Coconut water (coconut liquid endosperm), with its many applications, is one of the world's most versatile natural product. This refreshing beverage is consumed worldwide as it is nutritious and beneficial for health. There is increasing scientific evidence that supports the role of coconut water in health and medicinal applications. Coconut water is traditionally used as a growth supplement in plant tissue culture/micropropagation. The wide applications of coconut water can be justified by its unique chemical composition of sugars, vitamins, minerals, amino acids and phytohormones. This review attempts to summarise and evaluate the chemical composition and biological properties of coconut water.

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The Chemical Composition and Biological Properties of Coconut (Cocos nucifera L.) Water

Free radicals are generated by the collapse of ultrasound-induced cavitation bubbles when they are forcefully compressed by dynamic stimuli. Radical generation occurs as a result of the extremely high temperatures induced by adiabatic compression during the violent collapse process. It is generally believed that extreme conditions are required for this type of radical generation. However, we have demonstrated free-radical generation from the collapse of microbubbles (diameter = <50 μm) in the absence of a harsh dynamic stimulus. In contrast to ultrasound-induced cavitation bubbles, which collapse violently after microseconds, the microbubbles collapsed softly under water after several minutes. Electron spin-resonance spectroscopy confirmed free-radical generation by the collapsing microbubbles. The increase of the surface charges (ζ potentials) of the microbubbles, which were measured during their collapse, supported the hypothesis that the significant increase in ion concentration around the shrinking ga...

Free-radical generation from collapsing microbubbles in the absence of a dynamic stimulus.

Cardiovascular effects of flavonoids are not caused only by direct antioxidant activity

The product. Coconut water (Cocos nucifera L.) is an ancien t tropical beverage whose popularity on the international market has been continuously increasing in recent years. Uses. Besides its various traditional uses, this refreshing liqu id extracted from the coconut fruit has recently been described as a "sport beverage" and has drawn the attention of manufacturers as a natural functional drink. Composition. Coconut water has a low matter content (2% to 5% wet basis), mainly comprising sugars and minerals. Quality criteria, such as the water per nut ratio, Total Soluble Solids (TSS), total sugar per nut, and [reducing sugars / total sugars] ratio, are good indicators for estimating the suitability of coconut cultivars for the production of coconut water. Regarding these criteria, dwarf varieties are the most suitable cultivars to obtain a tasty product. Properties. The quality of coconut water can not only be attributed to sugars and minerals because it also has a typical flavour and some original properties. Although many authors have cited medicinal uses or growth-promoting activities, only a few publications have clearly identified the components responsible for these properties. Discussion. Results of former and recent investigations are discussed. Finally, suggestions are made for further research to increase our knowledge of this original tropical juice. (Resume d'auteur)

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Coconut water uses, composition and properties: a review

A number of drugs have been withdrawn from the market or severely restricted in their use because of unexpected toxicities that become apparent only after the launch of new drug entities. Circumstantial evidence suggests that, in most cases, reactive metabolites are responsible for these unexpected toxicities. In this review, a general overview of the types of reactive metabolites and the consequences of their formation are presented. The current approaches to evaluate bioactivation potential of new compounds with particular emphasis on the advantages and limitation of these procedures will be discussed. Reasonable reasons for the excellent safety record of certain drugs susceptible to bioactivation will also be explored and should provide valuable guidance in the use of reactive-metabolite assessments when nominating drug candidates for development. This will, in turn, help us to design and bring safer drugs to the market.

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Deleterious effects of reactive metabolites.

Inhibitory activity of kinetin on free radical formation of activated platelets in vitro and on thrombus formation in vivo

ESR spin trapping of a carbon-centered free radical from agonist-stimulated human platelets.

The pro-oxidant activities of baicalein, morin, myricetin, quercetin, and rutin were examined in various cell-containing systems including human platelets, rat vascular smooth muscle cells, human umbilical vein endothelial cells (HUVECs), human THP-1 cells, and fibroblast cells. Electron spin resonance (ESR) results showed that only baicalein generated hydroxyl radicals in a resting human platelet suspension, whereas the other flavonoids showed no effects on any of the resting cell systems. A low concentration of arachidonic acid (AA) increased the intensity of hydroxyl radicals, but a high concentration inhibited it. Collagen and thrombin, platelet aggregatory agents that can cause the release of AA by platelets, enhanced baicalein-induced hydroxyl radical formation, whereas ADP and U44619 showed no significant effects. Quinacrine and 5,8,11,14-eicosatetraenoic trifluoromethyl ketone, both PLA2 inhibitors, significantly attenuated baicalein-induced hydroxyl radical formation. These results suggest that baicalein-induced hydroxyl radical formation is associated with AA metabolite enzymes in human platelets. The formation of hydroxyl radicals was significantly inhibited by lipoxygenase inhibitors including nordihydroguaiaretic acid, (-)-epicatechin, (-)-epicatechin gallate, and hinokitiol, but was not affected by desferroxamine or the heme protein inhibitors KCN and NaN3. On the other hand, semiquinone free radicals were generated when baicalein was incubated with horseradish peroxidase/H2O2 or platelets/AA. The semiquinone radicals formed in the platelets/AA system could be extensively inhibited by desferroxamine, diethylenetriaminepentaacetic acid, KCN, and NaN3, indicating that prostaglandin H synthase (PGHS)-peroxidase may be involved. The results of this study led to the proposal that baicalein induces hydroxyl radical formation via 12-lipoxygenase and induces semiquinone radical formation via PGHS-peroxidase in human platelets.

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Baicalein Induction of Hydroxyl Radical Formation via 12-Lipoxygenase in Human Platelets: An ESR Study

The aim of this study was to systematically examine the inhibitory mechanisms of the flavonoid α-naphthoflavone (α-NF) in platelet activation. In this study, α-NF concentration dependently (5−20 μM) inhibited platelet aggregation stimulated by agonists. α-NF (5 and 10 μM) inhibited intracellular Ca2+ mobilization, phosphoinositide breakdown, and thromboxane A2 formation stimulated by collagen (1 μg/mL) in human platelets. In addition, α-NF (5 and 10 μM) markedly increased levels of cyclic GMP and cyclic GMP-induced vasodilator-stimulated phosphoprotein (VASP) Ser157 phosphorylation. Rapid phosphorylation of a platelet protein of Mr 47 000 (P47), a marker of protein kinase C activation, was triggered by phorbol-12,13-dibutyrate (60 nM). This phosphorylation was markedly inhibited by α-NF (5 and 10 μM). However, α-NF (5 and 10 μM) did not reduce the electron spin resonance (ESR) signal intensity of hydroxyl radicals in collagen (1 μg/mL)-activated platelets. These results indicate that the antiplatelet acti...

α-Naphthoflavone, a potent antiplatelet flavonoid, is mediated through inhibition of phospholipase C activity and stimulation of cyclic GMP formation

The detailed mechanisms underlying morphine-signaling pathways in platelets remain obscure. Therefore, we systematically examined the influence of morphine on washed human platelets. In this study, washed human platelet suspensions were used for in vitro studies. Furthermore, platelet thrombus formation induced by irradiation of mesenteric venules with filtered light in mice pretreated with fluorescein sodium was used for an in vivo thrombotic study. Morphine concentration dependently (0.6, 1, and 5 µM) potentiated platelet aggregation and the ATP release reaction stimulated by agonists (i.e., collagen and U46619) in washed human platelets. Yohimbine (0.1 µM), a specific α2-adrenoceptor antagonist, markedly abolished the potentiation of morphine in platelet aggregation stimulated by agonists. Morphine also potentiated phosphoinositide breakdown and intracellular Ca2+ mobilization in human platelets stimulated by collagen (1 µg/ml). Moreover, morphine (0.6–5 µM) markedly inhibited prostaglandin E1 (10 µM)-induced cyclic AMP formation in human platelets, while yohimbine (0.1 µM) significantly reversed the inhibition of cyclic AMP by morphine (0.6 and 1 µM) in this study. The thrombin-evoked increase in pHi was markedly potentiated in the presence of morphine (1 and 5 µM). Morphine (2 and 5 mg/g) significantly shortened the time require to induce platelet plug formation in mesenteric venules. We concluded that morphine may exert its potentiation in platelet aggregation by binding to α2-adrenoceptors in human platelets, with a resulting inhibition of adenylate cyclase, thereby reducing intracellular cyclic AMP formation followed by increased activation of phospholipase C and the Na+/H+ exchanger. This leads to increased intracellular Ca2+ mobilization, and finally potentiation of platelet aggregation and of the ATP release reaction.

https://link.springer.com/content/pdf/10.1007/BF02256448.pdf

Tzeng-Fu Chen

Papers

Inhibitory activity of kinetin on free radical formation of activated platelets in vitro and on thrombus formation in vivo

ESR spin trapping of a carbon-centered free radical from agonist-stimulated human platelets.

Baicalein Induction of Hydroxyl Radical Formation via 12-Lipoxygenase in Human Platelets: An ESR Study

α-Naphthoflavone, a potent antiplatelet flavonoid, is mediated through inhibition of phospholipase C activity and stimulation of cyclic GMP formation

Morphine-potentiated platelet aggregation in in vitro and platelet plug formation in in vivo experiments.