Abstract
Studies have reported that exposure to diesel exhaust particles (DEPs) induces lung inflammation and increases oxidative stress, and both effects are susceptible to changes via regular aerobic exercise in rehabilitation programs. However, the effects of exercise on lungs exposed to DEP after the cessation of exercise are not clear. Therefore, the aim of this study was to evaluate the effects of high-intensity swimming on lung inflammation and oxidative stress in mice exposed to DEP concomitantly and after exercise cessation. Male Swiss mice were divided into 4 groups: Control (n = 12), Swimming (30 min/day) (n = 8), DEP (3 mg/mL—10 μL/mouse) (n = 9) and DEP+Swimming (n = 8). The high-intensity swimming was characterized by an increase in blood lactate levels greater than 1 mmoL/L between 10th and 30th minutes of exercise. Twenty-four hours after the final exposure to DEP, the anesthetized mice were euthanized, and we counted the number of total and differential inflammatory cells in the bronchoalveolar fluid (BALF), measured the lung homogenate levels of IL-1β, TNF-α, IL-6, INF-ϫ, IL-10, and IL-1ra using ELISA, and measured the levels of glutathione, non-protein thiols (GSH-t and NPSH) and the antioxidant enzymes catalase and glutathione peroxidase (GPx) in the lung. Swimming sessions decreased the number of total cells (p<0.001), neutrophils and lymphocytes (p<0.001; p<0.05) in the BALF, as well as lung levels of IL-1β (p = 0.002), TNF-α (p = 0.003), IL-6 (p = 0.0001) and IFN-ϫ (p = 0.0001). However, the levels of IL-10 (p = 0.01) and IL-1ra (p = 0.0002) increased in the swimming groups compared with the control groups, as did the CAT lung levels (p = 0.0001). Simultaneously, swimming resulted in an increase in the GSH-t and NPSH lung levels in the DEP group (p = 0.0001 and p<0.002). We concluded that in this experimental model, the high-intensity swimming sessions decreased the lung inflammation and oxidative stress status during DEP-induced lung inflammation in mice.
Highlights
Nowadays air contamination is a real problem of public health in urban areas, and motor vehicle emissions, undoubtedly, are a major source of airbone pollutants
The present study provides the first demonstration that mice subjected to high-intensity swimming sessions and diesel exhaust particles (DEPs) administration for 10 days showed a decrease in the number of total cells, neutrophils and lymphocytes in bronchoalveolar fluid (BALF), even when the exercise was interrupted and the DEP administration was continued for 5 more days
Exercise decreased the levels of pro-inflammatory cytokines, such as interleukin 1β (IL-1β), interleukin 6 (IL-6), tumor necrosis factor α (TNF-α) and IFN-ϫ, in the lung homogenates, whereas exercises increased the levels of anti-inflammatory cytokines, such as interleukin 1ra (IL-1ra) and interleukin 10 (IL-10)
Summary
Nowadays air contamination is a real problem of public health in urban areas, and motor vehicle emissions, undoubtedly, are a major source of airbone pollutants. One of the classic pollutants composing the biomass in the air is particulate matter (PM). This term describes a mixture of solid or liquid particles dispersed in the air; the exhaust from vehicles and industries is the main source of PM [5,6]. The particles that result from burning diesel are essentially composed of metals, polycyclic aromatic hydrocarbons, and other organic species are called diesel exhaust particles (DEP), and affect different aspects of human health and disease [7,8,9,10,11]. The component of DEP responsible for the oxidative stress and subsequent pro-inflammatory signaling is especially the organic fraction, transition metals may be involved [7,8]
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