Takisawa Shoko, Takino Yuka, Lee Jaewon, Machida Shuichi, Ishigami Akihito
Molecular Regulation of Aging, Tokyo Metropolitan Institute of Gerontology, Tokyo 173-0015, Japan.
Department of Pharmacy, College of Pharmacy, Pusan National University, Busan 46241, Korea.
Biology (Basel). 2022 Jun 23;11(7):955. doi: 10.3390/biology11070955.
Vitamin C (L-ascorbic acid, VC) is a water-soluble antioxidant essential for collagen polymerization. Previously, we reported that long-term VC deficiency causes muscle atrophy and deterioration in physical ability using female senescence marker protein-30 (SMP30)-deficient mice with a lack of VC synthesis, which is similar to that observed in humans. To determine whether these findings also hold true for male SMP30-deficient mice, two-month-old male SMP30-deficient mice were divided into two groups: the VC-treated group (VC(+)) was administered 1.5 g/L VC, and the VC-untreated group (VC(-)) was supplied water without VC. The VC level at four weeks in the gastrocnemius muscles from the VC(+) and VC(-) groups was 205.7 ± 8.5 nmol/g tissue and 13.1 ± 0.6 nmol/g tissue, respectively. Thus, four weeks was enough to reduce the VC level in the skeletal muscle in the VC-untreated group. On the other hand, muscle weights of the gastrocnemius, soleus, plantaris, tibialis anterior, and extensor digitorum longus in the VC(-) group were significantly reduced by VC deficiency after twelve weeks. The physical endurance of the VC(-) group at eight weeks was markedly lower than that of the VC(+) group. The grasping strength and activity in the cage in the nocturnal phases of the VC(-) group were markedly lower at twelve and sixteen weeks than those of the VC(+) group. Interestingly, muscle atrophy and declined physical ability were completely restored with VC supplementation for twelve weeks after VC deficiency. Thus, VC is essential for maintaining skeletal muscle function in both male and female SMP30-deficient mice with a lack of VC synthesis.
维生素C（L-抗坏血酸，VC）是胶原蛋白聚合所必需的水溶性抗氧化剂。此前，我们报道过，利用缺乏VC合成能力的雌性衰老标记蛋白-30（SMP30）缺陷小鼠，长期VC缺乏会导致肌肉萎缩和体能下降，这与在人类身上观察到的情况相似。为了确定这些发现对于雄性SMP30缺陷小鼠是否也成立，将两个月大的雄性SMP30缺陷小鼠分为两组：VC处理组（VC(+)）给予1.5 g/L VC，未处理组（VC(-)）给予不含VC的水。VC(+)组和VC(-)组腓肠肌在四周时的VC水平分别为205.7±8.5 nmol/g组织和13.1±0.6 nmol/g组织。因此，四周时间足以使未处理组骨骼肌中的VC水平降低。另一方面，VC(-)组的腓肠肌、比目鱼肌、跖肌、胫骨前肌和趾长伸肌的肌肉重量在十二周后因VC缺乏而显著降低。VC(-)组在八周时的体能耐力明显低于VC(+)组。VC(-)组在十二周和十六周夜间的抓握力和笼内活动明显低于VC(+)组。有趣的是，在VC缺乏后补充VC十二周，肌肉萎缩和体能下降完全恢复。因此，对于缺乏VC合成能力的雄性和雌性SMP30缺陷小鼠，VC对于维持骨骼肌功能至关重要。
