Gasparotto Juciano, Petiz Lyvia Lintzmaier, Girardi Carolina Saibro, Bortolin Rafael Calixto, de Vargas Amanda Rodrigues, Henkin Bernardo Saldanha, Chaves Paloma Rodrigues, Roncato Sabrina, Matté Cristiane, Zanotto-Filho Alfeu, Moreira José Cláudio Fonseca, Gelain Daniel Pens
Centro de Estudos em Estresse Oxidativo, Departamento de Bioquímica, Instituto de Ciências Básicas da Saúde, Universidade Federal do Rio Grande do Sul, Porto Alegre, RS, Brazil.
Appl Physiol Nutr Metab. 2015 Dec;40(12):1253-61. doi: 10.1139/apnm-2015-0218. Epub 2015 Aug 17.
Exercise training induces reactive oxygen species production and low levels of oxidative damage, which are required for induction of antioxidant defenses and tissue adaptation. This process is physiological and essential to improve physical conditioning and performance. During exercise, endogenous antioxidants are recruited to prevent excessive oxidative stress, demanding appropriate intake of antioxidants from diet or supplements; in this context, the search for vitamin supplements that enhance the antioxidant defenses and improve exercise performance has been continuously increasing. On the other hand, excess of antioxidants may hinder the pro-oxidant signals necessary for this process of adaptation. The aim of this study was to investigate the effects of vitamin A supplementation (2000 IU/kg, oral) upon oxidative stress and parameters of pro-inflammatory signaling in lungs of rats submitted to aerobic exercise (swimming protocol). When combined with exercise, vitamin A inhibited biochemical parameters of adaptation/conditioning by attenuating exercise-induced antioxidant enzymes (superoxide dismutase and glutathione peroxidase) and decreasing the content of the receptor for advanced glycation end-products. Increased oxidative damage to proteins (carbonylation) and lipids (lipoperoxidation) was also observed in these animals. In sedentary animals, vitamin A decreased superoxide dismutase and increased lipoperoxidation. Vitamin A also enhanced the levels of tumor necrosis factor alpha and decreased interleukin-10, effects partially reversed by aerobic training. Taken together, the results presented herein point to negative effects associated with vitamin A supplementation at the specific dose here used upon oxidative stress and pro-inflammatory cytokines in lung tissues of rats submitted to aerobic exercise.
运动训练会诱导活性氧的产生以及低水平的氧化损伤，这是诱导抗氧化防御和组织适应所必需的。这个过程是生理性的，对于改善身体状况和运动表现至关重要。在运动过程中，内源性抗氧化剂被调动起来以防止过度的氧化应激，这就要求从饮食或补充剂中适当摄入抗氧化剂；在这种情况下，寻找能够增强抗氧化防御并改善运动表现的维生素补充剂的研究一直在不断增加。另一方面，过量的抗氧化剂可能会阻碍这种适应过程所需的促氧化信号。本研究的目的是调查补充维生素A（2000国际单位/千克，口服）对进行有氧运动（游泳方案）的大鼠肺部氧化应激和促炎信号参数的影响。当与运动相结合时，维生素A通过减弱运动诱导的抗氧化酶（超氧化物歧化酶和谷胱甘肽过氧化物酶）并降低晚期糖基化终产物受体的含量，抑制了适应/调节的生化参数。在这些动物中还观察到蛋白质（羰基化）和脂质（脂质过氧化）的氧化损伤增加。在久坐不动的动物中，维生素A降低了超氧化物歧化酶并增加了脂质过氧化。维生素A还提高了肿瘤坏死因子α的水平并降低了白细胞介素-10，有氧运动训练部分逆转了这些影响。综上所述，本文给出的结果表明，在此使用的特定剂量的维生素A补充剂对进行有氧运动的大鼠肺组织中的氧化应激和促炎细胞因子具有负面影响。
