Michels Alexander J, Joisher Neha, Hagen Tory M
Linus Pauling Institute and Department of Biochemistry and Biophysics, Oregon State University, 571 Weniger Hall, Corvallis, OR 97331, USA.
Arch Biochem Biophys. 2003 Feb 1;410(1):112-20. doi: 10.1016/s0003-9861(02)00678-1.
This study investigated whether the age-related decline in hepatic ascorbic acid (AA) levels in rats was due to altered AA uptake. AA concentrations were 68% lower in freshly isolated hepatocytes from old (24-26 months) versus young (3-5 months; p<0.0005) Fischer 344 rats. When incubated with 100 microM AA, cells from old as compared to young rats showed a 66% decline in both the rate of AA transport and the steady state intracellular levels. Sodium-free media significantly reduced AA uptake, suggesting that the sodium-dependent vitamin C transporter (SVCT) was largely responsible for declines in AA transport. Analysis of SVCT messenger RNA (mRNA) levels shows that one isoform of this transport protein, SVCT1, declines 45% with age, with no significant changes in SVCT2 mRNA levels. These results show for the first time that sodium-dependent AA transport declines during the aging process, which may account for much of the loss in tissue AA content.
本研究调查了大鼠肝脏中与年龄相关的抗坏血酸(AA)水平下降是否归因于AA摄取的改变。与年轻(3 - 5个月)的Fischer 344大鼠相比,老年(24 - 26个月)大鼠新鲜分离的肝细胞中AA浓度低68%(p<0.0005)。当与100微摩尔AA一起孵育时,老年大鼠的细胞与年轻大鼠相比,AA转运速率和细胞内稳态水平均下降了66%。无钠培养基显著降低了AA摄取,表明钠依赖性维生素C转运体(SVCT)在很大程度上导致了AA转运的下降。对SVCT信使核糖核酸(mRNA)水平的分析表明,这种转运蛋白的一种同工型SVCT1随着年龄增长下降了45%,而SVCT2 mRNA水平没有显著变化。这些结果首次表明,钠依赖性AA转运在衰老过程中下降,这可能是组织中AA含量损失的主要原因。