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Vitamin E in sarcopenia: current evidences on its role in prevention and treatment.

Khor SC, Abdul Karim N, Ngah WZ, Yusof YA, Makpol S - Oxid Med Cell Longev (2014)

Bottom Line: Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways.Previous studies have shown its possible beneficial effects on aging and age-related diseases.Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and current in vitro and in vivo studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.

ABSTRACT
Sarcopenia is a geriatric syndrome that is characterized by gradual loss of muscle mass and strength with increasing age. Although the underlying mechanism is still unknown, the contribution of increased oxidative stress in advanced age has been recognized as one of the risk factors of sarcopenia. Thus, eliminating reactive oxygen species (ROS) can be a strategy to combat sarcopenia. In this review, we discuss the potential role of vitamin E in the prevention and treatment of sarcopenia. Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways. Previous studies have shown its possible beneficial effects on aging and age-related diseases. Although there are evidences suggesting an association between vitamin E and muscle health, they are still inconclusive compared to other more extensively studied chronic diseases such as neurodegenerative diseases and cardiovascular diseases. Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and current in vitro and in vivo studies.

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Related in: MedlinePlus

Effects of reactive oxygen species (ROS) on muscle cells. Accumulation of ROS will affect organelles and cell membranes. Alteration on genes and proteins expression leads to muscle wasting during aging. The important mechanisms involved are apoptosis and proteolysis.
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Related In: Results  -  Collection


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fig2: Effects of reactive oxygen species (ROS) on muscle cells. Accumulation of ROS will affect organelles and cell membranes. Alteration on genes and proteins expression leads to muscle wasting during aging. The important mechanisms involved are apoptosis and proteolysis.

Mentions: How does increased activation of skeletal muscle NF-κB in aging lead to muscle atrophy? NF-κB induces muscle breakdown by promoting proteolysis in skeletal muscle. A previous study using a transgenic mice model has shown that NF-κB increased murine ring finger-1 (MuRF-1) by binding to its promoter, supporting the notion of NF-κB regulated ubiquitin-proteasome pathway (UPS) [65]. This pathway can be regulated by ROS and contributes to muscle mass loss [76]. Furthermore, p38 which is affected by ROS was found to increase the expression of E3 ubiquitin ligases (atrogin-1) in myotube [77]. In senescent muscle cells, the expression of E3 ubiquitin ligases, atrogin-1, and MuRF-1 can either increase [78], remain unchanged [79], or decrease [80]. Even though inconsistent results were reported, their roles in sarcopenia are still worth exploring. Researchers suggested that Akt and FOXO may contribute to the decrease of atrogenes expression in the muscle old rats [80]. However, atrogin-1 and MuRF-1 at transcription level may not represent their actual protein concentrations [81]. Findings on the degradation of oxidized protein without ubiquitination in proteasome 20S served as evident that these atrogenes play an important role in accelerating proteolysis in response to oxidative stress [82]. In addition, reactive nitrogen species (RNS) can activate NF-κB and its cascade response on UPS and matrix metalloproteinases (MMPs), as well as degrading muscle-specific proteins in L6 myotubes [83]. Protein catabolism that occurs during oxidative stress via the activation of NF-κB and other proteins leading to muscle wasting is summarized in Figure 2.


Vitamin E in sarcopenia: current evidences on its role in prevention and treatment.

Khor SC, Abdul Karim N, Ngah WZ, Yusof YA, Makpol S - Oxid Med Cell Longev (2014)

Effects of reactive oxygen species (ROS) on muscle cells. Accumulation of ROS will affect organelles and cell membranes. Alteration on genes and proteins expression leads to muscle wasting during aging. The important mechanisms involved are apoptosis and proteolysis.
© Copyright Policy - open-access
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC4109111&req=5

fig2: Effects of reactive oxygen species (ROS) on muscle cells. Accumulation of ROS will affect organelles and cell membranes. Alteration on genes and proteins expression leads to muscle wasting during aging. The important mechanisms involved are apoptosis and proteolysis.
Mentions: How does increased activation of skeletal muscle NF-κB in aging lead to muscle atrophy? NF-κB induces muscle breakdown by promoting proteolysis in skeletal muscle. A previous study using a transgenic mice model has shown that NF-κB increased murine ring finger-1 (MuRF-1) by binding to its promoter, supporting the notion of NF-κB regulated ubiquitin-proteasome pathway (UPS) [65]. This pathway can be regulated by ROS and contributes to muscle mass loss [76]. Furthermore, p38 which is affected by ROS was found to increase the expression of E3 ubiquitin ligases (atrogin-1) in myotube [77]. In senescent muscle cells, the expression of E3 ubiquitin ligases, atrogin-1, and MuRF-1 can either increase [78], remain unchanged [79], or decrease [80]. Even though inconsistent results were reported, their roles in sarcopenia are still worth exploring. Researchers suggested that Akt and FOXO may contribute to the decrease of atrogenes expression in the muscle old rats [80]. However, atrogin-1 and MuRF-1 at transcription level may not represent their actual protein concentrations [81]. Findings on the degradation of oxidized protein without ubiquitination in proteasome 20S served as evident that these atrogenes play an important role in accelerating proteolysis in response to oxidative stress [82]. In addition, reactive nitrogen species (RNS) can activate NF-κB and its cascade response on UPS and matrix metalloproteinases (MMPs), as well as degrading muscle-specific proteins in L6 myotubes [83]. Protein catabolism that occurs during oxidative stress via the activation of NF-κB and other proteins leading to muscle wasting is summarized in Figure 2.

Bottom Line: Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways.Previous studies have shown its possible beneficial effects on aging and age-related diseases.Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and current in vitro and in vivo studies.

View Article: PubMed Central - PubMed

Affiliation: Department of Biochemistry, Faculty of Medicine, Universiti Kebangsaan Malaysia, Jalan Raja Muda Abdul Aziz, 50300 Kuala Lumpur, Malaysia.

ABSTRACT
Sarcopenia is a geriatric syndrome that is characterized by gradual loss of muscle mass and strength with increasing age. Although the underlying mechanism is still unknown, the contribution of increased oxidative stress in advanced age has been recognized as one of the risk factors of sarcopenia. Thus, eliminating reactive oxygen species (ROS) can be a strategy to combat sarcopenia. In this review, we discuss the potential role of vitamin E in the prevention and treatment of sarcopenia. Vitamin E is a lipid soluble vitamin, with potent antioxidant properties and current evidence suggesting a role in the modulation of signaling pathways. Previous studies have shown its possible beneficial effects on aging and age-related diseases. Although there are evidences suggesting an association between vitamin E and muscle health, they are still inconclusive compared to other more extensively studied chronic diseases such as neurodegenerative diseases and cardiovascular diseases. Therefore, we reviewed the role of vitamin E and its potential protective mechanisms on muscle health based on previous and current in vitro and in vivo studies.

Show MeSH
Related in: MedlinePlus