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首页> 外文期刊>Biological research for nursing >Changes in Oxidant Defense, Apoptosis, and Cognitive Abilities During Treatment for Childhood Leukemia
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Changes in Oxidant Defense, Apoptosis, and Cognitive Abilities During Treatment for Childhood Leukemia

机译：儿童白血病治疗过程中氧化剂防御，细胞凋亡和认知能力的变化

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Aggressive central nervous system (CNS)-directed treatment for acute lymphoblastic leukemia (ALL), the most prevalent cancer among children and adolescents, prevents metastasis of leukemia cells into the brain. Up to 60% of survivors experience cognitive problems, but knowledge about risk factors for and mechanisms of neurologic injury is lacking. Objectives of the present study were to (1) quantify changes in oxidant defense and apoptosis over the course of ALL therapy and (2) elucidate risk factors for long-term cognitive problems. The sample included 71 children with ALL. Cerebrospinal fluid (CSF) samples were collected at diagnosis and during intrathecal chemotherapy administration. Oxidant defense was measured by reduced glutathione (GSH), oxidized glutathione (GSSG), and the ratio of GSH:GSSG. Apoptosis was measured by activity of several cysteine-dependent aspartate-specific protease (abbreviated as caspase) enzymes that initiate (caspases 8 and 9) or execute (caspases 3/7) apoptosis. Cognitive abilities were assessed by standardized measures of short-term memory, visual-motor integration, and attention 3 years after ALL diagnosis. GSH and GSSG concentration increased significantly during ALL therapy, and a low GSH:GSSG ratio was indicative of an oxidized extracellular environment. Caspase enzyme activity increased significantly, and caspases 3/7 activity was significantly and negatively associated with performance on measures of cognitive abilities. Younger age at time of ALL diagnosis was associated with some measures of attention. Efflux of glutathione into CSF maintains oxidant defense by scavenging free radicals and other reactive oxygen species and is an early event in apoptosis. These mechanisms may be involved in neurologic injury associated with CNS-directed treatment and subsequent cognitive problems.
机译：侵略性的中枢神经系统（CNS） - 对急性淋巴细胞白血病（ALL），儿童和青少年中最普遍的癌症的侵略性治疗，可防止白血病细胞转移到大脑中。高达60％的幸存者体验认知问题，但缺乏关于危险因素的知识和神经系统损伤机制。本研究的目的是（1）在所有治疗过程中量化氧化剂防御和细胞凋亡的变化和（2）阐明的长期认知问题的危险因素。该样品包括所有全部的71名儿童。在诊断和鞘内化疗施用时收集脑脊髓液（CSF）样品。通过降低的谷胱甘肽（GSH），氧化谷胱甘肽（GSSG）和GSH：GSSG的比例测量氧化剂防御。通过几种半胱氨酸依赖性天冬氨酸特异性蛋白酶（缩写为Caspase）酶的活性来测量细胞凋亡，其引发（半胱天冬酶8和9）或执行（半胱天冬酶3/7）凋亡。通过在所有诊断后3年的短期记忆，视觉电动机集成和注意力的标准化测量评估了认知能力。在所有治疗过程中GSH和GSSG浓度显着增加，并且低GSH：GSSG比率指示氧化细胞外环境。 Caspase酶活性显着增加，并且Caspases 3/7活性显着且与认知能力措施的性能显着和负面相关。所有诊断时的年龄较小与一些注意措施有关。通过清除自由基和其他活性氧物质，将谷胱甘肽的流出保持氧化剂防御，并且是细胞凋亡的早期事件。这些机制可以参与与CNS的治疗和随后的认知问题相关的神经系统损伤。

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