AGE-RELATED CHANGES IN GLUTATHIONE METABOLISM

谷胱甘肽代谢与年龄相关的变化

• 批准号: 7605792
• 负责人: NAOMI K FUKAGAWA
• 金额: $ 22.44万
• 依托单位: UNIVERSITY OF VERMONT & ST AGRIC COLLEGE
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-03-01 至 2008-02-29
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7605792
• 关键词: Aging-Related Process; Antioxidants; Cardiovascular Diseases; Cells; Complex; Computer Retrieval of Information on Scientific Projects Database; Cytoprotection; Diabetes Mellitus; Disease; Drug Metabolic Detoxication; Elderly; Funding; Glutathione; Glutathione Metabolism Pathway; Grant; Human; Institution; Intervention; Maintenance; Mammalian Cell; Measurement; Measures; Oxidants; Oxidative Stress; Pathway interactions; Play; Rate; Reaction; Relative (related person); Reporting; Research; Research Personnel; Resources; Role; Source; Thinking; Tissues; Toxic effect; United States National Institutes of Health; Variant; age related; impaired glucose tolerance; in vivo; interest

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Oxidative stress is thought to be one of the mechanisms leading to the initiation or progression of specific diseases as well as to the general process of aging. Glutathione (GSH), a tripeptide present in high concentrations in all mammalian cells, is the body's major endogenous antioxidant and plays a vital role in detoxification reactions and in the protection of cells from the toxic effects of oxidants. Maintenance of body GSH stores is a complex, integrated phenomenon, and there has been a resurgence of interest in potential interventions that may modulate GSH levels in the whole body and in specific tissues and cells. Advancing age, known to be associated with increased oxidative stress, is also reported to be associated with cardiovascular disease, impaired glucose tolerance, and diabetes mellitus; the latter has also been shown to be accompanied by lower GSH concentrations. The mechanisms that could be responsible for a compromised GSH status include decreased synthesis and/or increased utilization relative to synthetic capacity. Ideally, one would like to measure in vivo rates of both GSH synthesis and utilization. Unfortunately, the multitude of pathways consuming GSH, as well as tissue variation, makes it impossible to have meaningful simultaneous measurements of utilization by all of the different pathways in the human. Hence, the focus of this proposal will be on GSH synthesis rates.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 氧化应激被认为是导致特定疾病引发或进展的机制之一，以及衰老的一般过程。 谷胱甘肽（GSH）是所有哺乳动物细胞中高浓度的三肽，是人体主要的内源性抗氧化剂，在排毒反应和保护细胞免受氧化剂毒性的保护中起着至关重要的作用。 人体GSH商店的维持是一种复杂的综合现象，并且对潜在干预措施的兴趣兴起，这些干预措施可能调节全身以及特定的组织和细胞中的GSH水平。 据报道，已知与氧化应激增加有关的年龄也与心血管疾病，葡萄糖耐受性受损和糖尿病有关。后者也已显示出较低的GSH浓度。 可能导致GSH状态损害的机制包括降低合成和/或相对于合成能力的利用率增加。 理想情况下，人们希望测量GSH合成和利用率的体内速率。 不幸的是，消耗GSH的多种途径以及组织变化使得人类所有不同途径的利用都无法同时测量有意义的测量。 因此，该提案的重点将放在GSH合成率上。