inner medulla (apparent dissociation constant, KD = 8.5 X 10(-9) M). [Asu1,6, Phe (p-N3)3] AVP was found to be biologically active in triggering the characteristic increase in toad bladder permeability to water. Photolysis of the analog in the presence of the toad bladder results in a hydroosmotic response which persists, in spite of repeated washings, for more than 18 h. The irreversible stimulation of the bladder is inhibited when photolysis is carried out in the presence of vasopressin. Our findings indicate that with photoactivation [Asu1,6, Phe(p-N3)3]AVP binds covalently to hormonal receptors and forms an active hormone-receptor complex. This analog, therefore, is a suitable tool for studies of hydroosmotic receptor function and for receptor isolation.

Affinity Labels↗
PubMed1983

Structure-activity and dose-effect relationships of the antagonism of picrotoxin-induced seizures by cholecystokinin, fragments and analogues of cholecystokinin in mice.

Intraperitoneal administration of cholecystokinin octapeptide sulphate ester (CCK-8-SE) and nonsulphated cholecystokinin octapeptide (CCK-8-NS) enhanced the latency of seizures induced by picrotoxin in mice. Experiments with N- and C-terminal fragments revealed that the C-terminal tetrapeptide (CCK-5-8) was the active centre of the CCK octapeptide molecule. The analogues CCK-8-SE and CCK-8-NS (dose range 0.2-6.4 mumol/kg) and caerulein dose range 0.1-0.8 mumol/kg) showed bell-shaped dose-effect curves, with the greatest maximum inhibition for CCK-8-NS. The peptide CCK-5-8 had weak anticonvulsant activity in comparison to the octapeptides, 3.2 mumol/kg and larger doses of the reference drug, diazepam, totally prevented picrotoxin-induced seizures and mortality. The maximum effect of the peptides tested was less than that of diazepam. Experiments with analogues and derivatives of CCK-5-8 demonstrated that the effectiveness of the beta-alanyl derivatives of CCK-5-8 were enhanced and that they were equipotent with CCK-8-SE. Of the CCK-2-8 analogues, Ser(SO3H)7-Ac-CCK-2-8-SE and Thr(SO3H)7-Ac-CCK-2-8-SE and Hyp(SO3H)-Ac-CCK-2-8-SE were slightly more active than CCK-8-SE.

Animals↗
PubMed1983

(3H)-imipramine binding and plasmid replication sites in Escherichia coli.

Binding of (3H)-imipramine to F'lac plasmid-carrying E.coli was studied. The binding was saturated at 500 mM imipramine in the case of F'lac cells, and the imipramine binding of plasmid-carrying bacteria was inhibited by several tricyclic compounds, such as acridine orange, desimpramine and promethazine. Methylene blue enhanced the (3H)-imipramine binding of bacteria. Binding of radioactively labelled pBR322 plasmid DNA to the internal membrane was more efficient in the presence of plasmid-eliminating drugs than in that of their ineffective derivatives. It is concluded that a structural association exists between imipramine binding and plasmid replication sites in bacteria. The plasmid DNA is assumed to bind irreversibly to its replication site in the presence of the drug and this process can lead to plasmid elimination.

Antidepressive Agents, Tricyclic↗
PubMed1983

Gastric cytoprotective effects of vitamin A and other carotenoids.

The effects of vitamin A and some carotenoids (beta-carotene, beta-cryptoxanthin, zeaxanthin, lutein, capsorubin, capsanthin, capsanthol and lycopene) were studied (a) on the development of acute gastric mucosal lesions produced by topical application of 0.6 M HCl and (b) on gastric secretion in 4-h pylorus-ligated rats. It was found (a) that vitamin A, beta-carotene, beta-cryptoxanthin, zeaxanthin and lutein significantly inhibited the development of gastric mucosal lesions produced by 0.6 M HCl, while capsorubin, capsanthin, capsanthol and lycopene failed to prevent the development of such lesions; and (b) that vitamin A, beta-carotene, beta-cryptoxanthin, zeaxanthin and lutein, i.e., the carotenoids which exerted a cytoprotective effect, had no inhibitory effect on gastric acid secretion in 4-h pylorus-ligated rats. The possible relationship between chemical structure and gastric cytoprotection is discussed.

Animals↗