Adamo A M, Llesuy S F, Pasquini J M, Boveris A
Departamento de Quimica Biologica-IQUIFIB, Facultad de Farmacia y Bioquimica, Universidad de Buenos Aires-CONICET, Argentina.
Biochem J. 1989 Oct 1;263(1):273-7. doi: 10.1042/bj2630273.
Newborn Wistar rats were made hyperthyroid by injection of tri-iodothyronine and assayed for survival, brain oxygen uptake, brain chemiluminescence and activity of antioxidant enzymes. Brain chemiluminescence was measured (1) by removing the parietal bones or (2) through the translucid parietal bones. Control animals showed a brain chemiluminescence of 130 +/- 12 c.p.s./cm2 and 99 +/- 10 c.p.s./cm2 for procedures (1) and (2) respectively. Hyperthyroid rats showed increases in the spontaneous brain photoemission of 46 and 70% compared with controls, measured by procedures 1 and 2 respectively. The hyperthyroid state did not modify the oxygen-dependent chemiluminescence of brain homogenates. The hyperthyroid animals showed a 30% increase in the oxygen uptake of brain slices and a dramatic shortening of life-span to about 16 weeks. Superoxide dismutase (the Cu-Zn enzyme), catalase and Se-dependent glutathione peroxidase activities of brain homogenates were increased by 18, 36 and 30% respectively in the hyperthyroid animals. Isolated brain mitochondria produced 0.18-0.20 nmol of H2O2/min per mg of protein in state 4 in the presence of succinate as substrate. No difference was observed between control and hyperthyroid animals. It is concluded that hyperthyroidism leads to hypermetabolism and oxidative stress in the brain. The increased levels of oxygen and peroxyl radicals may contribute to premature ageing in these animals.
通过注射三碘甲状腺原氨酸使新生Wistar大鼠甲状腺功能亢进,并对其进行存活、脑氧摄取、脑化学发光和抗氧化酶活性测定。脑化学发光的测量方法为:(1)去除顶骨;(2)透过半透明的顶骨。对照组动物在方法(1)和(2)下的脑化学发光分别为130±12计数/秒/平方厘米和99±10计数/秒/平方厘米。甲状腺功能亢进大鼠通过方法1和2测量,其自发脑光发射分别比对照组增加了46%和70%。甲状腺功能亢进状态并未改变脑匀浆的氧依赖性化学发光。甲状腺功能亢进动物的脑切片氧摄取增加了30%,寿命显著缩短至约16周。甲状腺功能亢进动物脑匀浆中的超氧化物歧化酶(铜锌酶)、过氧化氢酶和硒依赖性谷胱甘肽过氧化物酶活性分别增加了18%、36%和30%。在以琥珀酸为底物的状态4下,分离的脑线粒体每毫克蛋白质每分钟产生0.18 - 0.20纳摩尔过氧化氢。对照组和甲状腺功能亢进动物之间未观察到差异。结论是甲状腺功能亢进导致脑内代谢亢进和氧化应激。氧和过氧自由基水平的升高可能导致这些动物过早衰老。