Aydın Birsen
Department of Biology, Science and Art Faculty, Amasya University, 05100, İpekköy, Amasya, Turkey.
Biomed Pharmacother. 2017 Mar;87:476-481. doi: 10.1016/j.biopha.2016.12.124. Epub 2017 Jan 6.
Argan oil (AO) is rich in minor compounds such as polyphenols and tocopherols which are powerful antioxidants. Acrylamide (ACR) has been classified as a neurotoxic agent in animals and humans. Mitochondrial oxidative stress and dysfunction is one of the most probable molecular mechanisms of neurodegenerative diseases. Female Sprague Dawley rats were exposed to ACR (50mg/kg i.p. three times a week), AO (6ml/kg,o.p, per day) or together for 30days. The activities of cytosolic enzymes such as xanthine oxidase (XO), glucose 6-phosphate dehydrogenase (G6PDH), glutathione-S-transferase (GST), mitochondrial oxidative stress, oxidative phosphorylation (OXPHOS) and tricarboxylic acid cycle (TCA) enzymes, mitochondrial metabolic function, adenosine triphosphate (ATP) level and acetylcholinesterase (AChE) activity were assessed in rat brain. Cytosolic and mitochondrial antioxidant enzymes were significantly diminished in the brains of rats treated with ACR compared to those in control. Besides, ACR treatment resulted in a significant reduction in brain ATP level, mitochondrial metabolic function, OXPHOS and TCA enzymes. Administration of AO restored both the cytosolic and mitochondrial oxidative stress by normalizing nicotinamide adenine dinucleotide phosphate (NADPH) generating enzymes. In addition, improved mitochondrial function primarily enhancing nicotinamide adenine dinucleotide (NADH) generated enzymes activities and ATP level in the mitochondria. The reason for AO's obvious beneficial effects in this study may be due to synergistic effects of its different bioactive compounds which is especially effective on mitochondria. Modulation of the brain mitochondrial functions and antioxidant systems by AO may lead to the development of new mitochondria-targeted antioxidants in the future.
阿甘油（AO）富含多种微量成分，如多酚和生育酚，这些都是强大的抗氧化剂。丙烯酰胺（ACR）已被归类为对动物和人类具有神经毒性的物质。线粒体氧化应激和功能障碍是神经退行性疾病最可能的分子机制之一。将雌性斯普拉格 - 道利大鼠暴露于ACR（腹腔注射50mg/kg，每周三次）、AO（口服6ml/kg，每天）或两者联合处理30天。评估大鼠脑中胞质酶如黄嘌呤氧化酶（XO）、葡萄糖6 - 磷酸脱氢酶（G6PDH）、谷胱甘肽 - S - 转移酶（GST）的活性、线粒体氧化应激、氧化磷酸化（OXPHOS）和三羧酸循环（TCA）酶、线粒体代谢功能、三磷酸腺苷（ATP）水平以及乙酰胆碱酯酶（AChE）活性。与对照组相比，用ACR处理的大鼠脑中胞质和线粒体抗氧化酶显著减少。此外，ACR处理导致脑ATP水平、线粒体代谢功能、OXPHOS和TCA酶显著降低。给予AO通过使烟酰胺腺嘌呤二核苷酸磷酸（NADPH）生成酶正常化，恢复了胞质和线粒体的氧化应激。此外，改善了线粒体功能，主要是增强了烟酰胺腺嘌呤二核苷酸（NADH）生成酶的活性以及线粒体中的ATP水平。本研究中AO产生明显有益作用的原因可能是其不同生物活性化合物的协同作用，这对线粒体尤其有效。AO对脑线粒体功能和抗氧化系统的调节可能会在未来促成新型线粒体靶向抗氧化剂的开发。
