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Participation of some radical products in isolated nerve cell response to blue laser microirradiation

机译:某些自由基产物参与离体神经细胞对蓝色激光微辐射的反应

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Abstract: For the study of some primary photochemical mechanisms of neuron response to laser microirradiation it was modified with quenchers of intermediate photochemical products. Dibunol (0.02 mM), inhibitor of lipid peroxidation, did not shift impulse activity itself, but changed neuron response to microirradiation: impulse frequency acceleration was lower than control, spike generation ceased at higher frequency levels, and neuron lifetime increased by 1.7 times. Hence, impulse acceleration phase is probably connected with membrane lipid peroxidation induced by blue light and dibunol protects cells from laser injury. The study of hydroxyl radicals (important in ionizing radiation cell damage) participation using quencher D- mannite (10 mM) did not show reliable changes of neuron response parameters, i.e., these radicals were not significant for blue laser light induced neuron activity changes. Observation of flavin-like action spectrum with a maximum near 460 nm forced us to use a flavin triplet quencher. Ten mM NaJ did not shift impulse frequency level but changed neuron response to irradiation: cell lifetime increased by 1.4 times due to inhibition phase increase. It is not proved that flavin triplets were involved in neuron response and its lifetime increase was due to rather physiological than photochemical causes. !6
机译:摘要:为了研究神经元对激光微辐照反应的一些主要光化学机理,用中间光化学产物的淬灭剂对其进行了修饰。脂质过氧化抑制剂Dibunol(0.02 mM)本身并未改变脉冲活动,但改变了神经元对微辐照的反应:脉冲频率加速低于对照组,峰值频率在较高频率下停止了,神经元寿命增加了1.7倍。因此,脉冲加速阶段可能与蓝光诱导的膜脂质过氧化有关,地丁酚可以保护细胞免受激光伤害。使用淬灭剂D-甘露石(10 mM)进行的羟基自由基(对电离辐射细胞损伤很重要)参与的研究没有显示出可靠的神经元反应参数变化,即这些自由基对于蓝色激光诱导的神经元活性变化没有显着影响。观察到最大在460 nm附近有类黄素作用谱,这迫使我们使用黄素三重态猝灭剂。 10 mM NaJ不会改变脉冲频率水平,但会改变神经元对辐照的反应:由于抑制期增加,细胞寿命增加了1.4倍。没有证明黄素三联体参与神经元反应,其寿命增加是由于生理原因而非光化学原因。 !6

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