Sodium Fluoride Mimics the Effect of Prostaglandin E2 on Catecholamine Release from Bovine Adrenal Chromaffin Cells

We have reported recently that prostaglandin E2 (PGE2) stimulated phosphoinositide metabolism in bovine adrenal chromaffin cells and that PGE2 and ouabain, an inhibitor of Na+, K(+)-ATPase, synergistically induced a gradual secretion of catecholamines from the cells. Here we examined the involvement of a GTP-binding protein(s) in PGE receptor-induced responses by using NaF. In the presence of Ca2+ in the medium, NaF stimulated the formation of all three inositol phosphates, i.e., inositol monophosphate, bisphosphate, and trisphosphate, linearly over 30 min in a dose-dependent manner (15-30 mM). This effect on phosphoinositide metabolism was accompanied by an increase in cytosolic free Ca2+. NaF also induced catecholamine release from chromaffin cells, and the dependency of stimulation of the release on NaF concentration was well correlated with those of NaF-enhanced inositol phosphate formation and increase in cytosolic free Ca2+. Although the effect of NaF on PGE2-induced catecholamine release in the presence of ouabain was additive at concentrations below 20 mM, there was no additive effect at 25 mM NaF. Furthermore, the time course of catecholamine release stimulated by 20 mM NaF in the presence of ouabain was quite similar to that by 1 microM PGE2, and both stimulations were markedly inhibited by amiloride, with half-maximal inhibition at 10 microM. Pretreatment of the cells with pertussis toxin did not prevent, but rather enhanced, PGE2-induced catecholamine release over the range of concentrations examined. These results demonstrate that NaF mimics the effect of PGE2 on catecholamine release from chromaffin cells and suggest that PGE2-evoked catecholamine release may be mediated by the stimulation of phosphoinositide metabolism through a putative GTP-binding protein insensitive to pertussis toxin.     

Adenosine and Glutamate Modulate Each Other's Release from Rat Hippocampal Synaptosomes

Abstract: In rat hippocampal synaptosomes, adenosine decreased the K⁺ (15 mM) or the kainate (1 mM) evoked release of glutamate and aspartate. An even more pronounced effect was observed in the presence of the stable adenosine analogue, R-phenylisopropyladenosine. All these effects were reversed by the selective adenosine A₁ receptor antagonist 8-cyclo-pentyltheophylline. In the same synaptosomal preparation, K⁺ (30 mM) strongly stimulated the release of the preloaded [³H]adenosine in a partially Ca²⁺-dependent and tetrodotoxin (TTX)-sensitive manner. Moreover, in the same experimental conditions, both l -glutamate and l -aspartate enhanced the release of [³H]adenosine derivatives ([³H]ADD). The gluta-mate-evoked release was dose dependent and appeared to be Ca²⁺ independent and tetrodotoxin insensitive. This effect was not due to metabolism because even the nonmetabolizable isomers d -glutamate and d -aspartate were able to stimulate [³H]ADD release. In contrast, the specific glutamate agonists N-methyl-d -aspartate, kainate, and quisqualate failed to stimulate [³H]ADD release, suggesting that glutamate and aspartate effects were not mediated by known excitatory amino acid receptors. Moreover, NMDA was also ineffective in the absence of Mg²⁺ and l -glutamate-evoked release was not inhibited by adding the specific antagonists 2-amino-5-phosphonovaleric acid or 6–7-dinitroquinoxaline-2, 3-dione. The stimulatory effect did not appear specific for only excitatory amino acids, as γ-anunobutyric acid stimulated [³H]ADD release in a dose-related manner. These results suggest that, at least in synaptosomal preparations from rat hippocampus, adenosine and glutamate modulate each other's release. The exact mechanism of such interplay, although still, unknown, could help in the understanding of excitatory amino acid neurotoxicity.     

Optical Feedback Loop Involving Dinoflagellate Symbiont and Scleractinian Host Drives Colorful Coral Bleaching

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Selective Alterations in Presynaptic Cytomatrix Protein Organization Induced by Calcium and Other Divalent Cations That Modulate Exocytosis

Rises in intracellular calcium cause several events of physiological significance, including the regulated release of neuronal transmitters. In this study, the effects of divalent cations on the structural organization of cytomatrix in presynaptic terminals was examined. [35S]Methionine-radiolabeled guinea pig retinal ganglion cell cytomatrix proteins were axonally transported [in slow component b (SCb) of axonal transport] to the neuron terminals in the superior colliculus. When the peak of radiolabeled cytomatrix proteins reached the terminals, synaptosomes containing the radiolabeled cytomatrix proteins were prepared. Approximately 40% of each SCb protein was soluble after hypoosmotic lysis of the radiolabeled synaptosomes in the presence of divalent cation chelators. Lysis of synaptosomes in the presence of calcium ions over a range of concentrations, however, caused a dramatic decrease in solubility of the presynaptic SCb proteins. The cytoplasmic effects may result from a calcium-dependent condensation of cytoplasm around presynaptic terminal membrane systems. There are two major presynaptic SCb proteins (at 60 and 35 kDa), that exhibited exceptional behavior: they remained as soluble in the presence of calcium as under control conditions, suggesting that they were relatively unaffected by the mechanism causing the decrease in SCb protein solubility. Also examined were the effects of other alkaline earth and transition metal divalent cations on the presynaptic SCb proteins.     

Do soft drinks affect metal ions release from orthodontic appliances?

ObjectiveThe effect of orange juice and Coca Cola^® on the release of metal ions from fixed orthodontic appliances.Materials and methodsA continuous flow system designed for in vitro testing of orthodontic appliances was used. Orange juice/Coca Cola^® was flowing through the system alternately with artificial saliva for 5.5 and 18.5 h, respectively. The collected samples underwent a multielemental ICP-OES analysis in order to determine the metal ions release pattern in time.ResultsThe total mass of ions released from the appliance into orange juice and Coca Cola^® (respectively) during the experiment was calculated (μg): Ni (15.33; 37.75), Cr (3.604; 1.052), Fe (48.42; ≥156.1), Cu (57.87, 32.91), Mn (9.164; 41.16), Mo (9.999; 30.12), and Cd (0.5967; 2.173).ConclusionsIt was found that orange juice did not intensify the release of metal ions from orthodontic appliances, whereas Coca Cola^® caused increased release of Ni ions.     

Responses of nitrogen and phosphorus resorption from leaves and branches to long-term nitrogen deposition in a Chinese fir plantation

为了解森林养分内循环对全球变化的响应, 基于长期模拟氮沉降试验, 研究了杉木(Cunninghamia lanceolata)人工林不同龄级(一年生、二年生和衰老)叶和枝的氮(N)、磷(P)养分分配及其再吸收特征, 并分析了不同模拟N沉降处理时间(7年和14年)杉木叶N、P养分再吸收差异。在12年生杉木中开展模拟N沉降试验, 以尿素(CO(NH₂)₂)为N源, 设N0、N1、N2和N3 4个处理水平, 施氮量分别为0、60、120和240 kg·hm ^-2·a ^-1, 每个处理重复3次。结果表明: (1)叶和枝在衰老过程中碳(C)、N和P含量逐渐降低, 且叶的C、N和P含量比枝高; N含量大小依次为一年生叶>二年生叶>衰老叶>一年生枝>二年生枝>衰老枝, 且N3 > N2 > N1 > N0, 而C:N则呈现相反的趋势; 衰老器官的C:N、C:P、N:P比新鲜器官高; N沉降增加了不同龄级叶和枝(除二年生叶外)的N、N:P和C:P, 但降低了P和C:N。(2)叶和枝的N、P养分再吸收率(RE_N、RE_P)随龄级的增加至衰老有规律地递减, 且RE_P > RE_N; 受长期N沉降的影响, RE_N叶(28.12%) <枝(30.00%), 而RE_P则为叶(45.82%) >枝(30.42%); 杉木叶和枝N:P与RE_N:RE_P之间存在极显著的线性相关关系。(3)随N沉降处理时间的增加, 叶RE_N呈降低态势, 各处理(N1、N2和N3)分别降低了9.85%、3.17%和11.71%; 而RE_P则明显上升, 分别增加了71.98%、42.25%和9.60%。研究结果表明: 不同器官、不同龄级的养分再吸收率随氮沉降处理的水平、处理时间而所有不同; RE_N:RE_P与N:P之间存在紧密关系。     

Release kinetics of ATP in cells exposed to nonionic detergents

We have previously shown that the protein binding of intracellular ATP could be examined by monitoring the ATP release kinetics from Triton X-100 and Brij 58 nonionic detergent permeabilized cells. We have now analysed the protein binding of ATP in an isotonic medium using intact and partially ATP depleted Brij 58 treated human erythrocytes. The effects of Triton X-100 below the critical micelle concentration (CMC) was studied in normal and tumorous tissue culture cells and human red blood cells. Our results showed that the protein association of ATP was altered in the partially ATP depleted erythrocytes. Below the CMC value, but above a critical level Triton X-100 treatment was effective in mobilizing the intracellular ATP in both cell types. The ATP release curves were sigmoidal and an ‘all or none’ type of response was observed, especially in erythrocytes. The use of Triton X-100 (< CMC) delays the detergent-induced cell decomposition time thus providing a new approach to investigating the physical state of intracellular ATP.