目的将评估一个环境致癌物 benzo (a) 分核(BaP ) 的可能的脉管的效果。BaP 和老鼠肝 S9 (0.25 mg/mL ) 的 cytotoxicit 激活 BaP 的方法被 MTT 试金检验。胸的大动脉的戒指从 Sprague-Dawley 老鼠被把。大动脉的戒指的收缩被 60 mmol/L KCl 或 106 mol/L phenylephrine (PE ) 在 BaP (100 mol/L ) 以后在一个 ex-vivo 灌注系统导致为 6 h 的孵化。[Ca2+] 我用 Fluo-4/AM 被测量。为 in-vivo 处理,老鼠与 BaP 被注射 4 个星期(10 mg/kg,每周 i.p ) 。结果 BaP (1500 m ) 显著地没影响房间生存能力;激活 S9 的 BaP 刺激了房间增长。BaP 没影响内皮细胞层未经触动或剥光的大动脉的戒指的可收缩的功能。BaP 没影响导致 ATP ([Ca2+] 我) 人的脐的静脉 endothelial 房间的增加。在对待 BaP 的老鼠,心率和传播煽动性的房间的数字没被影响。当血压显著地增加了时,身体重量减少了。对 PE 和 KCl 的最大的大动脉的可收缩的回答和对醋胆素的最大的大动脉的松驰反应被 25.0% , 34.2% ,和 10.4% 显著地分别地减少。这些结果建议的结论根据它的损坏 DNA 性质,那新陈代谢的激活是为导致 BaP 的心血管的毒性的一个前提。
Abstract Objective To evaluate the possible vascular effects of an environment carcinogen benzo(a)pyrene (BaP). Methods The cytotoxicit of BaP and rat liver S9 (0.25 mg/mL)-activated BaP were examined by MTT assay. Thoracic aortic rings were dissected from Sprague-Dawley rats. Contraction of aortic rings was induced by 60 mmol/L KCl or 10-6 mol/L phenylephrine (PE) in an ex-vivo perfusion system after BaP (100 tlmol/L) incubation for 6 h. [Ca^2+]i was measured using Fluo-4/AM. For in-vivo treatment, rats were injected with BaP for 4 weeks (10 mg/kg, weekly, i.p.). Results BaP (1-500 μm) did not significantly affect cell viability; S9-activated BaP stimulated cell proliferation. BaP did not affect the contractile function of endothelium-intact or -denuded aortic rings. BaP did not affect ATP-induced ([Ca2+]i) increases in human umbilical vein endothelial cells. In BaP-treated rats, heart rate and the number of circulating inflammatory cells were not affected. Body weight decreased while blood pressure increased significantly. The maximum aortic contractile responses to PE and KCI and the maximum aortic relaxation response to acetylcholine were significantly decreased by 25.0%, 34.2%, and 10.4%, respectively. Conclusion These results suggest, in accordance with its DNA-damaging properties, that metabolic activation is a prerequisite for BaP-induced cardiovascular toxicity.