Barth A, Bauer R, Gedrange T, Walter B, Klinger W, Zwiener U
Institute of Pharmacology and Toxicology, Friedrich Schiller University Jena, Germany.
Exp Toxicol Pathol. 1998 Sep;50(4-6):402-10. doi: 10.1016/S0940-2993(98)80026-2.
Glutathione (reduced (GSH) and oxidized (GSSG)), lipid peroxidation products (TBAR) and in vitro production of reactive oxygen species (ROS, by means of stimulated lipid peroxidation, H2O2 formation and amplified chemiluminescence (CL) in 9000 xg brain supernatants) were studied in the cerebellum (C) and temporoparietal area (TP) of the brain of normal weight (NW) and spontaneously intra-uterine growth-restricted newborn piglets (IUGR) after 1 hour hypoxia (fractional inspired oxygen concentration (FiO2) 8%), and in combination with 10% CO2, followed by 3 hours recovery (FiO2 30%). The strong GSH depletion accompanied by an increased concentration of GSSG and TBAR, more distinct in IUGR, is the most important result in the brain after hypoxia and reoxygenation. Hypercapnia-related acidosis seems to protect the brain of IUGR from hypoxia/reoxygenation induced injury by reducing GSH depletion as well as GSSG and TBAR increases. But stimulated lipid peroxidation and H2O2 formation in 9000 xg supernatants of C and TP were found to be higher in acidosis and hypercapnia. Decreased or unchanged amplified CL, demonstrating lower in vitro production of ROS, cannot explain the GSH depletion after hypoxia and reoxygenation. The scarce changes in erythrocyte GSH and GSSG as well as plasma TBAR concentrations did not reflect the findings in the brain. Nevertheless, the changes in the brain support the hypothesis that oxidative stress plays a role in neuronal damage after hypoxic stress, but the brain of IUGR did not reveal a special response to moderate hypoxia.
研究了正常体重（NW）和自发性宫内生长受限新生仔猪（IUGR）在缺氧1小时（吸入氧分数（FiO2）8%）并联合10%二氧化碳，随后恢复3小时（FiO2 30%）后，大脑小脑（C）和颞顶叶区域（TP）中的谷胱甘肽（还原型（GSH）和氧化型（GSSG））、脂质过氧化产物（TBAR）以及活性氧（ROS，通过9000 xg脑上清液中刺激的脂质过氧化、H2O2形成和增强化学发光（CL）来测定）。缺氧和复氧后，大脑中最重要的结果是GSH强烈耗竭，同时GSSG和TBAR浓度增加，在IUGR中更为明显。高碳酸血症相关酸中毒似乎通过减少GSH耗竭以及GSSG和TBAR增加来保护IUGR的大脑免受缺氧/复氧诱导的损伤。但发现在酸中毒和高碳酸血症时，C和TP的9000 xg上清液中刺激的脂质过氧化和H2O2形成更高。增强化学发光降低或不变，表明体外ROS产生较低，无法解释缺氧和复氧后的GSH耗竭。红细胞GSH和GSSG以及血浆TBAR浓度变化稀少，并未反映大脑中的情况。然而，大脑中的变化支持了氧化应激在缺氧应激后神经元损伤中起作用的假说，但IUGR的大脑对中度缺氧并未表现出特殊反应。
