Effects of Litoralon (gamma-L-glutamyl-taurine) and its analogues on fear-motivated behaviour of rats

The effects of a single post-trial intraperitoneal administration of the dipeptide Litoralon (gamma-L-glutamyl-taurine) and some of its analogues were tested on the passive avoidance latency of male and female Wistar rats. The avoidance latency was significantly decreased by Litoralon and gamma-aminobutyryl-ethanolamine phosphate but lengthened by DL-beta-aminoisobutyryl-ethanolamine phosphate. No differences were observed between the responses of immature male and female rats following Litoralon treatment. The observed inter-group differences in passive avoidance behaviour following dipeptide administration were also demonstrable in tests of the open-field activity of the animals examined immediately after the 24-hour retention test. The results are discussed on the basis of a central Litoralon effect on emotional arousal and the anti-conflict potencies of the dipeptide.     

Antiepileptic effects of amphetamine may require GABA (benzodiazepine) activity

Secondary components of visual evoked potentials (slow negative wave-SNW, and photically-evoked sensory afterdischarge-SAD) are known to be precursors of experimentally activated wave-spike discharges, similar to wave-spikes of petit mal epilepsy. Both SNW and SAD may be potently suppressed wither by amphetamine or GABAergic compounds such as diazepam and sodium valproate. A hypothesis was tested in the present study, that amphetamine-induced suppression of wave-spike discharges may require GABA-benzodiazepine activity for its expression.Electrocortical activity was recorded and averaged in unrestrained albino rats with chronically implanted epicortical electrodes. SNW and SAD obtained in habituated rats in the predrug state were potently suppressed by amphetamine (1 mg/kg, i.p.). Fifteen minutes after amphetamine injection, a challenging drug (metrazol, picrotoxin, convulsant benzodiazepine, Ro 5-3663, or imidazodiazepine, Ro 15-1788) was administered intraperitoneally. Subconvulsive doses of metrazol (10 mg/kg) reversed amphetamine suppression; imidazodiazepine (20 mg/kg) and picrotoxin (1.5 mg/kg) reliably opposed the SNW suppression; convulsant benzodiazepine, Ro 5-3663 (2 mg/kg), showed modest and nonsignificant effect in the same direction. It is proposed that the antiepileptic potency of amphetamine may be associated with its ability, apparently via modulatory effect of norepinephrine, to facilitate the activation of benzodiazepine-GABA receptors.     

Experiences with a new type of microcarrier

Summary Two new microcarriers were tested and showed good properties in cell attachment, cell growth and production of Human--Interferon. Cell densities up to 5·10⁶ cells/ml on microcarriers were reached in 1 l bioreactors.     

Serum and tissue levels of tocopherols in cultured turbot (Scophthalmus maximus L.) fed vitamin E enriched diets

Turbot (Scophthalmus maximus) of approximate 110 g mean wet weight were fed three different diets supplemented with DL-alpha-tocopherol (1.4 g and 2.45 g · kg^-1 basal diet) and with non-alphatocopherols (0.29 g beta-, 1.29 g gamma-and 0.68 g delta-tocopherol kg^-1 basal diet). High dosages of alpha-tocopherol caused a linear increase of liver tocopherol (ninefold to controls). Spleen and blood serum accumulated also tocopherol. The level in muscle tissue was only poorly influenced by high vitamin E dosage. Non-alpha-tocopherols which normally do nct occur in blood and tissue have been resorbed from experiment diets and deposed in tissues in the same manner as alpha-tocopherol. The distribution of various tocopherols in the diets was reflected in muscle, spleen and serum of the fishes in the experiment. In the liver the distribution pattern of tocopherols was different to that of the diet. Conversion of alpha-tocopherol to non-alpha-tocopherpls in-vivo has not been found.     

Enhancement of spontaneous and lymphokine activated human macrophage cytotoxicity by hyperthermia

Human macrophages grown on hydrophobic teflon membranes from blood-born monocytes were incubated at hyperthermic temperatures for various time periods and then tested for their ability to inhibit the growth of an allogeneic lymphoma cell line (U 937). Incubation at 40.5 degrees C greatly enhanced macrophage cytotoxicity. This effect of hyperthermia developed slowly with an optimal incubation period of 48 h. In addition, lymphokine activation of macrophages for cytotoxicity appeared to be more effective at elevated temperatures.     

Nuclear medicine-important advances in clinical medicine: the role of nuclear and ultrasonic thyroid imaging

The Scientific Board of the California Medical Association presents the following inventory of items of progress in nuclear medicine. Each item, in the judgment of a panel of knowledgeable physicians, has recently become reasonably firmly established, both as to scientific fact and important clinical significance. The items are presented in simple epitome and an authoritative reference, both to the item itself and to the subject as a whole, is generally given for those who may be unfamiliar with a particular item. The purpose is to assist busy practitioners, students, research workers or scholars to stay abreast of these items of progress in nuclear medicine that have recently achieved a substantial degree of authoritative acceptance, whether in their own field of special interest or another.The items of progress listed below were selected by the Advisory Panel to the Section on Nuclear Medicine of the California Medical Association and the summaries were prepared under its direction.     

Metabolism of 4-pentenoic acid and inhibition of thiolase by metabolites of 4-pentenoic acid

The metabolism of 4-pentenoic acid, a hypoglycemic agent and inhibitor of fatty acid oxidation, has been studied in rat heart mitochondria. Confirmed was the conversion of 4-pentenoic acid to 2,4-pentadienoyl coenzyme A (CoA), which either is directly degraded via beta-oxidation or is first reduced in a NADPH-dependent reaction before it is further degraded by beta-oxidation. At pH 6.9, the NADPH-dependent reduction of 2,4-pentadienoyl-CoA proceeds 10 times faster than its degradation by beta-oxidation. At pH 7.8, this ratio is only 2 to 1. The direct beta-oxidation of 2,4-pentadienoyl-CoA leads to the formation of 3-keto-4-pentenoyl-CoA, which is highly reactive and spontaneously converts to another 3-ketoacyl-CoA derivative (compound X). 3-Keto-4-pentenoyl-CoA is a poor substrate of 3-ketoacyl-CoA thiolase (EC 2.3..1.16) whereas compound X is not measurably acted upon by this enzyme. The effects of several metabolites of 4-pentenoic acid on the activity of 3-ketoacyl-CoA thiolase were studied. 3,4-Pentadienoyl-CoA is a weak inhibitor of this enzyme that is protected against the inhibition by acetoacetyl-CoA. The most effective inhibitor of 3-ketoacyl-CoA thiolase was found to be 3-keto-4-pentenoyl-CoA, which inhibits the enzyme in both a reversible and irreversible manner. The reversible inhibition is possibly a consequence of the inhibitor being a poor substrate of 3-ketoacyl-CoA thiolase. It is concluded that 4-pentenoic acid is metabolized in mitochondria by two pathways. The minor yields 3-keto-4-pentenoyl-CoA, which acts both as a reversible and as a irreversible inhibitor of 3-ketoacyl-CoA thiolase and consequently of fatty acid oxidation.