Microalgae Produce Antioxidant Molecules with Potential Preventive Effects on Mitochondrial Functions and Skeletal Muscular Oxidative Stress

Abstract

In recent years, microalgae have become a source of molecules for a healthy life. Their composition of carbohydrates, peptides, lipids, vitamins and carotenoids makes them a promising new source of antioxidant molecules. Skeletal muscle is a tissue that requires constant remodeling via protein turnover, and its regular functioning consumes energy in the form of adenosine triphosphate (ATP), which is produced by mitochondria. Under conditions of traumatic exercise or muscular diseases, a high production of reactive oxygen species (ROS) at the origin of oxidative stress (OS) will lead to inflammation and muscle atrophy, with life-long consequences. In this review, we describe the potential antioxidant effects of microalgae and their biomolecules on mitochondrial functions and skeletal muscular oxidative stress during exercises or in musculoskeletal diseases, as in sarcopenia, chronic obstructive pulmonary disease (COPD) and Duchenne muscular dystrophy (DMD), through the increase in and regulation of antioxidant pathways and protein synthesis.

Keywords: antioxidant molecules; exercise; microalgae; mitochondrial function; musculoskeletal diseases; oxidative stress; redox homeostasis.

Figure 1

Microalgal bioactive molecules [15,16].

Figure 2

RONS production and cellular fate. The mitochondrial function produces superoxide anion O₂^·−, which is transformed into H₂O₂ due to the antioxidant enzymes Mn-SOD, CAT and GPx. Muscular damage, oxidation of L-arginine (L-Arg) and increased calcium level (↑) activates iNOS and the production of NO. An overproduction of H₂O₂ or the action of O₂^·− with NO will induce OS through OH⁻ and ONOO⁻, respectively, resulting in DNA, lipid and protein damage. Contrarily, a controlled H₂O₂ level will be in favor of muscle health. Non-enzymatic antioxidants such as vitamins C and E inhibit the production of O₂^·−, and thus also limit the oxidant stress. Created using Biorender.com (accessed on 28 April 2023).

Figure 3

The roles of RONSs during skeletal muscle pathologies. Redox pathways in COPD, DMD and sarcopenia, mitochondria dysfunction and sarcomere NO leakage produce OS, which causes muscle damage leading to muscle atrophy. Protein balance pathways: the IGF1/PI3K/Akt/mTOR protein synthesis pathway is impacted by OS. Mitochondrial dysfunction due to the RONS active, AMPK, inhibiting mTOR and leading to rapid atrophy. Inflammatory pathways: inflammation is increased by OS via (+) NF-κB and TNF-α, activating UPS and resulting in muscle atrophy. In addition, OS triggers the release of antioxidant enzymes via Nrf2; however, SOD, CAT and GPx are insufficient to compensate for the overproduction of OH⁻ and ONOO⁻. According to the roles played by RONSs and their consequences, the described pathologies support OS-induced muscle atrophy and damage. Created using Biorender.com (accessed on 28 April 2023).

Figure 4

Microalgal effects described on skeletal muscle. Microalgal biomasses have been shown to prevent muscle atrophy and damage through contraction strength. Moreover, they increase antioxidant enzymatic activities, such as SOD, CAT and GPx. Microalgal compounds, such as gallic acid, ferulic acid and ω3-PUFAs, prevent muscle atrophy and damage, and activate mitochondrial biogenesis via the activation of Nrf1, TFAM and PGC-1α. The ω3-PUFA, Asx and Fcx are able to activate protein synthesis via the phosphorylation of mTOR. Then, these three molecules and β-1,3 glucan increase the activation of AMPK. All these reported microalgal molecules have an antioxidant activity against ROS. Created using Biorender.com (accessed on 28 April 2023).