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出生时葡萄糖对大鼠肝脏线粒体成熟的抑制作用。磷脂与氧化代谢。

Inhibitory effect of glucose on the maturation of rat liver mitochondria at birth. Phospholipid and oxidative metabolism.

作者信息

Meister R, Comte J, Baggetto L, Godinot C, Gautheron D C

出版信息

Biochim Biophys Acta. 1983 Jan 13;722(1):36-42. doi: 10.1016/0005-2728(83)90154-8.

Abstract

(1) The rate of ATP synthesis coupled with succinate oxidation in rat liver mitochondria is low at birth and increases rapidly during the first postnatal hours (Nakazawa, T., Asami, K., Suzuki, H. and Yakawa, O. (1973) J. Biochem. 73, 397-406). A glucose injection given to newborn rats immediately after birth seemed to delay this maturation process. (2) Glucose administration specifically diminished the rate of 32Pi incorporation into phosphatidylcholine both in microsomes and in mitochondria while other phospholipids remained unaffected. (3) In newborn rat liver, 32Pi incorporation into phospholipids can be explained by de novo synthesis of phospholipids in microsomes followed by transfer to mitochondria with two exceptions phosphatidylserine and sphingomyelin. Indeed, after a 20-min incorporation of 32Pi into phospholipids, the specific radioactivity of phosphatidylserine and sphingomyelin was higher in mitochondria than in microsomes. (4) As far as phospholipid synthesis is concerned, no precursor-product relationship could be observed between light and heavy mitochondria.

摘要

(1) 大鼠肝线粒体中与琥珀酸氧化偶联的ATP合成速率在出生时较低,并在出生后的最初几个小时内迅速增加(中泽,T.,浅见,K.,铃木,H.和矢川,O.(1973年)《生物化学杂志》73,397 - 406)。出生后立即给新生大鼠注射葡萄糖似乎会延迟这一成熟过程。(2) 葡萄糖给药特异性降低了微粒体和线粒体中32Pi掺入磷脂酰胆碱的速率,而其他磷脂不受影响。(3) 在新生大鼠肝脏中,32Pi掺入磷脂可通过微粒体中磷脂的从头合成来解释,随后转移至线粒体,但磷脂酰丝氨酸和鞘磷脂除外。实际上,在32Pi掺入磷脂20分钟后,线粒体中磷脂酰丝氨酸和鞘磷脂的比放射性高于微粒体。(4) 就磷脂合成而言,在轻、重线粒体之间未观察到前体 - 产物关系。

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