Piedimonte G, Guetard D, Magnani M, Corsi D, Picerno I, Spataro P, Kramer L, Montroni M, Silvestri G, Torres Roca J F, Montagnier L
Istituto di Patologia Generale e Anatomia Patologica e Dipartimento di Igiene e Medicina Preventiva, Università di Messina, Italy.
J Infect Dis. 1997 Sep;176(3):655-64. doi: 10.1086/514087.
It has been proposed that oxidative stress is the common mediator of apoptotic cell death in AIDS. However, mechanistic relationships between oxidative damage and cell death are far from clear. It is reported here that the mitogenic activation of T lymphocytes from human immunodeficiency virus-positive subjects involves perturbation of redox balance, as indicated by the increase in hydroethydine intracellular oxidation and manganese superoxide dismutase adaptive induction. Principal molecular targets of oxidative injury are cellular proteins whose content in carbonyl groups increases together with a dramatic increase in degradation of newly synthesized proteins catalyzed by the ATP- and ubiquitin-dependent proteolytic system. The major consequence of this metabolic anomaly is the decrease in protein cell mass leading to cells that are smaller than normal at lethal mitosis.
有人提出氧化应激是艾滋病中凋亡性细胞死亡的常见介质。然而，氧化损伤与细胞死亡之间的机制关系尚不清楚。据报道，人类免疫缺陷病毒阳性受试者的T淋巴细胞有丝分裂激活涉及氧化还原平衡的扰动，这表现为氢乙锭细胞内氧化增加和锰超氧化物歧化酶适应性诱导。氧化损伤的主要分子靶点是细胞蛋白，其羰基含量增加，同时由ATP和泛素依赖性蛋白水解系统催化的新合成蛋白降解显著增加。这种代谢异常的主要后果是蛋白质细胞质量减少，导致细胞在致死性有丝分裂时比正常细胞小。
