Abstract
L-Ascorbic acid (AsA) is a water-soluble antioxidant. We examined the effect of AsA deficiency on skeletal muscle using senescence marker protein-30 (SMP30)-knockout (KO) mice that are defective in AsA biosynthesis, which makes this mouse model similar to humans, to clarify the function of AsA in skeletal muscle. Eight-week-old female SMP30-KO mice were divided into the following two groups: an AsA-sufficient group [AsA(+)] that was administered 1.5 g/L AsA and an AsA-deficient group [AsA(−)] that was administered tap (AsA-free) water. At 4 weeks, the AsA content in the gastrocnemius muscle of AsA(−) mice was 0.7% compared to that in the gastrocnemius muscle of AsA(+) mice. Significantly lower weights of all muscles were observed in AsA(−) mice than those in AsA(+) mice at 12 and 16 weeks. The cross-sectional area of the soleus was significantly smaller in AsA(−) mice at 16 weeks than that in AsA(+) mice. The physical performance of AsA(−) mice was significantly less than that of AsA(+) mice at 12 weeks. Following AsA deficiency for 12 weeks, the expression of ubiquitin ligases, such as atrogin1/muscle atrophy F-box (MAFbx) and muscle RING-finger protein 1 (MuRF1), was upregulated. Furthermore, all detected effects of AsA deficiency on muscles of the AsA(−) group at 12 weeks were restored following AsA supplementation for 12 weeks. Thus, longer-term AsA deficiency is associated with muscle wasting, that this can be reversed by restoring AsA levels.
Highlights
L-Ascorbic acid (AsA, vitamin C) is a water-soluble antioxidant that scavenges reactive oxygen species (ROS), such as hydroxyl radicals, singlet oxygen, and superoxide radicals[1]
Eight-week-old female senescence marker protein-30 (SMP30)-KO mice were divided into two groups and housed with either free access to 1.5 g/L AsA water [AsA(+)] or AsA-free tap water [AsA(−)]and an AsA-free diet (Fig. 1a)
A slightly higher ROS level was detected in the skeletal muscles of the AsA(−) group at 4 weeks, but no significant differences were observed between the AsA(+) and AsA(−) groups (Fig. 1c)
Summary
L-Ascorbic acid (AsA, vitamin C) is a water-soluble antioxidant that scavenges reactive oxygen species (ROS), such as hydroxyl radicals, singlet oxygen, and superoxide radicals[1]. Primates, including humans, and guinea pigs are unable to synthesize AsA since these organisms carry multiple mutations in the Gulo gene encoding L-gulono-γ-lactone oxidase, the last enzyme in the AsA biosynthesis pathway[4]. In community-dwelling older people (Hertfordshire Cohort Study), higher AsA intake is only associated with physical performance (short chair rise time) in women[22]. These results prompted the hypothesis that AsA in muscle might act to maintain muscle weight and function through its function as an antioxidant by preventing excess oxidative states. All these observed effects of AsA deficiency in muscles were restored by AsA supplementation
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