گروه سمشناسی، دانشکده علوم پزشکی، دانشگاه تربیت مدرس، تهران ایران
چکیده
هدف: ترکیبات کروم شش ظرفیتی [(VI)cr] از جمله آلودهکنندههای محیطزیست است که از طریق فعالیتهای صنعتی ایجاد میشود. مطالعات متعددی در رابطه با آثار مضرر کروم VI بر اندامهای مختلف انجام گرفته است اما درباره سمیت عصبی آن اطلاعات کمی وجود دارد. هدف از این تحقیق بررسی سمیت عصبی کروم VI بر سلولهای PC12 است. مواد و روشها: سلولهای PC12 براساس روش استاندارد کشت داده شدند و با غلظتهای مختلف پتاسیمدیکرومات (1-100 میکرومولار) بهمدت 24، 48 و 72 ساعت مواجه شدند؛ بعد از مواجهه بقای سلولها بهوسیله روش MTT ارزیابی شد. علاوه بر این؛ میزان گونههای فعال اکسیژن و پراکسیداسیون لیپید نیز ارزیابی شد. نتایج: پتاسیمدیکرومات بهطور معنیداری باعث مرگ سلولهای PC12 شد. IC50 محاسبه شده برای سمیت کروم 01/22، 88/1 و 85/1 میکرومولار بهترتیب برای زمانهای 24، 48 و 72 ساعت بود که در بین زمان 24 با بقیه زمانها دارای اختلاف معنیداری است (05/0>P). میزان تولید گونههای فعال اکسیژن و همچنین پراکسیداسیون لیپید، در گروههای تیمار شده با کروم VI نسبت به گروه کنترل افزایش معنیداری نشان داده است (05/0>P). نتیجهگیری: نتایج این تحقیق نشان میدهد که کروم VI بهصورت وابسته به دوز و زمان باعث ایجاد سمیت سلولی در سلولهای PC12 میشود که بیانگر سمیت عصبی این ترکیب است. مکانیسم سمیت عصبی ایجاد شده بهوسیله کروم VI بهطور کامل مشخص نیست؛ اما افزایش گونههای فعال اکسیژن و پراکسیداسیون لیپید در گروههای مواجه شده با کروم VI نشان دهنده امکان درگیر بودن استرس اکسیداتیو در سمیت عصبی کروم VI است.
Evaluation of Cr (VI) induced Neurotoxicity and Oxidative Stress in PC12 Cells
نویسندگان [English]
Abolfazl Dashti؛ Maliheh Soodi؛ Nahid Amani
Department of Toxicology, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
چکیده [English]
Objective: Hexavalent chromium [Cr (VI)] compounds are well-known environmental contaminants generated from industrial processes. Several studies have reported the harmful effects of Cr (VI) on different organs, however, little is known about neurotoxic effects of Cr (VI). The aim of this study is to investigate the toxic effects of Cr (VI) on PC12 cells. Methods: PC12 cells were cultured following standard protocol and exposed to various concentrations (1-100 μM) of potassium dichromate (K2Cr2O7) for 24, 48 and 72 h. After exposure, cell viability was measured by the MTT assy. Also following exposure, production of reactive oxygen species (ROS) and lipid peroxidation were measured. Results: Potassium dichromate induced significant cell death in PC12 cells. The IC50 values for cytotoxicity were 22.02 for 24 h, 1.88 for 48 h, and 1.85 for 72 h of exposure. Significant differences between IC50 for 24 h of exposure compared to 48 and 72 h of exposure were observed (p<0.05). ROS production and lipid peroxidation significantly increased in the Cr (VI) treated groups compared to the control group (p<0.05). Conclusion: The results indicated that Cr (VI) induced dose and time dependent cytotoxicity in PC12 cells which indicated neurotoxic effects of Cr (VI). Mechanisms of Cr (VI) induced toxicity have not been fully determined, however increased production of ROS and lipid peroxidation in Cr (VI) treated groups demonstrated that oxidative stress might be involved in neurotoxicity of Cr (VI).
کلیدواژه ها [English]
Cr (VI), Neurotoxicity, Oxidative stress
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