Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.
Indian J Pharmacol. 2010 Apr;42(2):78-81. doi: 10.4103/0253-7613.64501.
Extended exposure to low levels of lead causes high blood pressure in human and laboratory animals. The mechanism is not completely recognized, but it is relatively implicated with generation of free radicals, oxidant agents such as ROS, and decrease of available nitric oxide (NO). In this study, we have demonstrated the effect of ascorbic acid as an antioxidant on nitric oxide metabolites and systolic blood pressure in rats exposed to low levels of lead.
The adult male Wistar rats weighing 200-250 g were divided into four groups: control, lead acetate (receiving 100 ppm lead acetate in drinking water), lead acetate plus ascorbic acid (receiving 100 ppm lead acetate and 1 g/l ascorbic acid in drinking water), and ascorbic acid (receiving 1 g/l ascorbic acid in drinking water) groups. The animals were anesthetized with ketamin/xylazine (50 and 7 mg/kg, respectively, ip) and systolic blood pressure was then measured from the tail of the animals by a sphygmomanometer. Nitric oxide levels in serum were measured indirectly by evaluation of its stable metabolites (total nitrite and nitrate (NOchi)).
After 8 and 12 weeks, systolic blood pressure in the lead acetate group was significantly elevated compared to the control group. Ascorbic acid supplementation could prevent the systolic blood pressure rise in the lead acetate plus ascorbic acid group and there was no significant difference relative to the control group. The serum NOchi levels in lead acetate group significantly decreased in relation to the control group, but this reduction was not significantly different between the lead acetate plus ascorbic acid group and the control group.
Results of this study suggest that ascorbic acid as an antioxidant prevents the lead induced hypertension. This effect may be mediated by inhibition of NOchi oxidation and thereby increasing availability of NO.
长期接触低水平的铅会导致人类和实验动物的高血压。其机制尚未完全阐明，但与自由基的产生、ROS 等氧化剂以及可用一氧化氮 (NO) 的减少有关。在这项研究中，我们已经证明了抗氧化剂抗坏血酸对暴露于低水平铅的大鼠的一氧化氮代谢物和收缩压的影响。
成年雄性 Wistar 大鼠体重 200-250 克，分为四组：对照组、醋酸铅组（饮用水中含 100ppm 醋酸铅）、醋酸铅加抗坏血酸组（饮用水中含 100ppm 醋酸铅和 1g/l 抗坏血酸）和抗坏血酸组（饮用水中含 1g/l 抗坏血酸）。动物用氯胺酮/甲苯噻嗪（分别为 50 和 7mg/kg，ip）麻醉，然后用血压计从动物尾巴测量收缩压。通过评估其稳定代谢物（总亚硝酸盐和硝酸盐（NOchi）），间接测量血清中的一氧化氮水平。
8 周和 12 周后，醋酸铅组的收缩压明显高于对照组。抗坏血酸补充可防止醋酸铅加抗坏血酸组收缩压升高，与对照组相比无显著差异。与对照组相比，醋酸铅组血清 NOchi 水平显著降低，但醋酸铅加抗坏血酸组与对照组之间无显著差异。
本研究结果表明，抗氧化剂抗坏血酸可预防铅引起的高血压。这种作用可能是通过抑制 NOchi 的氧化从而增加 NO 的可用性来介导的。
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