易卒中型自发性高血压大鼠的氧化性DNA损伤增加。

Increased oxidative DNA damage in stroke-prone spontaneously hypertensive rats.

Negishi H, Ikeda K, Sagara M, Sawamura M, Yamori Y

Environmental Conservation and Development, Graduate School of Human and Environmental Studies, Kyoto University, Japan.

Clin Exp Pharmacol Physiol. 1999 May-Jun;26(5-6):482-4. doi: 10.1046/j.1440-1681.1999.03055.x.

Abstract

The amount of urinary 8-hydroxy-2'-deoxyguanosine (8-OHdG), a biomarker of the total systemic oxidative stress in vivo, in stroke-prone spontaneously hypertensive rats (SHRSP) was not different from that in control normotensive Wistar-Kyoto (WKY) rats at 6 weeks of age, but became higher than control values after the development of severe hypertension at 14-17 weeks of age. 2. The amount of urinary 8-OHdG was not significantly different between SHRSP treated with anti-hypertensive agents and those not treated at 14 weeks of age. 3. Stroke-prone spontaneously hypertensive rats were exposed to DNA damage by oxidative stress at the early stage when they developed severe hypertension, but this increase in DNA damage was not the secondary effect of hypertension.

摘要

尿8-羟基-2'-脱氧鸟苷（8-OHdG）是体内全身性氧化应激的生物标志物，在6周龄时，易患中风的自发性高血压大鼠（SHRSP）的尿8-OHdG含量与对照正常血压的Wistar-Kyoto（WKY）大鼠无差异，但在14至17周龄出现严重高血压后，其含量高于对照值。2. 14周龄时，接受抗高血压药物治疗的SHRSP与未接受治疗的SHRSP的尿8-OHdG含量无显著差异。3. 易患中风的自发性高血压大鼠在出现严重高血压的早期阶段受到氧化应激导致的DNA损伤，但这种DNA损伤的增加并非高血压的继发效应。