Liu J, Mori A
Division of Biochemistry and Molecular Biology, University of California, Berkeley 94720-3202, USA.
Neurochem Res. 1999 Nov;24(11):1479-97. doi: 10.1023/a:1022597010078.
Stress may contribute to aging acceleration and age-related degenerative diseases. Stress and adaptation to stress require numerous homeostatic adjustments including hormones, neurotransmitters, oxidants, and other mediators. The stress-induced hormones, neurotransmitters, and oxidants all have beneficial, but also harmful effects if out of balance. Therefore, the homeostasis of stress and adaptation should be governed by the hormone balance, neurotransmitter balance, and oxidant balance, as well as the interactions among these substances. The imbalance and the over-interaction of these balances may ultimately cause increased oxidant generation and oxidative damage to biomolecules. This increased oxidative damage may add to the oxidant burden associated with normal aerobic metabolism, which in itself, generates oxidants, causes accumulation of oxidative damage in mitochondria, and contributes to normal aging. Therefore, the stress-associated increase of oxidative damage may, in part, contribute to stress-associated aging acceleration and age-related neurodegenerative diseases.
压力可能会导致衰老加速以及与年龄相关的退行性疾病。压力以及对压力的适应需要众多的稳态调节,包括激素、神经递质、氧化剂及其他介质。应激诱导产生的激素、神经递质和氧化剂都有有益作用,但如果失衡也会产生有害影响。因此,压力和适应的稳态应由激素平衡、神经递质平衡、氧化剂平衡以及这些物质之间的相互作用来调控。这些平衡的失衡和过度相互作用最终可能导致氧化剂生成增加以及对生物分子的氧化损伤。这种增加的氧化损伤可能会加重与正常有氧代谢相关的氧化剂负担,正常有氧代谢本身会产生氧化剂,导致线粒体中氧化损伤的积累,并促成正常衰老。因此,与压力相关的氧化损伤增加可能部分导致与压力相关的衰老加速以及与年龄相关的神经退行性疾病。