Kaushik Susmita, Kaur Jyotdeep
Department of Biochemistry, Postgraduate Institute of Medical Education and Research, Chandigarh 160 012, India.
Clin Chim Acta. 2003 Jul 1;333(1):69-77. doi: 10.1016/s0009-8981(03)00171-2.
Chronic exposure to stress alters the normal body homeostasis and, hence, leads to the development of various human pathologies, which might involve alterations in the antioxidant defense system. We studied the effect of chronic cold exposure on oxidative stress and antioxidant defense system in various rat tissues.
Male albino rats (Wistar strain), 2-3 months old, were exposed to 3 weeks of cold treatment. Antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione S-transferase (GST) were measured in addition to the antioxidants, ascorbic acid (AsA) and glutathione (GSH), and the prooxidants, lipid peroxides (LPO) and xanthine oxidase (XOD), in brain, heart, kidney, liver and small intestine using standard protocols.
Chronic cold exposure resulted in a significant increase in LPO in all the tissues studied while XOD was increased in the brain and intestine. Total SOD activity was significantly decreased in all the tissues, whereas CAT activity was significantly increased in the kidney and decreased in heart, liver and intestine in the animals exposed to cold. GPx activity was increased only in the brain and intestine of stressed rats. Chronic cold exposure resulted in significant decrease in GR activity in heart, liver and intestine. GST activity was increased (except heart) and GSH was significantly decreased in all the tissues in treated rats. AsA was increased in kidney and intestine but decreased in heart of stressed animals.
The observed changes in the antioxidant defense system are tissue specific, but it is evident that chronic exposure to cold leads to oxidative stress by displacing the prooxidant-antioxidant balance of this defense system by increasing the prooxidants while depleting the antioxidant capacities.
长期暴露于压力会改变正常的身体内稳态,从而导致各种人类疾病的发生,这可能涉及抗氧化防御系统的改变。我们研究了长期冷暴露对大鼠不同组织中氧化应激和抗氧化防御系统的影响。
选用2 - 3月龄的雄性白化大鼠(Wistar品系),进行3周的冷处理。采用标准方案,测定大脑、心脏、肾脏、肝脏和小肠中的抗氧化酶,如超氧化物歧化酶(SOD)、过氧化氢酶(CAT)、谷胱甘肽过氧化物酶(GPx)、谷胱甘肽还原酶(GR)和谷胱甘肽S - 转移酶(GST),以及抗氧化剂抗坏血酸(AsA)和谷胱甘肽(GSH),还有促氧化剂脂质过氧化物(LPO)和黄嘌呤氧化酶(XOD)。
长期冷暴露导致所有研究组织中的LPO显著增加,而大脑和肠道中的XOD增加。所有组织中的总SOD活性显著降低,而冷暴露动物的肾脏中CAT活性显著增加,心脏、肝脏和肠道中的CAT活性降低。GPx活性仅在应激大鼠的大脑和肠道中增加。长期冷暴露导致心脏、肝脏和肠道中的GR活性显著降低。处理大鼠所有组织中的GST活性增加(心脏除外),GSH显著降低。应激动物肾脏和肠道中的AsA增加,但心脏中的AsA降低。
抗氧化防御系统中观察到的变化具有组织特异性,但很明显,长期冷暴露通过增加促氧化剂同时消耗抗氧化能力,打破了该防御系统的促氧化剂 - 抗氧化剂平衡,从而导致氧化应激。