EFFECT OF VITAMIN B6 ON PHENYLALANINE METABOLISM IN THE BRAIN OF NORMAL AND p-CHLOROPHENYLALANINE-TREATED RATS

Abstract— A phenylketonuria-like state was produced in the preweanling rat, and the metabolism of phenylalanine in the normal and phenylketonuric brain was compared. The effect of B₆ vitamers on the disposition of phenylalanine was also investigated. Phenylalanine was metabolized mainly by transamination and to a lesser extent by decarboxylation in both the normal and phenylketonuric-like brain. Small amounts of amine were detected in all the brains throughout the experimental period. More than 95 percent of the metabolized amino acid appeared as aromatic acids, which steadily accumulated and remained in the brain for the duration of the experiment. No change in the metabolic pattern was produced by pyridoxol. In striking contrast, pyridoxamine prevented the accumulation of acidic metabolites in the brains of all animals tested. We suggest that pyridoxamine phosphate and/or pyridoxamine is actively associated with the removal of excess keto acids and aldehydes from the brain.     

SPECTROFLUORIMETRIC ASSAY OF VITAMIN B6 ANALOGUES IN BRAIN TISSUE

Abstract— —A method for the simultaneous assay of the predominant forms of vitamin B₆ occurring in brain tissue was developed. Quantitative release of the vitamers was effected by partial removal of lipids with an organic solvent followed by extraction with aqueous metaphosphoric acid. The compounds were separated by ion exchange column chromatography and estimated fluorimetrically.     

SOME EFFECTS OF DIETARY VITAMIN B6 DEFICIENCY AND 4-DEOXYPYRIDOXINE ON γ-AMINOBUTYRIC ACID METABOLISM IN RAT BRAIN

Abstract— Investigations of the respective effects of dietary vitamin B₆ deficiency and 4-deoxypyridoxine (a vitamin B₆ antagonist) on GABA metabolism in rat brain have been carried out. No convulsions were observed in rats subjected to either treatment. GABA levels were lowered by both treatments, the greatest diminutions being found with the dietary deficiency. Glutamic acid decarboxylase activity was reduced under both conditions, but the loss of activity in the B₆ deficiency experiments could be attributed to cofactor depletion, whereas in the deoxypyridoxine experiments the loss of activity appears to be due to lower levels of available apoenzyme. The activity of GABA-transaminase was not affected by deoxypyridoxine treatment and only moderately reduced in the B.5 deficient animals.     

THE STABILITY OF VITAMIN B6 ACCUMULATION AND PYRIDOXAL KINASE ACTIVITY IN RABBIT BRAIN AND CHOROID PLEXUS

The effects of changes in the concentrations of pyridoxal phosphate and blogenic amines in brain on: (I) pyridoxal kinase (EC 2.7.1.35) activity in brain and choroid plexus; and (2) vitamin B₆ accumulation by brain slices and isolated, intact choroid plexuses were studied. New Zealand white rabbits were treated parenterally with 200 mg/kg pyridoxine-HCl for 3 days or 120 mg/kg 4-deoxypyridoxine HCI or 5 mg/kg reserpine I day before death. After these treatments the mean concentration of pyridoxal phosphate in brain was elevated by 39% by pyridoxine and decreased by 57% by 4-deoxypyridoxine. Reserpine had no effect. However, the ability of brain slices and isolated, intact choroid plexuses from the treated rabbits to accumulate [³H] vitamin B₆ (with [³H]pyridoxine in the medium) was not different from untreated controls. Also, the specific activity of pyridoxal kinase in brain and choroid plexus of treated rabbits was not different from controls. These results show that vitamin B₆ accumulation and pyridoxal kinase activity in brain and choroid plexus are independent of both pyridoxal phosphate and reserpine-sensitive biogenic amine concentrations in brain. In vitro studies with pyridoxal kinase showed that. in both choroid plexus and brain. pyridoxal kinase was a single enzyme with a molecular weight of 43.000 and a K_m , for pyridoxine of 2.0 μM Crude and partially-purified pyridoxal kinase from brain was not inhibited by biogenic amines (1 mM) or pyridoxal phosphate (5 μM). These in vitro data are consistent with the lack of effect of changes in pyridoxal phosphate and biogenic amine concentrations (in brain) on pyridoxal kinase activity in brain in vivo.     

EFFECT OF HYPERPHENYLALANINEMIA ON VITAMIN B6, METABOLISM IN DEVELOPING RAT BRAIN

Abstract— The turnover of the different forms of B₆ vitamers in the brains of normal and hyperphenylalaninemic preweanling rats was compared after administration of a load of [¹⁴C]pyridoxol. Metabolic transformations occurred in the following sequence: oxidation of pyridoxol to pyridoxal, which was in turn phosphorylated to the 5'-phosphate ester. No significant amount of pyridoxamine was formed during the 8-h experimental period. Pyridoxamine 5'-phosphate was derived from pyridoxal 5'-phosphate. The specific radioactivity of pyridoxal phosphate in the hyperphenylalaninemic brain was significantly lower and increased at a slower rate than in control brains. This difference could not be accounted for by either a deficient supply or inhibited activity of the enzyme, pyridoxal kinase. The synthesis of pyridoxamine 5'-phosphate in the experimental animals also lagged behind the controls. Decreased activity of enzymes dependent on pyridoxal phosphate as cofactor would explain the slower turnover of this B₆-coenzyme.     

THE COMBINED EFFECTS OF LOW TEMPERATURE AND SO2+NO2 POLLUTION ON THE NEW SEASON'S GROWTH AND WATER RELATIONS OF PICEA SITCHENSIS

Picea sitchensis (Bong.) Carr. seedlings were exposed to SO₂, NO₂ and SO₂+ NO₂ during dormancy in controlled environments, and were taken to night temperatures of 4, 0, −5, −10 and −15 °C in a freezer. Conditions in the freezer were carefully monitored during the low–temperature treatments. In two experiments, different photoenvironments and temperature regimes were imposed prior to the cold treatments, and different effects were observed. In the first, only limited frost hardiness was achieved and night temperatures of −15 °C were lethal. Temperatures of −5 and − 10 °C led to poor survival of lateral buds, particularly in plants exposed to 45 ppb SO₂. The poor bud break in plants exposed to SO₂ and to − 5 °C resulted in a loss of the effectiveness of this temperature as a chill requirement. Pressure-volume analysis showed that the shoots of plants exposed to NO₂ had greater elasticity (lower elastic moduli, e), so that loss of turgor occurred at lower relative water contents. In contrast, a hardening period (2 weeks in night/day temperatures of 3/10 °C and 8 h days at 50 μmol m⁻² s⁻¹ PAR) gave decreased elasticity and lower solute potentials of spruce shoots. In the second experiment, exposure to 30 ppb SO₂ and SO₂+ NO₂ led to slight, but consistent, increases in frost injury to the needles of plants frozen to − 5 and − 10 °C. The results suggest that the main interaction of low temperatures and winter pollutants may be on bud survival rather than on needle damage, but that effects are subtle, only occurring with certain combinations of pollutant dose and cold treatment.     

HISTAMINE-SENSITIVE ADENYLATE CYCLASE IN HYPOTHALAMUS OF RAT BRAIN: H1 AND H2 RECEPTORS

Abstract— In in vitro experiments on rat hypothalamic homogenates the effects of biogenic amines such as histamine (HA), noradrenaline (NA), dopamine (DA), serotonin (5-HT) and drugs such as isoprenaline (ISP), 2-(2-pyridyl)ethylamine (H₂ stimulant—H_ls), 4-methyl-histamine (H₂ stimulant H_2s), mepyramine (H₁ antagonistp H_la), cimetidine (H₂ antagonist—H_2a) were tested on adenylate cyclase activity. HA possessed a powerful stimulating effect on hypothalamic adenylate cyclase activity, higher than that shown by the other substances.
The stimulating effect of HA was greatest in hypothalamic tissue from male rats, while tissue from females showed only a modest stimulation. H_2s, induced a greater stimulation of adenylate cyclase than H_ls. On the other hand, the H_2a inhibited HA stimulation to a greater extent than the H_la, H_la and H_2a, when used together, completely inhibited the HA stimulation. HA may have a neurotrans-mitter role in the hypothalamus, and in this area there appears to be a mixed population of H₁ and H₂ receptors, with a majority of H₂ receptors.     

高浓度CO2与磷浓度对葛仙米生长和光合作用的耦合效应

在不同CO₂(400和2000 ppm)和磷浓度下(0.088—0.350 mmol/L)培养葛仙米(拟球状念珠藻, Nostoc sphaeroides Kutzing), 研究CO₂和磷对葛仙米相对生长速率、色素含量、光系统Ⅱ光化学活性和光合速率等的影响。结果显示CO₂或磷浓度对葛仙米的相对生长速率、球体粒径和数量、光饱和光合速率、呼吸速率和光合效率均有显著影响, 且两者对球体粒径和数量、叶绿素a含量、呼吸速率和光合效率存在明显交互作用。高CO₂浓度培养明显提高磷对球体粒径和数量和光合效率的效应, 同时降低高磷浓度对叶绿素a合成的抑制作用, 但两者对相对生长速率、藻胆蛋白含量、光饱和光合速率、F_v/F_m和Yield的交互作用均不显著。以上研究结果表明高CO₂浓度或磷浓度增加促进葛仙米生长主要是通过提高光合速率和光合效率来实现; 两者交互作用表明高CO₂浓度可能通过提升磷的利用效率, 降低高磷浓度对叶绿素a合成的抑制, 提高光合效率, 使球体明显增大。     

不同氮源及CO_2浓度下湖泊微拟球藻的生长及产油特性分析

<正>工业生产排放的各种废气与污水污染人类赖以生存的环境。化石燃料燃烧除排放出大量CO2外,还释放出含有粉尘、SO[x和NOx等直接危害人类健康的有毒成分1]。其中NO]x与水结合后最终会转化成硝酸盐或亚硝酸盐等[2,导致污水中的含氮化合物氨氮、亚硝酸盐氮、硝酸盐氮和有机氮的含量通常偏高。如何有效去除污水中的氮是防治水体污染最关键的步骤之一,而利用微藻培养去除水体中的氮源是目前研究的热点。尽管生物燃料生产的成本远     

高浓度CO2对极大螺旋藻生长和光合作用的影响

以极大螺旋藻作为实验材料,研究了高CO2浓度对极大螺旋藻的生长和光合作用效应,结果表明在高光强下（400μmolm^-2s^-1),高浓度CO2对其生长和光合作用有明显的影响。高浓度CO2培养下,辈放荡中的比生长速率是低浓度CO2培养的1.2倍;而在低光强下,高浓度CO2对其生长和光合作用无明显影响。两种不同CO2浓度和光强下培养的极大螺旋藻,在不同的生长时期,分别测定其P-I曲线,结果表明,低光强下培养的极大螺旋藻,在5d、8d、11d,两者的Ik、α值均无显著差异,Pmax在第5d、11d差异不显著,但在第8d有显著差异。而在高光强培养条件下,第8、11d通高浓度CO2培养的极大螺旋藻,其Pmax、α值明显大于通低浓度CO2培养的极大螺旋藻,但两者在第5d无明显差异。     

EVIDENCE FOR INVOLVEMENT OF Ca2+ IN THE INCORPORATION OF 32Pi INTO THE PHOSPHATIDYLINOSITOL OF RAT DIAPHRAGM

Abstract— Ethyleneglycol-bis (β-aminoethyl ether)-N-N'-tetraacetic acid (EGTA) inhibited the incorporation of ³²P_i into phosphatidylinositol (PI) in rat diaphragm incubated in Ca²⁺-free Krebs-Ringer medium. Only the labelling of the PI was altered, and no effects on the pool size of PI or on the incorporation of ³²P_i into other phospholipids were observed. The effect of EGTA was concentration-dependent and appeared to be related to its Ca^a+-chelating properties; the inhibition of the incorporation of ³²P_i could be completely reversed by the addition of excess Ca²⁺ but not Mg²⁺. The inhibitory effect of the EGTA was progressively enhanced by lengthening the preincubation of the tissue with EGTA, an observation suggesting that chelation of intracellular or membrane-bound Ca²⁺, rather than extracellular Ca²⁺, was involved in the effect. In contrast to its inhibition of the incorporation of ³²P_i EGTA enhanced the incorporation of [³H]inositol into PI, but this effect was accompanied by an appreciable increase in total uptake of [³Hlinositol by the tissue. Our results suggest that the level of intracellular Ca²⁺ plays a role in the regulation of the incorporation of ³²P_i into PI. Addition of unlabelled α-glycerophosphate to the incubation medium of tissues which had been preincubated with 2-deoxy-d -glucose failed to cause a significant diminution in the inhibition by EGTA of the incorporation of ³²P_i into PI. This experiment suggests, but does not prove, that the effect of EGTA was not at the level of incorporation of ³²P_i into α-glycerophosphate.     

ON THE EXISTENCE OF 'ARRESTED G2 CELLS' IN MOUSE EPIDERMIS

It has been postulated that mouse epidermis contains two populations of resting cells, one of which is blocked at the G₁-S boundary and the other between G₂ and mitosis. the ‘arrested G₂ cells’ were estimated, by the labelled mitosis method, to comprise 510% of the epidermal population and presumed to function as a ‘reserve pool’ which could be activated by wounding. A comprehensive search has now been carried out for arrested G₂ cells in mouse epidermis using the direct methods of single cell and flow through cytophotometry. No evidence was obtained which supports the existence of such a cell compartment. Suitable control experiments were carried out to ensure that G₂ cells were not lost during the isolation of epidermal nuclei.