Ohishi S, Kizaki T, Ookawara T, Toshinai K, Haga S, Karasawa F, Satoh T, Nagata N, Ji L L, Ohno H
Department of Hygiene, National Defense Medical College, 3-2, Namiki, Tokorozawa 359, Japan.
Pflugers Arch. 1998 May;435(6):767-74. doi: 10.1007/s004240050582.
The aim of the current study was to elucidate the synergism of dietary calcium restriction and exhaustive exercise in the antioxidant enzyme system of rat soleus muscle, and to investigate the involvement of neutrophils in exercise-induced muscle damage. Forty-eight male Wistar rats were assigned to the following groups: control (C) or calcium-restricted [1 month (1 M) or 3 months (3 M)]. Each group was subdivided into acutely exercised or non-exercised groups. Soleus muscle from each rat was analysed to determine the levels of antioxidant enzymes [Mn-superoxide dismutase (SOD), Cu, Zn-SOD, glutathione peroxidase (GPX), and catalase (CAT)]. Dietary calcium restriction resulted in calcium deficiency and upregulated the antioxidant enzymes examined except GPX. Conversely, exhaustive exercise significantly decreased GPX and CAT, but not SODs activities in the calcium-restricted (1 M and/or 3 M) rats. Contents of immunoreactive Mn-SOD and Cu,Zn-SOD were only increased in the 3 M rats. During calcium restriction, the mRNA expression of both forms of SOD showed initial upregulation, followed by downregulation. Exhaustive exercise significantly increased the mRNA expressions only in the 3 M rats. Moreover, exhaustive exercise markedly increased myeloperoxidase activity in soleus muscles from the 1 M and 3 M rats compared with the C rats, and significantly enhanced the ability of neutrophils to generate superoxide in the 3 M rats. The results demonstrate that dietary calcium restriction upregulates certain antioxidant enzyme activities in rat soleus muscle, indicating an enhanced resistance to potential increases in intracellular reactive oxygen species. The results also suggest that exhaustive exercise may cause oxidative damage in soleus muscle of calcium-deficient rats through the activation of neutrophils.
本研究的目的是阐明饮食钙限制与力竭运动对大鼠比目鱼肌抗氧化酶系统的协同作用，并研究中性粒细胞在运动诱导的肌肉损伤中的作用。48只雄性Wistar大鼠被分为以下几组：对照组（C）或钙限制组[1个月（1M）或3个月（3M）]。每组再细分为急性运动组或非运动组。分析每只大鼠的比目鱼肌，以确定抗氧化酶[锰超氧化物歧化酶（SOD）、铜锌超氧化物歧化酶、谷胱甘肽过氧化物酶（GPX）和过氧化氢酶（CAT）]的水平。饮食钙限制导致钙缺乏，并上调了除GPX外所检测的抗氧化酶。相反，力竭运动显著降低了钙限制（1M和/或3M）大鼠的GPX和CAT，但不影响SOD的活性。免疫反应性锰超氧化物歧化酶和铜锌超氧化物歧化酶的含量仅在3M大鼠中增加。在钙限制期间，两种形式的超氧化物歧化酶的mRNA表达最初上调，随后下调。力竭运动仅在3M大鼠中显著增加了mRNA表达。此外，与C组大鼠相比，力竭运动显著增加了1M和3M大鼠比目鱼肌中的髓过氧化物酶活性，并显著增强了3M大鼠中性粒细胞产生超氧化物的能力。结果表明，饮食钙限制上调了大鼠比目鱼肌中某些抗氧化酶的活性，表明对细胞内活性氧潜在增加的抵抗力增强。结果还表明，力竭运动可能通过激活中性粒细胞在缺钙大鼠的比目鱼肌中引起氧化损伤。
