衰老损害整体生理功能,特别是对环境压力的反应。反复的热应激会增加老年动物肝脏中的活性氧和大分子损伤,可能是由于线粒体功能障碍.本研究的目的是通过评估关键的氧化还原敏感和抗氧化蛋白(Sirt-3,MnSOD,Trx-2和Ref-1)。我们假设热应激会导致这些蛋白质的线粒体丰度增加,但是衰老会减弱这种反应。为此,年轻(6个月)和老年(24个月)的Fisher344大鼠连续两天暴露于热应激。在每次加热试验期间,在最初的60分钟内,结肠温度升高到41°C,然后在此温度下夹紧30分钟。未加热的动物作为对照。在第二次热应激后2小时和24小时,从每只动物中分离肝线粒体,然后对Sirt-3,乙酰化赖氨酸残基(Ac-K)进行免疫印迹,MnSOD,Trx-2和Ref-1。老化增加了Sirt-3并降低了Ac-K。为了应对热应力,Sirt-3,AC-K,MnSOD,和Ref-1在年轻和老年动物的线粒体部分中增加。在第二次热应激后2h,线粒体Trx-2在年老时下降,但不是在年轻的动物。我们的结果表明,随着年龄的增长,对热应激反应的某些成分得以保留。然而,Trx-2的下降代表了热应激后与年龄相关的线粒体损伤和功能障碍的潜在机制。
Aging impairs overall physiological function, particularly the response to environmental stressors. Repeated heat stress elevates reactive oxygen species and macromolecular damage in the livers of aged animals, likely due to mitochondrial dysfunction. The goal of this investigation was to determine potential mechanisms for mitochondrial dysfunction after heat stress by evaluating key redox-sensitive and antioxidant proteins (Sirt-3, MnSOD, Trx-2, and Ref-1). We hypothesized that heat stress would result in greater mitochondrial abundance of these proteins, but that aging would attenuate this response. For this purpose, young (6 mo) and old (24 mo) Fisher 344 rats were exposed to heat stress on two consecutive days. During each heating trial, colonic temperature was elevated to 41°C during the first 60 min, and then clamped at this temperature for 30 min. Nonheated animals served as controls. At 2 and 24 h after the second heat stress, hepatic mitochondria were isolated from each animal, and then immunoblotted for Sirt-3, acetylated lysine residues (Ac-K), MnSOD, Trx-2, and Ref-1. Aging increased Sirt-3 and lowered Ac-K. In response to heat stress, Sirt-3, Ac-K, MnSOD, and Ref-1 increased in mitochondrial fractions in both young and old animals. At 2 h after the second heat stress, mitochondrial Trx-2 declined in old, but not in young animals. Our results suggest that some components of the response to heat stress are preserved with aging. However, the decline in Trx-2 represents a potential mechanism for age-related mitochondrial damage and dysfunction after heat stress.NEW & NOTEWORTHY Our results suggest heat stress-induced mitochondrial translocation of Sirt-3, MnSOD, and Ref-1 in young and old animals. Aged rats experienced a decline in Trx-2 after heat stress, suggesting a potential mechanism for age-related mitochondrial dysfunction.