Mukhopadhyay C K, Ghosh M K, Chatterjee I B
Department of Biochemistry, University College of Science, Calcutta, India.
Mol Cell Biochem. 1995 Jan 12;142(1):71-8. doi: 10.1007/BF00928915.
It has recently been indicated that in the absence of free iron, NADPH initiates oxidative damage of proteins in guinea pig liver microsomes and also lipid peroxidation and protein damage in cardiac microsomes and that ascorbic acid specifically inhibits both the lipid peroxidation and protein damage [Mukhopadhyay CK, Chatterjee IB: J Biol Chem 269: 13390-13397, 1994; Mukhopadhyay M et al.: Mol Cell Biochem 126: 69-75, 1993]. In this paper we demonstrate that Fe(III)-independent NADPH-initiated lipid peroxidation and oxidative damage of proteins occur in the microsomes of all the extrahepatic tissues including lung, kidney, adrenal gland and brain and that both the lipid peroxidation and protein damage are specifically prevented by ascorbic acid. We further demonstrate that when NADPH is replaced by O2 as the electron donor, the O2-initiated lipid peroxidation and protein damage are also inhibited by ascorbic acid.
最近有研究表明，在没有游离铁的情况下，NADPH会引发豚鼠肝微粒体中蛋白质的氧化损伤，以及心脏微粒体中的脂质过氧化和蛋白质损伤，并且抗坏血酸能特异性抑制脂质过氧化和蛋白质损伤[Mukhopadhyay CK, Chatterjee IB: 《生物化学杂志》269: 13390 - 13397, 1994; Mukhopadhyay M等人: 《分子与细胞生物化学》126: 69 - 75, 1993]。在本文中，我们证明了不依赖Fe(III)的NADPH引发的脂质过氧化和蛋白质氧化损伤发生在包括肺、肾、肾上腺和脑在内的所有肝外组织的微粒体中，并且脂质过氧化和蛋白质损伤均能被抗坏血酸特异性抑制。我们进一步证明，当用O2替代NADPH作为电子供体时，O2引发的脂质过氧化和蛋白质损伤也能被抗坏血酸抑制。
