Abstract
Exercise-induced reactive oxygen and nitrogen species are increasingly considered as beneficial health promotion. Astaxanthin (ASX) has been recognized as a potent antioxidant suitable for human ingestion. We investigated whether ASX administration suppressed antioxidant enzyme activity in moderate-intensity exercise. Seven-week-old male C57BL/6 mice (n = 8/group) were treated with ASX (5, 15, and 30 mg/kg BW) combined with 45 min/day moderate-intensity swimming training for four weeks. Results showed that the mice administrated with 15 and 30 mg/kg of ASX decreased glutathione peroxidase, catalase, malondialdehyde, and creatine kinase levels in plasma or muscle, compared with the swimming control group. Beyond that, these two (15 and 30 mg/kg BW) dosages of ASX downregulated gastrocnemius muscle erythroid 2p45 (NF-E2)-related factor 2 (Nrf2). Meanwhile, mRNA of Nrf2 and Nrf2-dependent enzymes in mice heart were also downregulated in the ASX-treated groups. However, the mice treated with 15 or 30 mg/kg ASX had increased constitutive nitric oxidase synthase and superoxide dismutase activity, compared with the swimming and sedentary control groups. Our findings indicate that high-dose administration of astaxanthin can blunt antioxidant enzyme activity and downregulate transcription of Nrf2 and Nrf2-dependent enzymes along with attenuating plasma and muscle MDA.
Highlights
Regular, nonexhaustive physical exercise has been considered beneficial for improving health and physical fitness
glutathione peroxidase (GPx) the training compared with two higher dose groups seemed not tonot affect
We found that supplementation of ASX affected NOS level in plasma
Summary
Regular, nonexhaustive physical exercise has been considered beneficial for improving health and physical fitness. Many studies show that chronic physical exercise can prevent several chronic diseases (e.g., cardiovascular disease, diabetes, cancer, hypertension, obesity, depression, and osteoporosis) and premature death. During high-intensity exercise, reactive oxygen and nitrogen species (RONS) are yielded simultaneously, which may damage important macromolecules such as lipids, protein, and DNA [1,2]. Organisms have evolved complicated endogenous antioxidant defense mechanisms to minimize the potential damage caused by increased oxidative stress [3]. Key antioxidant enzymes, such as glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT), synergistically eliminate damaging free radical species.
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