正常及实验二恶英中毒大鼠大脑皮层细胞超微结构

M. Salnikova, V. Саитов, А. Яковлева, А. Голубев
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摘要

目的研究正常和实验性二恶英中毒大鼠大脑皮层超微结构的变化。材料和方法。研究了小剂量二恶英(2,3,7,8-四氯二苯并对二恶英或TCDD)慢性中毒大鼠大脑皮层锥体层细胞的超微结构。形态计量学分析测定突触间隙长度、单位面积突触数量、突起髓鞘层厚度和髓鞘包裹层数量。结果。从光学和超微结构两方面观察了神经元的病理变化。其特点是细胞核减少、细胞死亡、髓鞘变薄和脱髓鞘。中毒的剂量与神经元的破坏程度相关:随着二恶英剂量的增加,变化变得更加显著。突触接触的数量减少,但它们的平均长度显著增加。结论。脱髓鞘、细胞呼吸受损和突触接触破坏的过程表明,二恶英能够间接导致神经元加速老化和死亡(细胞凋亡)。
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Ultrastructure of rat cerebral cortex cells in normal and experimental dioxin poisoning
Purpose the study of the ultrastructure of the cerebral cortex of rats in normal and experimental poisoning with dioxin. Materials and methods. We studied the ultrastructure of the cells of the pyramidal layer of the cerebral cortex of rats of the control and experimental groups that were chronic poisoned with small doses of dioxin (2,3,7,8-tetrachlorodibenzo-para-dioxin or TCDD). Morphometric analysis was carried out to determine the length of synaptic clefts, the number of synapses per unit area, the thickness of the myelin layer of the processes and the number of wrappers of myelin sheaths. Results. The pathology of neurons has been observed both at the optical and ultrastructural levels. It is characterized by a decrease in nuclei, cell death, thinning of myelin sheaths and demyelination. The dose of poisoning correlates with the degree of destruction of neurons: with an increase in the dose of dioxin, changes become more significant. The number of synaptic contacts decreases but there is a significant increase in their average length. Conclusions. The processes of demyelination, impaired cellular respiration and destruction of synaptic contacts indicate the ability of dioxin to indirectly cause accelerated aging of neurons and their death (apoptosis).
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