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慢性接触自来水中的砷会降低雌性大鼠主动脉中乙酰胆碱诱导的松弛,并增加氧化应激。

Chronic exposure to arsenic in tap water reduces acetylcholine-induced relaxation in the aorta and increases oxidative stress in female rats.

机构信息

Departamento de Químicas y Farmacia, Facultad de Ciencias, Universidad Católica del Norte, Angamos 0610. Antofagasta, Chile.

出版信息

Int J Toxicol. 2009 Nov-Dec;28(6):534-41. doi: 10.1177/1091581809345924.

Abstract

The aim of this work is to determine whether consuming tap water containing arsenic (20 microg/L) alters oxidative stress levels in female rats and changes vascular response. Whereas nitric oxide produces complete relaxation, arsenic (7 months of exposure) impairs the acetylcholine-induced endothelial relaxation in the rat aorta compared with control rats. Arsenic exposure results in a marked elevation in reactive oxygen species in blood, and delta-aminolevulinic acid dehydratase activity, which is a sensitive biomarker for arsenic toxicity and oxidative stress, is significantly decreased in erythrocytes from 7-month-old rats. Diastolic blood pressure increases significantly in 7-month-old arsenic-treated versus control rats. The percentage of change in peripheral resistance increases. The results indicate that chronic environmental exposure to low levels of arsenic alters the release of vasoactive substances, causes changes in oxidative stress, and increases blood pressure in female rats.

摘要

本研究旨在探讨摄入含砷(20μg/L)的自来水是否会改变雌性大鼠的氧化应激水平,并改变血管反应。虽然一氧化氮可产生完全松弛,但与对照组大鼠相比,砷(暴露 7 个月)可损害大鼠主动脉中乙酰胆碱诱导的内皮松弛。砷暴露导致血液中活性氧显著升高,而δ-氨基酮戊酸脱水酶活性(一种砷毒性和氧化应激的敏感生物标志物)在 7 月龄大鼠的红细胞中显著降低。与对照组大鼠相比,7 月龄砷处理大鼠的舒张压显著升高。外周阻力的变化百分比增加。结果表明,慢性环境暴露于低水平的砷会改变血管活性物质的释放,导致氧化应激的变化,并增加雌性大鼠的血压。

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