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Pyrroloquinoline quinone protects against exercise‐induced fatigue and oxidative damage via improving mitochondrial function in mice
Author(s) -
Liu Lixia,
Zhang Yingyong,
Liu Tao,
Ke Chongrong,
Huang Jianzhong,
Fu Yajuan,
Lin Zhang,
Chen Fengjuan,
Wu Xiuqin,
Chen Qi
Publication year - 2021
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fj.202001977rr
Subject(s) - pyrroloquinoline quinone , lactate dehydrogenase , oxidative stress , reactive oxygen species , mitochondrion , malondialdehyde , chemistry , oxidative phosphorylation , creatine kinase , biochemistry , antioxidant , adenosine triphosphate , bioenergetics , enzyme , cofactor
Abstract Pyrroloquinoline quinone (PQQ) has a variety of biological functions. However, rare attention has been paid to its effects on exercise‐induced damage. Here, we assessed the potential protective effects of PQQ against the fatigue and oxidative damage caused by repeated exhaustive exercise, and studied the underlying mechanism. The models for exercise‐induced fatigue were established, and the parameters were measured, including the time to exhaustion (TTE), biochemical indicators, the expression of nuclear factor kappa B (NF‐κB) and inflammatory cytokines and so on. Besides, the mitochondrial function was evaluated by the morphology, membrane potential, respiratory function, adenosine triphosphate (ATP) levels, and the application of the mitochondrial complex I inhibitor. The results demonstrate that PQQ prolongs TTE, causes the decrease in the activity of serum creatine kinase and lactate dehydrogenase, increases the activity of antioxidant enzymes, inhibits the production of reactive oxygen species (ROS) and malondialdehyde (MDA), and diminishes the over expression of NF‐κB (p65) and inflammatory mediators. Furthermore, PQQ preserves normal mitochondrial function. Particularly, PQQ reduces the accumulation of ROS triggered by the mitochondrial complex I inhibitor. These data suggest that PQQ can significantly protect mice from exercise‐induced fatigue and oxidative damage by improving mitochondrial function. These data also suggest that PQQ controls mitochondrial activity through directly affecting the NADH dehydrogenase.