Fulle S, Belia S, Di Tano G
Dipartimento di Scienze del Farmaco, Università G. d'Annunzio, Chieti-Pescara, Via dei Vestini 29, I-66013 Chieti Scalo.
Arch Ital Biol. 2005 Sep;143(3-4):229-34.
Sarcopenia is a complex process that appears in aged muscle associated with a decrease in mass, strength, and velocity of contraction. This process is the result of many molecular, cellular and functional alterations. It has been suggested that sarcopenia may be triggered by reactive oxygen species (ROS) that have accumulated throughout one's lifetime. We found a significant increase in oxidation of DNA and lipids in the elderly muscle, more evident in males, and a reduction in catalase and glutathione transferase activities. Experiments on Ca2+ transport showed an abnormal functional response of aged muscle after exposure to caffeine, which increases the opening of Ca2+ channels, as well a reduced activity of the Ca2+ pump in elderly males. From these results we concluded that oxidative stress play an important role in muscle aging and that oxidative damage is much more evident in elderly males, suggesting a gender difference may be related to hormonal factors. The progression of sarcopenia is directly related to a significant reduction of the regenerative potential of muscle normally due to a type of adult stem cells, known as satellite cells, which lie outside the sarcolemma and remain quiescent until external stimuli trigger as growth factors (IGF-1 or mIGF-1) their re-entry into the cell cycle. One possibility is that the anti oxidative capacity of satellite cells could also be altered and this, in turn, determines the decrease of their regenerative capacity. Data concerning this hypothesis are discussed
肌肉减少症是一个复杂的过程,出现在老年肌肉中,伴随着肌肉质量、力量和收缩速度的下降。这个过程是许多分子、细胞和功能改变的结果。有人提出,肌肉减少症可能是由一生中积累的活性氧(ROS)引发的。我们发现老年肌肉中DNA和脂质的氧化显著增加,在男性中更为明显,同时过氧化氢酶和谷胱甘肽转移酶的活性降低。关于钙离子运输的实验表明,老年肌肉在接触咖啡因后会出现异常的功能反应,咖啡因会增加钙离子通道的开放,老年男性的钙离子泵活性也会降低。从这些结果我们得出结论,氧化应激在肌肉衰老中起重要作用,并且氧化损伤在老年男性中更为明显,这表明性别差异可能与激素因素有关。肌肉减少症的进展通常与肌肉再生潜力的显著降低直接相关,这是由于一种称为卫星细胞的成体干细胞,它们位于肌膜外,直到外部刺激如生长因子(IGF-1或mIGF-1)触发它们重新进入细胞周期之前一直处于静止状态。一种可能性是卫星细胞的抗氧化能力也可能发生改变,进而决定了它们再生能力的下降。本文讨论了有关这一假设的数据