Superoxide dismutase, SOD, SOD2, SOD3

Discussion in 'Possible causes and predisposing factor discussion' started by Nightsong, Sep 12, 2024.

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  1. Nightsong

    Nightsong Senior Member (Voting Rights)

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    Post copied from Replicated blood-based biomarkers for Myalgic Encephalomyelitis not explicable by inactivity, 2024, Beentjes, Ponting et al
    That study of a UK Biobank sample found lower levels of SOD3 in both males and females reporting an ME/CFS diagnosis
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    * A review of the role of SOD3, the extracellular isoform of SOD. (The International Journal of Biochemistry & Cell Biology, 2005). Although old I thought it useful background.
    This post is going to become extremely long if I post snippets from different papers, so I'll just post my current list from Mendeley to begin with:

    * This 2019 paper attempts to document SOD3's potential role in various inflammatory disorders & discussing its potential immunological role ("Anti-oxidative effects of superoxide dismutase 3 on inflammatory diseases", J Mol Medicine, 2019).
    * This 2011 paper documents SOD3's potential role in hypertension ("Role of Vascular Extracellular Superoxide Dismutase in Hypertension", Hypertension, 2011) (also open-access PDF).
    * "Extracellular superoxide dismutase, a molecular transducer of health benefits of exercise" - link (Redox Biology, 2020, open access).
    * "Extracellular Superoxide Dismutase and Risk of COPD" - link (also open-access PDF).
    * "Extracellular superoxide dismutase and cardiovascular disease" - link (Cardiovascular Research, 2002, open-access PDF).
    * "Extracellular superoxide dismutase in biology and medicine" - link (Free Radical Biology and Medicine, 2003)

    As it may be useful to look at superoxide dismutase more generally, especially in relation to physical activity:

    * "Sex hormones modulate circulating antioxidant enzymes: impact of estrogen therapy" (Redox Biology, 2013, open-access PDF).
    * Lower levels of SOD were found in idiopathic chronic fatigue patients (Nature Scientific Reports, 2018).
    * This 2011 paper examines the role of SODs in redox signalling, vascular function & disease;
    * This 2015 paper regarding the effects of an antioxidant supplement found that chronic forced exercise in mice depleted levels of various antioxidant levels including SOD. In another forced-exercise mouse model (this one a claimed model of CFS, sigh) decreased levels of SOD were found following the exercise.
    * This 2020 paper - another forced running wheel one - examining numerous "oxidative stress" biomarkers reported that "exercise on an FRW significantly increased several serum biochemical parameters, malondialdehyde level and superoxide dismutase activity in all tissues of exercise rats compared with control rats".

    I also came across three ME/CFS papers implicating another isoform, mitochondrial SOD (SOD2):

    * "The most interesting observation was the downregulation in expression of the mitochondrial proteins pyruvate dehydrogenase phosphatase catalytic subunit 1 (PDP1) and manganese-dependent superoxide dismutase 2 (SOD2)" - a Prusty et al ME/CFS paper (link)
    * In this preprint (Davis/Stanford) Long COVID patients' (but not the ME/CFS patients') CD4 & CD8 T lymphocytes had lower mitochondrial SOD (SOD2) levels. Also: "sex hormones such as estradiol can regulate the serum levels of antioxidant enzymes, including catalase, glutathione peroxidase, and SOD2".
    * This 2009 muscle-biopsy transcription profile analysis found a downregulation of three mitochondrial genes encoding proteins the authors thought relevant to oxidative stress, including SOD2, in both male & female CFS patients.
     
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