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Development of oxidative stress and cell damage in the liver of rats with water-immersion restraint stress

机译:浸水抑制应激大鼠肝脏氧化应激和细胞损伤的发展

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We examined how oxidative stress and cell damage develop in the liver of rats subjected to water-immersion stress (WIRS). In rats subjected to WIRS for 1.5, 3 or 6 h, serum alanine aminotransferase and aspartate aminotransferase activities increased time-dependently. In the liver tissue, vacuolization and apoptosis occurred at 1.5 h of WIRS and vacuolization further developed without further appearance of apoptosis at 3 h or 6 h. Serum lipid peroxide (LPO) and NOx (nitriteitrate) concentrations increased at 3 h of WIRS and these increases were enhanced at 6 h. In liver tissue, increases in LPO and NOx concentrations and myeloperoxidase activity and decreases in ascorbic acid and reduced glutathione concentrations and superoxide dismutase activity occurred at 3 h of WIRS and these changes were enhanced at 6 h, although vitamin E concentration and xanthine oxidase activity were unchanged. These results indicate that oxidative stress in the liver of rats with WIRS develops after the appearance of cell damage in the tissue, and suggests that oxidative stress is caused through disruption of the antioxidant defense system and increases in NO generation and neutrophil infiltration in the liver, which may contribute to the progression of cell damage in the tissue.
机译:我们检查了水浸应激(WIRS)大鼠肝脏中氧化应激和细胞损伤的发展情况。在接受WIRS治疗1.5、3或6 h的大鼠中,血清丙氨酸氨基转移酶和天冬氨酸氨基转移酶活性随时间增加。在肝组织中,WIRS 1.5 h发生空泡化和凋亡,并且在3 h或6 h进一步空泡化而没有出现凋亡。 WIRS 3 h时血清脂质过氧化物(LPO)和NOx(亚硝酸盐/硝酸盐)浓度增加,而这些增加在6 h时增加。在肝组织中,WIRS 3 h时LPO和NOx浓度增加,髓过氧化物酶活性增加,抗坏血酸减少,谷胱甘肽浓度和超氧化物歧化酶活性降低,尽管维生素E浓度和黄嘌呤氧化酶活性降低,但这些变化在6 h增强。不变。这些结果表明,WIRS大鼠的肝脏中的氧化应激是在组织中出现细胞损伤后发展的,并且表明氧化应激是由抗氧化剂防御系统的破坏引起的,并且肝脏中NO的产生和中性粒细胞浸润的增加,这可能有助于组织中细胞损伤的发展。

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  • 来源
    《Redox Report 》 |2007年第3期| 139-147| 共9页
  • 作者单位

    Department of Chemistry, School of Medicine, Fujita Health University, Toyoake, Aichi, Japan Division of Metabolic and Functional Pathophysiology, Graduate School of Health Sciences, Fujita Health University, Toyoake, Aichi, Japan;

    Division of Metabolic and Functional Pathophysiology, Graduate School of Health Sciences, Fujita Health University, Toyoake, Aichi, Japan;

    Division of Metabolic and Functional Pathophysiology, Graduate School of Health Sciences, Fujita Health University, Toyoake, Aichi, Japan;

    Department of Clinical Biochemistry, Fujita Health University College, Toyoake, Aichi, Japan;

    Department of Nutrition, Faculty of Wellness, Chukyo Women's University, Ohbu, Aichi, Japan;

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