THERMAL INJURY, ATP DEPLETION, AND OXYGEN RADICALS

热损伤、ATP 耗竭和氧自由基

• 批准号: 3296344
• 负责人: GERD O TILL
• 金额: $ 9.13万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 1988
• 资助国家: 美国
• 起止时间: 1988-02-01 至 1991-01-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/3296344
• 关键词: NAD(H) phosphate; adenosine triphosphate; allergic pneumonitis; antioxidants; burns; glomerulonephritis; heat injury; hemolysis; hydroxyl group; hyperoxia; laboratory rat; lipid peroxides; neutrophil; peroxidation; phagocytosis; skin disorder; vasculitis; xanthine oxidase

Previously we have shown that thermal injury of skin in rats causes activation of the complement system, development of acute intravascular hemolysis and injury of the lung microvasculature, appearance of lipid peroxidation products, and pronounced functional defects in phagocytic cells. The proposed studies will evaluate the role of toxic oxygen products in the microvascular damage of thermally injured skin and the possible sources of these oxygen products (NADPH oxidase of phagocytic cells) or xanthine oxidase (in the thermally injured skin). We will also determine if ATP breakdown products appear during the course of thermal injury, if their appearance is prevented by the interposition of protective antioxidant interventions, and if the thermally injured skin is the likely source of the ATP breakdown products. Finally, we will evaluate further the dysfunctions of blood neutrophils in thermally injured animals, determine if the abnormalities are prevented by protective antioxidant interventions, and assess if defective neutrophils have diminished ATP levels which are not affected in oxidant-protected animals. These studies should provide important information on the pathogenesis of microvascular damage in thermally injured skin.

以前我们已经证明了大鼠皮肤的热损伤 补体系统的激活，急性的发展 血管内溶血和肺微血管造成的损伤， 脂质过氧化产物的外观，并发音 吞噬细胞中的功能缺陷。 拟议的研究将 评估有毒氧产品在微血管中的作用 损害热损伤的皮肤和可能的来源 氧气（吞噬细胞的NADPH氧化酶）或黄嘌呤 氧化酶（在热损伤的皮肤中）。 我们还将确定 如果在热过程中出现ATP分解产品 受伤，如果它们的外观是通过插入的介入来阻止的 保护性抗氧化剂干预措施，如果受伤 皮肤可能是ATP分解产品的来源。 最后， 我们将进一步评估血液中性粒细胞的功能障碍 热损伤的动物，确定异常是否为 通过保护性抗氧化剂的干预措施预防，并评估是否 中性粒细胞有缺陷的ATP水平降低了 受氧化剂保护动物的影响。 这些研究应该 提供有关微血管发病机理的重要信息 皮肤热损伤的损伤。