Iossa S, Lionetti L, Mollica M P, Barletta A, Liverini G
Department of General and Environmental Physiology, University of Naples Federico II, Italy.
Cell Biochem Funct. 1998 Dec;16(4):261-8. doi: 10.1002/(SICI)1099-0844(1998120)16:4<261::AID-CBF796>3.0.CO;2-1.
The purpose of this study was to evaluate the oxidative capacities in hepatic mitochondria isolated from prepubertal, young adult and adult rats (40, 90 and 180 days of age, respectively). In these rats, mitochondrial respiratory rates using FAD- and NAD-linked substrates as well as mitochondrial protein mass were measured. The results show that only the oxidative capacity of FAD-linked pathways significantly declined in mitochondria from 180-day-old rats compared with those from younger animals. When we consider FAD-linked respiration expressed per g liver, no significant difference was found among rats of different ages because of an increased mitochondrial protein mass found in 180-day-old rats. However, when FAD-linked and lipid-dependent respiratory rates were expressed per 100 g body weight, significant decreases occurred in 180-day-old rats. Therefore, the decrease in liver weight expressed per 100 g body weight rather than an impaired hepatic cellular activity may be the cause of body energy deficit in 180-day-old rats.
本研究的目的是评估从青春期前、年轻成年和成年大鼠（分别为40、90和180日龄）分离出的肝线粒体的氧化能力。对这些大鼠测量了使用黄素腺嘌呤二核苷酸（FAD）和烟酰胺腺嘌呤二核苷酸（NAD）连接底物时的线粒体呼吸速率以及线粒体蛋白含量。结果表明，与年幼动物的线粒体相比，180日龄大鼠线粒体中仅FAD连接途径的氧化能力显著下降。当我们考虑每克肝脏的FAD连接呼吸时，由于在180日龄大鼠中发现线粒体蛋白含量增加，不同年龄的大鼠之间未发现显著差异。然而，当以每100克体重表示FAD连接和脂质依赖性呼吸速率时，180日龄大鼠出现了显著下降。因此，每100克体重肝脏重量的下降而非肝细胞活性受损可能是180日龄大鼠身体能量不足的原因。
