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PubMed1985

Protection against acute ethanol toxicity in mice by zinc aspartate, glycols, levulose and pyritinol.

The lethality in mice after an acute intraperitoneal challenge with ethanol could be largely prevented by treatment with single doses of zinc aspartate. Other zinc salts or aspartates were not or clearly less effective than zinc aspartate. Marked protection was also provided by polyethylene glycol and propylene glycol. The antagonistic effects of levulose and pyritinol against acute ethanol intoxication were confirmed.

Alcoholic Intoxication↗
PubMed1994

Pyritinol facilitates the recovery of cortical cholinergic deficits caused by nucleus basalis lesions.

The effect of a nootropic, Pyritinol, on the recovery of cortical cholinergic deficits induced by injury of the nucleus basalis has been tested on two groups of unilateral quisqualic acid nbM-lesioned rats. The first group had a 30 nmol lesion producing a cortical cholinergic impairment at 21 days, with a spontaneous recovery at 45 days. The second group had a 50 nmol lesion that produced a deeper cholinergic deficit, which did not recover at 45 days. Pyritinol enhanced the recovery in the 30 nmol group of animals on the 21st day after surgery. The recovery was measured as an increase in the activities of acetylcholinesterase (AChE), choline acetyltransferase (ChAT) and the high affinity choline uptake system, and the histochemical densities of the cortical AChE network and the M2 receptor. Histochemical analysis of the nbM enabled cortical recovery to be related to the number of surviving neurons and also to their hypertrophy and AChE-ChAT hyperactivity. Pyritinol enhanced recovery in 30 nmol lesioned animals but in the other group, with a lower number of surviving neurons and a lower ability of the cells to become hypertrophic, the drug was unable to promote cortical recovery.

Animals↗
PubMed1986

Adverse effects profile of sulfhydryl compounds in man.

Many of the adverse reactions produced by penicillamine and other compounds with an active sulfhydryl group form a distinctive pattern when viewed as a class. Alterations in taste perception, mucocutaneous lesions, proteinuria due to immune-complex membranous glomerulopathy, and pemphigus are adverse reactions that have been encountered with all of the compounds discussed herein. Hematologic reactions such as neutropenia and thrombocytopenia occur rarely and with variable frequency. The angiotension converting enzyme inhibitor captopril has an active sulfhydryl group. When it was first given in high doses to patients with severe hypertension, adverse effects similar in pattern to those just outlined were reported. With reduced doses and more careful patient selection, the more serious reactions are no longer found, but disturbances of taste perception, rash, and oral mucosal ulcers are still encountered.

Anemia, Aplastic↗
PubMed1986

Effects of cerebro-protective agents on enzyme activities of rat primary glial cultures and rat cerebral cortex.

The effects of different cerebro-protective agents on selected key enzymes of the energy metabolism of rat primary glial cultures and rat cerebral cortex were studied. As indicators for the capacity of the most important pathways of energy metabolism the following enzyme activities were determined: hexokinase (HK), phosphofructokinase (PFK), pyruvate kinase (PK), lactate dehydrogenase (LDH), glucose-6-phosphate dehydrogenase (G-6-P-DH), malate dehydrogenase (MDH), glutamate dehydrogenase (GDH), and cytochrome-c-reductase (CCR). After a one week growth period, rat glial cultures were incubated for 3 or 4 weeks with the substances to be tested. Bencyclane (5 X 10(-5) mol/l) increased the activities of HK, G-6-P-DH, and LDH, whereas PFK and CCR were reduced. Pyritinol (10(-4) mol/l) led to a higher G-6-P-DH activity, simultaneously lowering the values for PFK, CCR, PK, LDH, and MDH. Under the influence of an extract of the leaves of Ginkgo bilobae (EGB; 100 mg/l) PFK, LDH, and MDH activities were reduced. All these alterations in enzyme activities went along with simultaneous reductions in protein content, therefore not allowing to exclude toxic effects with regard to the doses used. Moreover, direct interference with the analytical procedure was demonstrable for bencyclane and EGB. Piracetam (10(-3) mol/l), flunarizine (10(-6) mol/l), dihydroergocristine (5 X 10(-6) mol/l), and nicergoline (5 X 10(-6) mol/l) failed to induce any alteration in the employed doses. The most striking effects were obtained with meclofenoxate which was tested at 10(-3) and 10(-4) mol/l. The higher dose caused an elevation of HK, PFK, CCR, G-6-P-DH, GDH and MDH activities, while slightly reducing PK. With the lower dose of meclofenoxate CCR and G-6-P-DH activities were increased. Short-term incubation of the cultures with 10(-3) mol/l meclofenoxate for 24 hr led to an increase in LDH, G-6-P-DH, and GDH activities. Chronic incubation with meclofenoxate (10(-3) mol/l) followed by 48 hr deprivation of the drug resulted in elevated HK, PFK, CCR, G-6-P-DH, GDH, and MDH activities. These changes were accompanied by alterations in related metabolite levels. These include elevations in the concentration of creatine phosphate and fructose-1,6-bisphosphate, whereas glucose-6-phosphate levels were reduced. After one week of meclofenoxate deprivation the activities of CCR and G-6-P-DH were still elevated. The metabolites of meclofenoxate dimethylaminoethanol (DMAE; 10(-3) mol/l) and p-chlorophenoxyacetic acid (10(-3) mol/l) were also investigated.(ABSTRACT TRUNCATED AT 400 WORDS)

2,4-Dichlorophenoxyacetic Acid↗
PubMed1989

Testing drug effects against hypoxic damage of cultured neurons during long-term recovery.

Cultured neurons of chick cerebral embryo hemispheres were used to study drug effects against neuronal damage caused by hypoxia during long-term recovery. Sodium cyanide (NaCN, 1 mmol/l) induces hypoxia-like conditions by inhibiting oxydative phosphorylation. The sensitivity of the cultured neurons against this type of hypoxia was determined after 3, 4, 5 and 6 days of cultivation followed by 4, 3, 2 days and 1 day of recovery, respectively. The ATP level and the viability of cells as well as the total cell number and the protein content of the cultures were used to characterize the extent of posthypoxic neuronal damage. A hypoxic period of 30 min after 4 days of cultivation followed by 3 days of recovery seemed to be appropriate for determining protective drug effects. The drug effects obtained were comparable to those from in vivo models of cerebral ischemia or hypoxia. The results suggest that cultured neurons exposed to hypoxia and to long-term recovery could be suitable for studying post-hypoxic neuronal damage as well as neuroprotective drug effects.

Adenosine Triphosphate↗
PubMed1989

Protection of cell proteins against free-radical attack by nootropic drugs: scavenger effect of pyritinol confirmed by electron spin resonance spectroscopy.

The potency of nootropic drugs to protect cell proteins and lipids against free radical attack was studied. In an in vitro system, generating hydroxyl radicals by a Fenton-type reaction, the soluble proteins (bovine serum albumin and cytosol protein from brain) were quickly insolubilized and precipitated. Pyritinol (and tamitinol) exhibited the best protection against insolubilization of protein while centrophenoxine (meclophenoxate) and its dimethylaminoethanol moiety were less effective, piracetam (and oxiracetam) being without effect. The lipid peroxidation induced by free radicals from cyclic redox reactions of iron-ascorbate was not influenced by pyritinol, indicating the selectivity of its scavenger action. The efficient scavenging of hydroxyl radicals by pyritinol was confirmed by electron spin resonance spectroscopy measurement of hydroxyl radicals entrapped by spin trap. Millimolar concentrations of pyritinol competitively decreased the formation of spin adducts. The results suggest that the protective effect of pyritinol against free-radical induced derangement of cell proteins may be an important part of its antirheumatic, as well as nootropic, action.

Animals↗
PubMed1993

Effects of subchronic administration of pyritinol on receptor deficits and phosphatidylinositol metabolism in the brain of the aged mouse.

The effect of pyritinol, a commonly used nootropic drug, on receptor properties and function was investigated in different neuronal systems, possibly associated with age-related decline in brain function. Chronic treatment (15 days) of aged (22 months) female NMRI mice with pyritinol (200 mg/kg) restored the reduced density of N-methyl-D-aspartate receptors in the aged mouse brain. Furthermore, the total number of binding sites of the alpha 2-receptor ([3H]yohimbine binding) decreased after treatment with drug, while the number of high-affinity agonist binding sites ([3H]UK 14304 binding) was not changed. In both systems, receptor affinity was not influenced. The densities of other receptors investigated (muscarinic-cholinergic, benzodiazepine and beta-adrenergic) were not altered by treatment with pyritinol. Additionally, the effect of pyritinol on phosphatidylinositol (PI) metabolism was investigated in dissociated neurones from young and aged mice. Muscarinic-cholinergic induced accumulation of phosphatidylinositol and the inositol phosphate response due to activation of G-protein by fluoride was increased in aged animals, treated with drug. The inositolphosphate response after stimulation with pilocarpine was slightly but not significantly increased. The metabolism of phosphatidylinositol in young animals was not altered by treatment with drug. These results support the hypothesis of a nootropic-mediated restoration of age-related brain deficits. Changes caused by pyritinol may be due to beneficial effects on age-related alterations of the properties of the neuronal membrane.

Aging↗
PubMed1989

The influence of alpha-tocopherol and pyritinol on oxidative DNA damage and lipid peroxidation in human lymphocytes.

Unscheduled DNA synthesis (UDS) and lipid peroxidation (LPO) were measured in human peripheral lymphocytes from healthy volunteers. These processes were induced by the catalytic system Fe2+-sodium ascorbate. The degree of induced LPO was measured spectrophotometrically by the thiobarbituric acid assay. UDS was detected by scintillometric measurement of the incorporation of 3H-thymidine into DNA. The protective action by fat-soluble vitamin E (D,L-alpha-tocopherol) and the artificial antioxidant pyritinol on UDS and LPO was also investigated. The system Fe2+ (2 mumole/l)-sodium ascorbate (30 mumole/l) increased the LPO level in healthy volunteers approximately 2.5 times and the incorporation of 3H-thymidine by 60-70%. alpha-Tocopherol (0.2 mmole/l) very efficiently suppressed LPO processes (p less than 0.01) and the oxidative damage of DNA measured as UDS was also significantly diminished (p less than 0.05). Pyritinol had no effect on LPO and UDS under our experimental conditions.

Ascorbic Acid↗
PubMed1984

Changes in motor activity with age and the effects of pharmacologic treatment.

In a previous study the decline in the motor performance of old rats was determined to be differential. In this study, whether, and to what extent, this decline can be pharmacologically influenced was tested. Therefore, 27 month old rats were orally treated with several nootropics and d-amphetamine for six weeks. Food and water intake were determined. The rats were tested on spontaneous activity and on the tilting plane, climbing, and rotarod tests. The results showed that the nootropics only effected pronounced improvements on complex motor tasks such as on the rotarod test. In contrast, amphetamine treatment caused rather negative effects. This could be observed in the motor performance as well as in the food and water intake. Young rats did not have this sort of reaction to amphetamine. The nootropics were all well tolerated. Additionally, it was obvious that the untreated rats also showed a slight improvement in motor performance due to repeated practice.

Aging↗
PubMed1993

Source localization of brain electric field frequency bands during conscious, spontaneous, visual imagery and abstract thought.

This paper addresses the issue of mind-brain correspondence, using a novel way to reduce brain electric field data in the frequency domain to estimates of intracerebral model source locations, and applying this method to brain electric data collected during the 2-s epochs immediately before the randomly solicited reports of spontaneous, conscious, covert experiences from 12 normal volunteers. The mentation reports were classified into visual imagery and abstract thought. The mean locations of the EEG model sources associated with abstract thoughts were generally more anterior and deeper than those of visual imagery, particularly significant for the delta/theta band; the finding was common across subjects. Thus, different brain functional states involving different geometries of activated neural populations exist during conscious, spontaneous, task-free mentations of the visual imagery type and of the abstract thought type.

Acoustic Stimulation↗
PubMed1998

Acute pancreatitis due to pyritinol: an immune-mediated phenomenon.

A 23-year-old man experiencing three episodes of acute pancreatitis of undetermined etiology is described. Repeated questioning revealed that all three events had occurred after intake of the drug pyritinol. Controlled rechallenge with a single dose of the drug led to a fourth episode of acute pancreatitis. Skin testing was negative, but lymphocyte stimulation tests and double fluorescence analysis detected pyritinol-activated CD4 and CD8 lymphocytes. Together with the clinical observation that the intervals between drug intake and start of symptoms of acute pancreatitis became shorter with repeated exposure, the data are consistent with an immune-mediated origin of the pancreatitis. Pyritinol has to be added to the list of drugs capable of inducing acute pancreatitis.

Acute Disease↗
PubMed1986

Contact dermatitis caused by airborne agents. A review and case reports.

A general review is given of airborne-induced contact dermatoses, particularly of the irritant and allergenic types. Because the reports in the literature often omit the term airborne, 12 volumes of Contact Dermatitis (January 1975-July 1985) were screened, and the cases cited were classified in function of the anamnesis, lesion locations, causative irritants and allergens, and other factors. The present article also discusses differential diagnoses, in particular with regard to contact dermatitis of the face, ears, and neck. Finally, seven case reports of occupational and nonoccupational contact dermatitis problems caused by airborne agents are presented. In some of the cases the allergens have not been mentioned in published literature previously.

Adult↗