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心脏、肾脏和肝脏线粒体抗氧化防御的围产期发育

Perinatal development of heart, kidney, and liver mitochondrial antioxidant defense.

作者信息

Vlessis A A, Mela-Riker L

机构信息

Department of Surgery, Oregon Health Sciences University, Portland 97201.

出版信息

Pediatr Res. 1989 Sep;26(3):220-6. doi: 10.1203/00006450-198909000-00013.

DOI:10.1203/00006450-198909000-00013
PMID:2587124
Abstract

Development of the mitochondrial antioxidant defense system was studied to assess its potential role in the newborn mammal's tolerance to oxidative challenge and to gain insight into the fetal adaptation to a relatively hyperoxic adult environment. Isolated heart, kidney, and liver mitochondria from fetal, newborn, and adult guinea pigs were used. In situ function of the antioxidant enzymes was estimated in mitochondrial suspensions after the addition to selenite or tert-butyl hydroperoxide by determining NAD(P)H oxidation rates spectrophotometrically at 340-375 nm. Kidney and liver mitochondria from newborn animals were less susceptible to selenite and tert-butyl hydroperoxide-induced NAD(P)H oxidation. The pattern of change, however, varied widely with tissue type. Kidney mitochondria displayed the largest change with a 3- to 4-fold increase in rate from the fetal to adult period. NAD(P)H oxidation rates in intact mitochondria did not correlate consistently with glutathione reductase and peroxidase activities in sonicated mitochondria suggesting in situ regulation by other endogenous factors. Immediately after birth, mitochondrial glutathione reductase and peroxidase activities dropped 38-50% and 50-70%, respectively, in all tissues studied. Total glutathione content of heart and liver mitochondria did not change with age. Adult kidney mitochondrial glutathione, however, declined to 24% of fetal values. Mitochondrial superoxide dismutase activity increased 150-300% from the fetal to the adult period in all tissues studied. Perinatal changes in the mitochondrial antioxidant system and their relationship to mitochondrial calcium metabolism are discussed in terms of the newborn's resistance to oxidative stress.

摘要

研究了线粒体抗氧化防御系统的发育,以评估其在新生哺乳动物耐受氧化应激中的潜在作用,并深入了解胎儿对相对高氧的成年环境的适应性。使用了来自胎儿、新生和成年豚鼠的离体心脏、肾脏和肝脏线粒体。通过在340 - 375nm处用分光光度法测定NAD(P)H氧化速率,在向亚硒酸盐或叔丁基过氧化氢中添加线粒体悬浮液后,估计抗氧化酶的原位功能。新生动物的肾脏和肝脏线粒体对亚硒酸盐和叔丁基过氧化氢诱导的NAD(P)H氧化较不敏感。然而,变化模式因组织类型而异。肾脏线粒体的变化最大,从胎儿期到成年期速率增加3至4倍。完整线粒体中的NAD(P)H氧化速率与超声处理后的线粒体中的谷胱甘肽还原酶和过氧化物酶活性并不一致相关,这表明存在其他内源性因素的原位调节。出生后立即,在所研究的所有组织中,线粒体谷胱甘肽还原酶和过氧化物酶活性分别下降了38 - 50%和50 - 70%。心脏和肝脏线粒体的总谷胱甘肽含量不随年龄变化。然而,成年肾脏线粒体谷胱甘肽下降至胎儿值的24%。在所研究的所有组织中,线粒体超氧化物歧化酶活性从胎儿期到成年期增加了150 - 300%。从新生儿对氧化应激的抵抗力方面讨论了线粒体抗氧化系统的围产期变化及其与线粒体钙代谢的关系。

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