PHOSPHOLIPIDS IN THE BOVINE TONGUE PAPILLAE

Lipids, especially phospholipids in the bovine tongue papillaeand the surrounding epithelium were analyzed with a view toexamine the role of phospholipids in the taste reception. Thetaste buds bearing papillae, the circumvallate and the fungiformpapillae showed much higher phospholipid content than thoseof the filiform papillae bearing no taste buds and those ofthe epithelium. Nine phospholipids in the papillae and epitheliumwere identified and quantified. It was shown that the main componentsof phospholipids were phosphatidylcholine, phosphatidylethanolamine,sphingomyelin and phosphatidylserine. The composition of phospholipidsin the papillae bearing taste buds was not appreciably differentfrom that in the filiform papillae and the epithelium. On thebasis of the obtained results, the role of lipid in taste receptionis discussed.     

THE NATURE OF BANDS IN PARASITIZED BOVINE ERYTHROCYTES

Anaplasma marginale is the etiological agent of a hemolytic disease of cattle, known as anaplasmosis. The organism appears as a marginal inclusion in parasitized erythrocytes, but certain isolates also have bands associated with the inclusion. Inclusions and associated bands in parasitized erythrocytes in the liver and peripheral circulation were studied by light microscope cytochemistry and electron microscopy. Bands were comet- and dumbbell-shaped by light microscopy and were stained by techniques used to demonstrate protein and fibrin. The same forms, as well as other shapes, were seen in infected erythrocytes which were sectioned and examined by electron microscopy. Bands had longitudinal and transverse periodicity. They did not appear to have a crystalline structure. Their appearance was collated with that of bovine fibrin. Bands were well differentiated in erythrocytes that were entensively hemolyzed by natural or artificial means, but poorly differentiated in mildly hemolyzed erythrocytes. Hemolysis methods appeared to influence the morphology of bands and their demonstration.     

THE CHANGES IN CHEMICAL COMPOSITION DURING DEVELOPMENT OF THE BOVINE NUCHAL LIGAMENT

Whole bovine nuchal ligaments, or portions thereof (in the case of commercially valuable animals), were obtained from 45 animals (28 fetal and 17 postnatal) ranging in age from 110 days of gestation to 10 yr. Insoluble elastin was quantitatively prepared from the fresh ligaments by extraction with hot alkali and by a combination of multiple extractions with alkaline buffer and then repeated autoclaving. When adult samples were examined, the yields of insoluble residue by these two methods were very similar, but with young fetal samples the second method gave significantly higher values, because of incomplete purification of the elastin residue. The changes in the concentration of collagen, alkali-insoluble elastin, and DNA have been examined. DNA concentration, and, thus, cell population density, fell progressively during the fetal period of development, to reach a steady value soon after birth. Collagen appeared in appreciable quantities before elastin, but its concentration was rapidly halved at about the time of birth. Insoluble elastin concentration was low until the end of the 7th fetal month, at which time it began to rise rapidly. The rate of increase in elastin concentration remained high throughout the next 10–12 wk, by which time the adult value had been reached. Quantitative studies, on the basis of the whole ligament, showed that the total cell content rises to a maximum at birth, but falls soon after to a level about half that at birth. Total collagen production and elastin deposition continue at a steady, maximal rate over the interval from 235 days of gestation to the end of the 1st postnatal month. It is concluded that the immediate postnatal period would be the most favorable phase in which to attempt the isolation of the soluble precursor elastin.     

CONVERSION EFFICIENCIES IN HETEROTROPHIC ORGANISMS

1. The maximum possible efficiency at which living systems are able to convert input nutrients to their own biomass is between 70 and 80 %. 2. Conversion efficiency in bacteria, protozoa and metazoan cells in culture approximates more closely to 60%. 3. Conversion efficiency during embryonic development begins below 60% and rises above this level in the later stages. 4. Very young, post-natal organisms have high net efficiencies; 50 to 70% in homeotherms and 50 to 80 % in poikilotherms. 5. In cellular systems, capable of proliferation, conversion efficiency is independent of food supply. This means that conversion is directly dependent on nutrient supply. 6. Control of growth at the tissue level may occur through the control of the supply of nutrients to the tissues and its entry into the cells. 7. Compensatory growth, after and during undernutrition, involves increased absorption efficiency and reduced metabolic costs.     

ENZYMES CATALYSING ETHANOL METABOLISM IN NEURAL AND SOMATIC TISSUES OF THE RAT

Abstract— The enzymes catalysing ethanol metabolism, alcohol dehydrogenase (EC 1.l.1.1) and aldehyde dehydrogenase (EC 1.2.1.3), were assayed in a variety of neural and somatic tissues of the rat, the human counterparts of which are known to be vulnerable to excessive ethanol. The activity of alcohol dehydrogenase was assayed by the coupled oxidation of ethanol and reduction of lactaldehyde, a method which we have recently found to be sufficiently sensitive and specific to measure the relatively low levels of activity in whole brain. Detectable activities of these enzymes were found in peripheral nerve, skeletal muscle, retina, optic nerve and various regions of brain, as well as in a variety of non-neural tissues. The levels of the enzymic activities in all tissues were markedly lower than those of liver, but probably sufficient to perform a local function in the metabolism of ethanol or other endogenous substrates. The activity of alcohol dehydrogenase in the various tissues, like that of liver, was confined to the cytosol and exhibited kinetic properties and responses to inhibitors almost identical to those of the liver enzyme. We consider the results to be consistent with the hypothesis that the pathological effects of alcohol may be related, at least in part, to local mechanisms for the metabolism of alcohol.     

胰多肽对急性胰腺炎大鼠的细胞保护作用

用5%牛磺胆酸钠-胰蛋白酶溶液直接注入大鼠胰导管,制备成急性出血坏死性胰腺炎模型。由腹腔于制备前预防性地和制备后治疗性地结合注射剂量为3μg/kg 的牛胰多肽,能使病鼠的死亡率由对照的100%降到33%,已死鼠平均存活时间由对照的13±3小时延长到20±2小时,血清淀粉酶浓度升高的峰值降为对照的35%,胰腺组织学切片呈轻度急性胰腺炎或向慢性胰腺炎转化。单纯在制备前预防性地注射牛胰多肽或仅在制备后作治疗性注射,也有同样作用,但效果较差。这项结果提示,胰多肽对急性出血坏死性胰腺炎具有预防和治疗两方面的功效,即对胰腺有细胞保护作用。抑制胰酶的分泌和释放可能是它的作用机制之一。     

GANGLIOSIDES OF THE BOVINE NEUROHYPOPHYSIS

The gangliosides of the bovine neurohypophysis were isolated and partially characterized. In terms of lipid-sialic acid, the concentration of gangliosides in the tissue was 1465 nmol/g wet wt. On the basis of chromatographic properties, sugar composition and the products of neuraminidase-treatment, the principal ganglioside (approx. 51 per cent of the lipid-sialic acid) was identified as N-acetylneuraminylgalactosyl- N-acetylgalactosaminyl-(N-acetylneuraminyl)-galactosyl- glucosyl-ceramide (GDta). The gland also contained galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl- N-acetylneuraminyl)-galactosyl-glucosyl-ceramide (GDtb), and a mixture of N-glycolyl-neuraminic acid-containing disialogangliosides with unknown structures, in addition to smaller quantities of galactosyl-N-acetylgalactosaminyl-(N-acetylneuraminyl)- galactosyl-glucosyl-ceramide (GM1) and two glucosamine-containing monosialogangliosides. Stearic acid was the principal fatty acid in all the gangliosides.     

THE REGIONAL DISTRIBUTION OF SIALOGLYCOPROTEINS, GANGLIOSIDES AND SIALIDASE IN BOVINE BRAIN

Abstract— Sialoglycoproteins and gangliosides were characterized in various bovine brain regions by determining the amount of sialic acid. Expressed per g dry weight, the gangliosidic sialic acid ranged from 11·20 to 1·93 μmol and the glycoprotein sialic acid from 8·93 to 1·84 μmol in grey and white matter respectively (values not corrected for incomplete release and breakdown during hydrolysis). Both the sialoglycoproteins and the gangliosides occur in highest concentration in areas predominating in neuronal cell bodies (cerebral grey, cerebellar grey, caudate nucleus). The lowest concentrations are found in those areas, consisting largely of myelinated fibre tracts and glial cells (pons, medulla, corpus callosum, cerebral white). Relative to the gangliosides the sialoglycoproteins are somewhat more concentrated in white matter.
The sialidase activity was investigated with endogenous substrate as well as with additional gangliosides or sialoglycopeptides. In all conditions the activity was much greater in grey matter than in white matter. The regional sialidase distribution more or less parallels the distribution of sialic acid in the various regions. At high substrate level the sialoglycopeptides inhibit the sialidase activity. There are indications that gangliosides are a far better substrate for brain sialidase than glycoproteins or glycopeptides. The possible significance of this phenomenon is discussed.     

METABOLIC CONSEQUENCES OF ETHANOL OXIDATION IN BRAINS FROM MICE CHRONICALLY FED ETHANOL

Abstract— Effects of the acute and chronic administration of ethanol have been investigated in mouse brain on the redox-state, citric acid cycle function, levels of adenine nucleotides and other metabolites. Cerebral oxidation of ethanol, activity of alcohol dehydrogenase and the permeability of brain and liver mitochondrial preparations after chronic ethanol administration have been also investigated. Acute or chronic administration of ethanol resulted in a small but significant increase in the reduced components of certain dehydrogenase-linked substrate pairs in brain. Pyrazole, an inhibitor of alcohol dehydrogenase, prevented the ethanol-induced changes in brain. ¹⁴CO₂ production from several substrates was inhibited in brains from chronically ethanol-fed animals. Addition of pyrazole, however, prevented the ethanol-mediated inhibition of ¹⁴CO₂ production. Chronic administration of ethanol resulted in decreased levels of ATP and creatine phosphate in the brain, and increased contents of ADP and AMP. The cerebral activities of alcohol dehydrogenase and succinic dehydrogenase, oxidation of ethanol, mitochondrial oxidation of a-glycerophosphate, and levels of NADH remained unaffected by the chronic administration of ethanol. In contrast to liver, where chronic administration of ethanol increased the contribution of 'substrate shuttles'resulting in increased oxidation of ethanol; in brain, the contribution of these 'shuttles'remained unaffected.     

THE EFFECTS OF INTOXICATING DOSES OF ETHANOL UPON INTERMEDIARY METABOLISM IN RAT BRAIN

Abstract— The effect of acute (8-min) and prolonged (13-h) exposures to high doses of ethanol upon the intermediary metabolites of rat brain has been studied, with the use of a new freezing technique which minimizes post-mortem changes. Injection of ethanol (80 mmol/kg body wt) produced general anaesthesia within 8 min after administration. At this time there were increases in the brain contents of glucose, glucose-6-phosphate and citrate; there was no change in arterial pCO₂. Rats under ethanol anaesthesia for 13 h showed increases in brain contents of glycogen, glucose and glucose 6-phosphate; and decreases in lactate, pyruvate, α-oxoglutarate and malate. Under similar experimental conditions, arterial pCO₂, increased from 37 to 51 Torr. The changes in levels of metabolites after injection of ethanol were similar to those after administration of many volatile anaesthetic agents or elevation of brain CO₂ by other means. Although brain levels of malate and α-oxoglutarate decreased after prolonged exposure to ethanol, the mitochondrial redox state was maintained. Accordingly, the levels of glutamate and aspartate fell in accordance with the law of mass action. The maintenance of the cytoplasmic and mitochondrial redox states in the brain during ethanol intoxication was in marked contrast to the effects on the liver. We suggest that the different effects observed in brain and liver result from the action of ethanol upon the nerve cell membrane in brain, whereas the primary target in liver is alcohol dehydrogenase.