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氧化应激适应能力丧失作为衰老大鼠主动脉损伤的一种机制。

Loss of adaptation to oxidative stress as a mechanism for aortic damage in aging rats.

作者信息

Mármol F, Sánchez J, López D, Martínez N, Roselló-Catafau J, Mitjavila M T, Puig-Parellada P

机构信息

Unitat de Farmacologia, Facultat de Medicina, Universitat de Barcelona, IDIBAPS, Casanova 143, 08036 Barcelona, Spain.

出版信息

J Physiol Biochem. 2007 Sep;63(3):239-47. doi: 10.1007/BF03165787.

Abstract

Cells are armed with a vast repertoire of antioxidant defence mechanisms to prevent the accumulation of oxidative damage. The cellular adaptive response is an important antioxidant mechanism against physiological and pathophysiological oxidative alterations in a cell's microenvironment. The aim of this paper was to study, in the rat aorta, whether this adaptive response and the inflammation associated with oxidative stress were expressed throughout the aging process. We examined the rat aorta, as it is a very sensitive tissue to oxidative stress. Male Wistar rats of 1.5, 3, 12, 18 and 24 months of age were used. Superoxide anion (O2(-)) generation; levels of two antioxidant enzymes, superoxide dismutase (SOD) and catalase; and the levels of prostaglandin E2 (PGE2), an inflammatory marker, were measured. The results for rats at different ages were compared with those for 3 months of age. A balance between production of O2(-) and SOD activity was found in the aorta of rats from 1.5 to 12 months old. Oxidative stress was present in the aorta of old animals (18-24 months), due to a failure in the mechanisms of adaptation to oxidative stress. The observed increase in PGE2 levels in these rats reflected an inflammatory response. All together suggest that vascular oxidative stress and the inflammatory process observed in the old groups of rats could be closely related to vascular aging. Our results also remark the importance of the adaptative response to oxidative stress.

摘要

细胞具备大量抗氧化防御机制,以防止氧化损伤的积累。细胞适应性反应是一种重要的抗氧化机制,可抵御细胞微环境中的生理和病理生理氧化改变。本文旨在研究在大鼠主动脉中,这种适应性反应以及与氧化应激相关的炎症在整个衰老过程中是否会表现出来。我们选择检查大鼠主动脉,因为它是对氧化应激非常敏感的组织。使用了1.5、3、12、18和24月龄的雄性Wistar大鼠。测量了超氧阴离子(O2(-))的生成;两种抗氧化酶超氧化物歧化酶(SOD)和过氧化氢酶的水平;以及炎症标志物前列腺素E2(PGE2)的水平。将不同年龄大鼠的结果与3月龄大鼠的结果进行了比较。在1.5至12月龄大鼠的主动脉中发现O2(-)生成与SOD活性之间存在平衡。老年动物(18 - 24月龄)的主动脉中存在氧化应激,这是由于对氧化应激的适应机制失效所致。在这些大鼠中观察到的PGE2水平升高反映了一种炎症反应。所有这些表明,老年大鼠组中观察到的血管氧化应激和炎症过程可能与血管衰老密切相关。我们的结果还强调了对氧化应激适应性反应的重要性。

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