Ascorbic acid prevents protein oxidation in livers of senescence marker protein-30/gluconolactonase knockout mice.
Ascorbic acid prevents protein oxidation in livers of senescence marker protein-30/gluconolactonase knockout mice.
复制标题
抗坏血酸可防止衰老标记蛋白 30/葡萄糖酸内酯酶敲除小鼠肝脏中的蛋白质氧化。
DOI：
10.1111/ggi.12162
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发表时间：
2014
影响因子：
3.3
通讯作者：
A.
中科院分区：
文献类型：
--
作者：
Sato;Y.;Amano;A.;Kishimoto;Y.;Takahashi;K.;Handa;S.;Maruyama;N.;Ishigami;A.
目的衰老标记蛋白30(SMP30)/葡糖内酯酶基因敲除(KO)小鼠在 体内不能合成L抗坏血酸(AA)。由于AA是一种已知的水溶性抗氧化剂，我们评估了处于AA缺乏状态的SMP30/GNL KO小鼠肝脏中蛋白质的氧化水平。方法采集3、6和12 龄雄性SMP30/GNL KO小鼠和3、6、12和24 龄野生型(WT)小鼠的肝脏。为了评估蛋白质的氧化，我们测量了蛋白质的主要氧化标志物--蛋白质羰基的含量。结果SMP30/GNL KO小鼠∼中AA含量仅为WT小鼠的5%，3~12 月龄SMP30/GNL KO小鼠体内AA含量仅为WT小鼠的5%。SMP30/GNL KO小鼠肝脏中的蛋白质羰基水平显著高于年龄匹配的WT小鼠的1.8到2.3倍。为了确定AA缺乏导致了这种差异，我们在一些饮用水中添加了AA，并检测了AA对SMP30/GNL KO和WT小鼠肝脏中AA和蛋白质羰基水平的影响。给予额外AA的SMP30/GNL KO小鼠的肝脏含量显著高于不给予AA的小鼠。此外，添加AA的SMP30/GNL KO小鼠肝脏中的蛋白质羰基水平显著低于未添加AA的SMP30/GNL KO小鼠。然而，添加AA并不影响WT小鼠体内的蛋白质羰基水平。结论这些结果有力地表明AA在防止 体内的蛋白质氧化从而提高整体健康方面起着重要作用。
AimSenescence marker protein‐30 (SMP30)/gluconolactonase (GNL) knockout (KO) mice are incapable of synthesizing L‐ascorbic acid (AA)in vivo. As AA is known to be a water‐soluble anti‐oxidant, we assessed protein oxidation levels in livers from SMP30/GNL KO mice maintained in an AA‐insufficient condition.MethodsLivers were collected from male SMP30/GNL KO mice at the ages of 3, 6 and 12 months, and wild‐type (WT) mice at the ages of 3, 6, 12 and 24 months. To assess protein oxidation, we measured the content of protein carbonyl, which is a major protein oxidation marker. AA levels were measured by 2,4‐dinitrophenylhydrazine method using high‐performance liquid chromatography.ResultsLivers of SMP30/GNL KO mice had just ∼5% as much AA as those of WT mice from 3 to 12 months‐of‐age. Protein carbonyl levels in livers from SMP30/GNL KO mice were a significant 1.8‐ to 2.3‐fold higher than those from age‐matched WT mice. To establish that the AA‐insufficiency caused this difference, we added AA to some drinking water, and examined the effect on AA and protein carbonyl levels in livers from SMP30/GNL KO and WT mice. Livers from SMP30/GNL KO mice given extra AA had a significantly higher content than those from their deprived counterparts. Furthermore, protein carbonyl levels in livers from AA‐supplemented SMP30/GNL KO mice were significantly lower than those from the SMP30/GNL KO mice without AA supplementation. However, added AA did not affect the protein carbonyl levels in WT mice.ConclusionsThese results strongly suggest that AA plays an important role in preventing protein oxidationin vivo, thus enhancing overall health.Geriatr Gerontol Int 2014; 14: 989–995.