Sawada M, Sester U, Carlson J C
Department of Biology, University of Waterloo, Ontario, Canada.
J Cell Biochem. 1992 Mar;48(3):296-304. doi: 10.1002/jcb.240480310.
Plasma membrane samples from rat brain, heart, and liver were examined for biochemical changes with age. A rise in superoxide radical (SOR) levels was followed by increases in thiobarbituric acid reactive substances and decreases in membrane fluidity with age. The earliest rise in SOR formation appeared in the plasma membrane from the brain. With age, protein synthesis also decreased significantly in tissue homogenates from brain and heart but was unchanged in the liver. Exposure of plasma membrane samples to in vitro-elevated SOR levels stimulated formation of lipid peroxides, as indicated by the thiobarbituric acid test, and resulted in a decrease in membrane fluidity in each tissue and in a decline in protein synthesis in brain and heart. Changes in brain lipid peroxidation and in membrane fluidity in brain and heart as a result of SOR supplementation were further enhanced due to age. In addition, the mechanism of SOR formation was examined in plasma membrane samples from the brain. SOR generation was Ca(2+)-sensitive, blocked by superoxide dismutase or vitamin E and inhibited by both indomethacin, a cyclooxygenase inhibitor, and bromophenacyl bromide, a phospholipase A2 inhibitor. These results show significant increases in SOR formation and biochemical alterations in plasma membranes from brain, heart, and liver in aging rats. SOR formation appears to be enzyme-mediated and elevated levels of this oxygen radical could be involved in membrane breakdown in older rats.
对来自大鼠脑、心脏和肝脏的质膜样本进行了研究，以观察其随年龄增长的生化变化。随着年龄增长，超氧自由基（SOR）水平升高，随后硫代巴比妥酸反应性物质增加，膜流动性降低。SOR形成最早的升高出现在脑质膜中。随着年龄增长，脑和心脏组织匀浆中的蛋白质合成也显著下降，但肝脏中的蛋白质合成没有变化。将质膜样本暴露于体外升高的SOR水平会刺激脂质过氧化物的形成，硫代巴比妥酸试验表明了这一点，并导致每个组织的膜流动性降低以及脑和心脏中蛋白质合成下降。由于年龄增长，补充SOR导致的脑脂质过氧化以及脑和心脏中膜流动性的变化进一步加剧。此外，还研究了脑质膜样本中SOR形成的机制。SOR的产生对Ca(2+)敏感，可被超氧化物歧化酶或维生素E阻断，并被环氧化酶抑制剂吲哚美辛和磷脂酶A2抑制剂溴苯甲酰溴抑制。这些结果表明，衰老大鼠脑、心脏和肝脏的质膜中SOR形成显著增加且存在生化改变。SOR的形成似乎是由酶介导的，这种氧自由基水平的升高可能与老年大鼠的膜破坏有关。
