Kuban State University, 350040 Krasnodar, Russia.
South Scientific Center of the Russian Academy of Sciences, 344006 Rostov-on-Don, Russia.
Molecules. 2021 Apr 2;26(7):2036. doi: 10.3390/molecules26072036.
The deuterium content modification in an organism has a neuroprotective effect during the hypoxia model, affecting anxiety, memory and stress resistance. The aim of this work was to elucidate the possible mechanisms of the medium D/H composition modification on nerve cells. We studied the effect of an incubation medium with a 50 ppm deuterium content compared to a medium with 150 ppm on: (1) the activity of Wistar rats' hippocampus CA1 field neurons, (2) the level of cultured cerebellar neuron death during glucose deprivation and temperature stress, (3) mitochondrial membrane potential (MMP) and the generation of reactive oxygen species in cultures of cerebellar neurons. The results of the analysis showed that the incubation of hippocampal sections in a medium with a 50 ppm deuterium reduced the amplitude of the pop-spike. The restoration of neuron activity was observed when sections were returned to the incubation medium with a 150 ppm deuterium content. An environment with a 50 ppm deuterium did not significantly affect the level of reactive oxygen species in neuron cultures, while MMP decreased by 16-20%. In experiments with glucose deprivation and temperature stress, the medium with 50 ppm increased the death of neurons. Thus, a short exposure of nerve cells in the medium with 50 ppm deuterium acts as an additional stressful factor, which is possibly associated with the violation of the cell energy balance. The decrease in the mitochondrial membrane potential, which is known to be associated with ATP synthesis, indicates that this effect may be associated with the cell energy imbalance. The decrease in the activity of the CA1 field hippocampal neurons may reflect reversible adaptive changes in the operation of fast-reacting ion channels.
生物体中的氘含量修饰在低氧模型中具有神经保护作用,影响焦虑、记忆和应激抗性。本工作的目的是阐明中重水组成修饰对神经细胞的可能机制。我们研究了与含有 150 ppm 的培养基相比,含有 50 ppm 氘的培养基对以下方面的影响:(1)Wistar 大鼠海马 CA1 场神经元的活性,(2)在葡萄糖剥夺和温度应激下培养的小脑神经元死亡水平,(3)小脑神经元培养物中的线粒体膜电位(MMP)和活性氧的产生。分析结果表明,在含有 50 ppm 氘的培养基中孵育海马切片会降低峰峰值的幅度。当将切片返回含有 150 ppm 氘含量的孵育培养基中时,观察到神经元活性的恢复。含有 50 ppm 氘的环境不会显著影响神经元培养物中活性氧的水平,而 MMP 降低了 16-20%。在葡萄糖剥夺和温度应激实验中,含有 50 ppm 的培养基会增加神经元的死亡。因此,神经细胞在含有 50 ppm 氘的培养基中短暂暴露会作为额外的应激因素,这可能与细胞能量平衡的破坏有关。线粒体膜电位的降低与 ATP 合成有关,表明这种效应可能与细胞能量失衡有关。海马 CA1 场神经元活性的降低可能反映了快速反应离子通道操作的可逆适应性变化。