Melatonin supplementation ameliorates oxidative stress and inflammatory signaling induced by strenuous exercise in adult human males

Abstract

Strenuous exercise induces inflammatory reactions together with high production of free radicals and subsequent muscle damage. This study was designed to investigate for the first time and simultaneously whether over-expression of inflammatory mediators, oxidative stress, and alterations in biochemical parameters induced by acute exercise could be prevented by melatonin. This indoleamine is a potent, endogenously produced free radical scavenger and a broad-spectrum antioxidant; consequently, it might have positive effects on the recovery following an exercise session. The participants were classified into two groups: melatonin-treated men (MG) and placebo-treated individuals (controls group, CG). The physical test consisted in a constant run that combined several degrees of high effort (mountain run and ultra-endurance). The total distance of the run was 50 km with almost 2800 m of ramp in permanent climbing and very changeable climatic conditions. Exercise was associated with a significant increase in TNF-α, IL-6, IL-1ra (in blood), and also an increase in 8-hydroxy-2'-deoxyguanosine (8-OHdG) and isoprostane levels (in urine), and indicated the degree of oxidative stress and inflammation induced. Oral supplementation of melatonin during high-intensity exercise proved efficient in reducing the degree of oxidative stress (lower levels of lipid peroxidation, with a significant increase in antioxidative enzyme activities); this would lead to the maintenance of the cellular integrity and reduce secondary tissue damage. Data obtained also indicate that melatonin has potent protective effects, by preventing over-expression of pro-inflammatory mediators and inhibiting the effects of several pro-inflammatory cytokines. In summary, melatonin supplementation before strenuous exercise reduced muscle damage through modulation of oxidative stress and inflammation signaling associated with this physical challenge.

Polysaccharides fromCordyceps sinensismycelium ameliorate exhaustive swimming exercise-induced oxidative stress

“…8-OHdG is a DNA base-modified product generated by reactive oxygen species and is a mutation prone to induce a G-C to T-A transversion during DNA replication and has recently been shown to be a new marker of oxidative damage (Fukushima et al, 2010;Huang et al, 1999;Ogonovszky et al, 2005a). Over the past two decades, there is growing evidence that exhaustive exercise increased the MDA and 8-OHdG level in blood, liver and muscle tissues in rat and mice (Liu et al, 2000;Ochoa et al, 2011;Ogonovszky et al, 2005b;Okudan et al, 2012;Voces et al, 1999;Yu et al, 2006). In this study, the data showed that the MDA and 8-OHdG levels in serum, liver and muscle of mice in the CSPtreated groups were significantly lower compared with that in the control group.…”

Multiple Facets of Melatonin in Immunity: Clinical Applications

“…By the opposite, melatonin counteracts the exacerbated production of infl ammatory cytokines, mainly TNF-α, IL-1β, or IL-6, in several experimental models of infl ammation such as exercise-induced cardiac injury [ 60 ], diabetes-associated low grade of infl ammation [ 61 ], traumatic brain injury [ 62 ], heatstroke-induced multiple organ dysfunction syndrome [ 63 ], ischemia-reperfusioninduced liver damage [ 64 ], neuroinfl ammation in experimental diabetic neuropathy [ 65 ], cerulean-induced pancreatitis [ 66 ], and lung ischemia-reperfusion injury [ 67 ], among many others (reviewed by Carrillo- Vico et al 2013, in press). Furthermore, melatonin reduces the production of infl ammatory markers in infants subjected to endotracheal intubation [ 68 ], preterm newborns with respiratory distress syndrome [ 69 ], and adults under strenuous exercise [ 70 ], as well as in Duchenne muscular dystrophy [ 71 ]. Despite the diversity of infl ammatory conditions tested, the molecular mechanisms of melatonin studied always share the downregulation of the NF-κB activity.…”

Melatonin Ameliorates Burn-Induced Liver Injury by Modulation of Nrf2 and Nf- kB Signaling Pathways

“…Melatonin, vitamins C and E, reduced glutathione and uric acid are non enzymatic scavengers [20,21]. Antioxidant enzymes such as Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPx), or Glutathione Reductase (GR) are important in the defense against the damaging effect of ROS and RNS [17,22]. Oxidative stress occurs as a result of an imbalance between the excessive production of ROS and RNS and impaired ability of tissue to detoxify free radical in burns.…”