32 research outputs found

    Exploring metabolic responses of potato tissue induced by electric pulses

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    In this study, we investigated the metabolic responses of potato tissue induced by pulsed electric field (PEF). Potato tissue was subjected to field strengths ranging from 30 to 500 V/cm, with a single rectangular pulse of 10 μs, 100 μs, or 1 ms. Metabolic responses were monitored using isothermal calorimetry, changes on electrical resistance during the delivery of the pulse, as well as impedance measurements. Our results show that the metabolic response involves oxygen consuming pathways as well as other unidentified events that are shown to be insensitive to metabolic inhibitors such as KCN and sodium azide. The metabolic response is strongly dependent on pulsing conditions and is independent of the total permeabilization achieved by the pulse. Evidence shows that calorimetry is a simple and powerful method for exploring conditions for metabolic stimulation, providing information on metabolic responses that can not be obtained from electrical measurements. This study set the basis for further investigations on defense-related consequences of PEF-induced stress.Sparbanksstiftelsen Färs & Frosta (Sweden).Fundação para a Ciência e a Tecnologia (FCT).Lund University (Sweden).Department of Cell and Organism Biology; Department of Plant Biochemistry

    Effects of pulsed electric field on the viscoelastic properties of potato tissue

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    We have investigated whether transient permeabilization caused by the application of pulsed electric field would give rise to transient changes in the potato tissue viscoelastic properties. Potato tissue was subjected to nominal field strengths (E) ranging from 30 to 500 V/cm, with a single rectangular pulse of 10−5, 10−4, or 10−3 s. The changes on the viscoelastic properties of potato tissue during pulsed electric fields (PEF) were monitored through small amplitude oscillatory dynamic rheological measurements. The elastic (G′) and viscous moduli (G″) were measured every 30 s after the delivery of the pulse and the loss tangent change (tan-δ) was calculated. The results were correlated with measurements of changes on electrical resistance during the delivery of the pulse. Results show a drastic increase of tan-δ in the first 30 s after the application of the pulse, followed by a decrease 1 min after pulsation. This response is strongly influenced by pulsing conditions and is independent of the total permeabilization achieved by the pulse. Our results, supported by similar measurements on osmotically dehydrated control samples, clearly show that PEF causes a rapid change of the viscoelastic properties of the tissue that could be attributed to a partial loss in turgor pressure. This would be an expected consequence of electroporation. The recovery of tan-δ to values similar to those before pulsation strongly suggests recovery of cell membrane properties and turgor, pointing at reversible permeabilization of the cells. A slight increase of stiffness traduced by a negative change of tan-δ after application of certain PEF conditions may also give an indication of events occurring on cell wall structure due to stress responses. This study set the basis for further investigations on the complex cell stress physiology involving both cell membrane functional properties and cell wall structure that would influence tissue physical properties upon PEF application.Fundação para a Ciência e a Tecnologia (FCT

    Role of nicotinic acetylcholine receptor subtypes on nicotine's enhancing effect on electrical field stimulation elicited contractile responses in rabbit urine bladder.

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    This study aims to investigate the contribution of presynaptic nicotinic acetylcholine receptors (nAChRs) sub-types to nicotine-induced enhancement in electrical field stimulation (EFS) EFS-mediated contractile responses in rabbit urine bladder smooth muscle preparations

    Role of nicotinic acetylcholine receptor subtypes on nicotine's enhancing effect on electrical field stimulation elicited contractile responses in rabbit urine bladder

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    SARIOGLU, YUSUF/0000-0002-9227-365XWOS: 000380260000030PubMed: 27160140OBJECTIVE: This study aims to investigate the contribution of presynaptic nicotinic acetylcholine receptors (nAChRs) sub-types to nicotine-induced enhancement in electrical field stimulation (EFS) EFS-mediated contractile responses in rabbit urine bladder smooth muscle preparations. MATERIALS AND METHODS: Rabbit urine bladder smooth muscle strips were placed in organ baths containing 20 ml of an aerated Krebs-Henseleit solution, and contractions were recorded using isometric force displacement transducers. Following the acquisition of control EFS (60 V, 8 Hz, 1 ms) responses, nicotine was added to the bath at a 3x10(-5) M concentration, and EFS responses were obtained. The effect of nAChR antagonists on nicotine-induced augmentation in EFS-mediated responses was investigated in the presence of hexamethonium, dihydro-beta-erythroidine, mecamy-lamine, and alpha-bungarotoxin. RESULTS: Tetrodotoxin (TTX; 10(-6) M) completely blocked EFS-induced contractile responses in smooth muscle strips. Similarly, Atropine (10(-6) M), when administered with alpha,beta-methylene adenosine triphosphate (alpha,beta-methylene-ATP) (10(-5) M), completely blocked EFS responses. Nicotine significantly enhanced EFS-mediated contractile responses (23.67% +/- 1.75). Nicotine-induced increases in EFS responses were largely inhibited by hexamethonium, mecamylamine, and dihydro-beta-erythroidine, whereas alpha-bungarotoxin only partly inhibited these enhancements. CONCLUSIONS: These findings demonstrate that EFS-induced neurogenic contractions in rabbit urine bladder smooth muscle strips are mediated by purinergic and cholinergic transmissions, and the alpha 4 beta 2, alpha 3 beta 4, and alpha 7 sub-types of nAChRs contribute to the enhancement effect of nicotine on EFS-induced contractile responses.Gazi University Unit of Scientific Research ProjectsGazi University [01/2006-17]This work was supported by the Gazi University Unit of Scientific Research Projects (Project number: 01/2006-17)
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