Stress in Morphine-Addicted Rats: Antistressor Properties of Comenic Acid

In chronic experiments carried out on 128 rats we demonstrated that the withdrawal syndrome revealed in morphine-addicted animals is combined with the development of stress. This was reflected in an increase in the total duration of grooming behavior and in changes in its temporal pattern. In morphine-addicted animals, only the initial and final phases of the seven successive grooming phases remained clearly pronounced, whereas intermediate stages were lost. A recycling of the initial grooming stage, which could result in self-inflicted damage to the skin, was observed. Under conditions of complete discontinuation of morphine, disturbances of grooming were even intensified, and during 18 days after discontinuation of the drug such disturbances gradually disappeared. Injections of comenic acid against the background of discontinuation of morphine significantly accelerated the process of normalization of both the duration and pattern of grooming (9 days after discontinuation of the drug). In intact rats, comenic acid did not induce noticeable disturbances of grooming. We conclude that comenic acid possesses antistressor properties under conditions of the withdrawal syndrome.     

Arrest of Morphine Withdrawal Syndrome Using Comenic Acid: an Experimental Study on Rats

Chronic experiments on rats with experimental morphine addiction demonstrated that injections of comenic acid are capable of significantly arresting the withdrawal syndrome after morphine discontinuation. Neither habituation nor addiction to comenic acid were developed. Optimum doses of comenic acid have been selected (34 to 50 mg/kg per day).     

Effect of Comenic Acid on the Activation of G Proteins by Agonists of Opioid Receptors in Plasma Membranes from the Rat Brain

We studied the effect of comenic acid on transmembrane opioid signaling (in particular, on that mediated by -opioid receptors, with the use of an agonist of these receptors, [D-Ala²]-leucine enkephalin (DALE), and mediated by -opiate receptors, with the use of morphine). It was demonstrated that comenic acid modulates agonist-dependent binding of [³⁵S]GTPS in plasma membranes from the rat brain. The effect of comenic acid on the activation of G proteins via -opioid receptors possessing high affinity for DALE depended on the ion composition of the medium: in the presence of K⁺ the activation decreased, while in the presence of Na⁺ it remained invariable. Under the influence of comenic acid, the agonist-dependent activation of G proteins mediated by receptors with low affinity for DALE was intensified in the presence of both Na⁺ and K⁺. Using morphine, we observed opposite effects: in the presence of Na⁺ or K⁺ comenic acid decreased or increased, respectively, the agonist-dependent activation of G proteins. We suggest that due to the comenic acid-induced modulation the relative intensity of activation of G proteins, which control signal pathways activated by opioid receptors of different types, can be significantly changed.     

乳酸菌酸胁迫反应机制研究进展

乳酸菌可发酵糖类产生乳酸,并广泛应用于食品、药物和饲料等工业。由于有机酸的积累,乳酸菌大部分的生长代谢都在低pH的酸性环境中进行,具有酸胁迫反应。pH的自我平衡、ATR反应机制、对大分子的保护和修复作用及细胞膜的变化等是乳酸菌酸胁迫反应的主要机制,其中,pH自我平衡包括F0F1-ATPase质子泵、精氨酸脱氨酶途径(ADI)和谷氨酸脱羧酶途径(GAD)等。由此可见,乳酸菌酸胁迫反应机制涉及到基因和蛋白的表达调控等,是非常复杂的网络调控体系。     

乌索酸与齐墩果酸衍生物的合成进展

乌索酸和齐墩果酸在多种植物中均有分布.二者互为同分异构体,均属于五环三萜类化合物,由于其结构多样性而具有广泛的生物活性,包括抗肿瘤、抗氧化、抗艾滋病、抗溃疡、抗炎、免疫调节等功能.有关这两种活性物质的衍生化研究一直为科研人员所关注,本文主要综述了近10年来二者衍生物合成方面的新进展,为寻找活性先导化合物、合理设计药物分子提供依据.     

Enzymatic Formation of Hexadecenoic Acid from Palmitic Acid

Desaturation of palmitic acid was investigated in an enzyme system prepared from rat liver. 2-trans-Hexadecenoic acid as well as 9-cis-hexadecenoic acid (palmitoleic acid) were found to be formed as monoenoic acid in this system.     

Biotransformation of Cinnamic Acid,p-Coumaric Acid,Caffeic Acid,and Ferulic Acid by Plant Cell Cultures of Eucalyptus perriniana

Biotransformations of phenylpropanoids such as cinnamic acid, p-coumaric acid, caffeic acid, and ferulic acid were investigated with plant-cultured cells of Eucalyptus perriniana. The plant-cultured cells of E. perriniana converted cinnamic acid into cinnamic acid β-D-glucopyranosyl ester, p-coumaric acid, and 4-O-β-D-glucopyranosylcoumaric acid. p-Coumaric acid was converted into 4-O-β-D-glucopyranosylcoumaric acid, p-coumaric acid β-D-glucopyranosyl ester, 4-O-β-D-glucopyranosylcoumaric acid β-D-glucopyranosyl ester, a new compound, caffeic acid, and 3-O-β-D-glucopyranosylcaffeic acid. On the other hand, incubation of caffeic acid with cultured E. perriniana cells gave 3-O-β-D-glucopyranosylcaffeic acid, 3-O-(6-O-β-D-glucopyranosyl)-β-D-glucopyranosylcaffeic acid, a new compound, 3-O-β-D-glucopyranosylcaffeic acid β-D-glucopyranosyl ester, 4-O-β-D-glucopyranosylcaffeic acid, 4-O-β-D-glucopyranosylcaffeic acid β-D-glucopyranosyl ester, ferulic acid, and 4-O-β-D-glucopyranosylferulic acid. 4-O-β-D-Glucopyranosylferulic acid, ferulic acid β-D-glucopyranosyl ester, and 4-O-β-D-glucopyranosylferulic acid β-D-glucopyranosyl ester were isolated from E. perriniana cells treated with ferulic acid.     

Synthesis of l-(+)-Tartaric Acid from l-Ascorbic Acid via 5-Keto-d-Gluconic Acid in Grapes

5-Keto-l-idionic acid (5-keto-d-gluconic acid, d-xylo-5-hexulosonic acid) was found as a metabolic product of l-ascorbic acid in slices of immature grapes, Vitis labrusca L. cv `Delaware'. Specifically labeled compounds, recognized as metabolic products of l-ascorbic acid in grapes, were fed to young grape tissues to investigate the metabolic pathway from l-ascorbic acid to l-(+)-tartaric acid.     

丙酮酸对细菌L-乳酸发酵的促进作用

研究了丙酮酸在不同浓度和添加时间对LactobacilluscaseiL 乳酸发酵过程中葡萄糖转化率和L 乳酸产量的影响。结果表明 ,当丙酮酸的添加量为 30g·L- 1 时 ,L 乳酸的产量达到 74g·L- 1 。在 72h的发酵周期内 ,丙酮酸在 2 4h和 42h添加的效果好于其他时间添加。     

Bacterial Degradation of 4-Hydroxyphenylacetic Acid and Homoprotocatechuic Acid

A species of Acinetobacter and two strains of Pseudomonas putida when grown with 4-hydroxyphenylacetic acid gave cell extracts that converted 3,4-dihydroxyphenylacetic acid (homoprotocatechuic acid) into carbon dioxide, pyruvate, and succinate. The sequence of enzyme-catalyzed steps was as follows: ring-fission by a 2,3-dioxygenase, nicotinamide adenine dinucleotide-dependent dehydrogenation, decarboxylation, hydration, aldol fission, and oxidation of succinic semialdehyde. Two new metabolites, 5-carboxymethyl-2-hydroxymuconic acid and 2-hydroxyhepta-2,4-diene-1,7-dioic acid, were isolated from reaction mixtures and a third, 4-hydroxy-2-ketopimelic acid, was shown to be cleaved by extracts to give pyruvate and succinic semialdehyde. Enzymes of this metabolic pathway were present in Acinetobacter grown with 4-hydroxyphenylacetic acid but were effectively absent when 3-hydroxyphenylacetic acid or phenylacetic acid served as sources of carbon.     

Abscisic Acid ELISA: Organic Acid Interference

Consideration must be exercised in determination of buffers and solutions used when carrying out enzyme-linked immunosorbent assays (ELISAs). A commercial monoclonal antibody kit for abscisic acid (Idetek, Inc.) gives significant false-positives with tricarboxylic acid cycle intermediates. The organic acids or contaminants interfered with ELISA assays for ABA as indicated by deviations in the slopes of standard curves of ABA in the organic acids. The interference, in the case of α-ketoglutarate, was caused by a contaminant. Of the organic buffers tested—Tris, Tricine, and Hepes—only Hepes showed false-positive ABA. In addition, we present data indicating the presence of ABA in commercial mannitol and provide a simple procedure for removal of the ABA.     

Role of Ribonucleic Acid Synthesis in Replication of Deoxyribonucleic Acid

An experiment previously interpreted to show a ribonucleic acid requirement for propagation of deoxyribonucleic replication is reexamined and the earlier interpretation is shown to be incorrect.     

Turnover of Free Sialic Acid, CMP-Sialic Acid, and Bound Sialic Acid In Rat Brain

Abstract: Adult male rats were injected intraventricularly with N-[³H]acetylmannosamine. After different time intervals the rats were killed and free sialic acid, CMP-sialic acid, lipid- and protein-bound sialic acid were isolated from brain and the specific radioactivities determined. Maximal specific radioactivity was reached after approximately 4 h for CMP-sialic acid, after 10–12 h for free sialic acid and after approximately 42 h for lipid-and protein-bound sialic acid. After some days the specific radioactivities of all four pools were the same and decreased equally, with a calculated turnover rate of approximately 3.5 weeks. The conclusion was that this phenomenon was the result of reutilisation of sialic acid and/or precursors. Therefore, the calculated turnover is not the turnover of bound sialic acid, but merely the rate of leakage of sialic acid and/or precursors out of the brain, so that no real turnover can be measured by this method. The first few hours after injection the specific radioactivity of CMP-sialic acid rose above that of free sialic acid. It is supposed that a compartmentalization exists of free sialic acid. The newly synthesized sialic acid molecules are not secreted into the cytoplasmic pool but are preferentially used for the synthesis of CMP-sialic acid. The results and conclusions are discussed in view of the general problems concerning turnover measurements of glycoconjugates.     

Hyaluronic Acid Degradation by Ascorbic Acid and Influence of Iron

The effects of ascorbic acid, iron and ADP on hyaluronic acid, a compound present in inflamed joints, were investigated in an in vitro system. Ascorbic acid induces degradation of hyaluronic acid which increased in the presence of FeCl, and which is additionally stimulated by ADP chelated ferric ions. The hyaluronic acid degrading reactions induced by the Fe-III/ADP/ascorbic acid system were inhibited by catalase and formate to various extents whereas the presence of superoxide dismutase did not exert any inhibitory effect. Desferrioxamine, a specific iron chelator, completely inhibited hyaluronic acid depolymerisation by ascorbic acid as well as in combination with FeCl₃ or FeCl₃/ADP, respectively. We suggest that the ultimate hyaluronic acid degrading species is OH', generated via the Fe-III/ADP catalysed Haber Weiss reaction. There is also an indication for the involvement of perferryl or/and ferryl species in the degradation process.