اثرات بلند مدت نانوپلاستیک‌های پلی‌اتیلن ترفتالات در بافت قلب در موش‌های صحرایی نر نژاد ویستار

هدف: با رها کردن پلاستیک‌های یکبار مصرف در محیط زیست، این پلاستیک‌ها فرسوده شده و در اثر عوامل مختلف در اندازه‫های کوچک‫تر می‌شکنند و تحت عنوان میکرو و نانوپلاستیک‌ها وارد اکوسیستم آبی و خاکی شده و ممکن است توسط موجودات آبزی بلعیده شوند و در بدن آن‌ها تجمع یابند. همچنین می‌توانند توسط ریشه‌ی گیاهان جذب شوند و وارد زنجیره غذایی ما انسان‫ها شوند. در نتیجه بررسی اثرات سمی آن‫ها در بافت‫های حیاتی از قبیل بافت قلب مهم به‫نظر می‫رسد. مواد و روش‌ها: در این پژوهش تجربی 12 سر موش صحرایی نر نژاد ویستار با سن  4 هفته ای (250 گرم) به‫طور تصادفی به دو گروه تقسیم شدند. حیوانات گروه آزمایش به‫مدت 90 روز و روزانه ppm 200 نانوپلاستیک‌های پلی‌اتیلن ترفتالات به‫صورت گاواژ دریافت کردند و به‫شکل هم‫زمان گروه کنترل نیز محلول نمکی بافر فسفات  (ph=7.4) دریافت کردند. بعد از این مدت موش‫ها بی‫هوش شدند و پس از جداسازی سرم، سطوح لاکتات دهیدروژناز و کراتین کیناز سنجیده شد. میزان پراکسیداسیون لیپیدی، ظرفیت آنتی اکسیدانتی کل و فعالیت آنزیم کاتالاز نیز در بافت قلب سنجیده شد، نتایج با گروه کنترل مقایسه شد. مطالعات آسیب شناسی بافتی نیز با میکروسکوپ نوری بررسی شد. نتایج: نتایج نشان داد نانوپلاستیک‌های پلی‌اتیلن ترفتالات باعث افایش معنی‫داری در سطوح لاکتات دهیدروژناز و کراتین‌کیناز می‌شوند. همچنین افزایش پراکسیداسیون لیپیدی، کاهش ظرفیت آنتی‫اکسیدانتی کل و کاهش فعالیت کاتالاز در بافت قلب حیوانات گروه آزمایش نسبت به گروه کنترل مشاهده شد. در مطالعات بافت شناسی، ادم بین عضلانی و انحطاط میوفیبریل ها در گروهی که نانوپلاستیک دریافت کرده بودند مشهود بود. نتیجه گیری: به‫نظر می رسد نانوپلاستیک‌های پلی‌اتیلن ترفتالات در بلند مدت توانایی آسیب زدن به بافت قلب را دارند.

long-term effects of polyethylene terephthalate nanoplastics on heart tissue in male wistar rats

aim: plastics, as diverse polymeric materials, have become an integral part of modern life due to their unique properties, including high resistance to various chemicals, a high strength-to-weight ratio, ease of preparation, and low cost. millions of tons of these materials are produced annually; however, only a small portion is recycled or reused. by leaving single-use plastics in the environment, these plastics are worn out and fragmented into smaller sizes due to various factors such as uv irradiation and oxidation and finally enter the aquatic and terrestrial ecosystems and based on their size are called micro and nanoplastics and may be uptaken by aquatic organisms such as fishes and also shrimps and accumulate in their tissues. they can also be absorbed by the roots of plants and enter the food chain of us humans. although various in vitro and in vivo studies have been conducted to investigate the different effects of various nanoplastics, and various mechanisms such as oxidative stress and inflammation have been reported for their effects, but subchronic studies have been conducted to investigate the effects of polyethylene terephthalate nanoparticles. it is very important on the tissue of the heart in the body. as a result, it seems important to investigate their toxic effects in vital tissues such as heart tissue.material and methods: in this experimental study, polyethylene terephthalate nanoplastics were prepared using aqueous solution and then characterized using dynamic light scattering and scanning electronic microscopy. four weeks old 12 male wistar rats (average weight=250 gr) were randomly divided into two groups. animals in the treatment group received 200 ppm of polyethylene terephthalate nanoplastics by gavage daily for 90 days and control group received only phosphate buffer saline (ph=7.4). after this period, the rats were anesthetized and after collecting the serum, lactate dehydrogenase and creatine kinase activity levels were measured using commercial colorimetric kit. the level of lipid peroxidation was analyzed using thiobarbituric acid reactive substance formation colorimetric assay, total antioxidant capacity was assessed using ferric reducing antioxidant power and catalase enzyme activity were also measured in the heart tissue homogenate using specific kit, the results data were analyzed by one-way analysis of variance. histopathological studies were also performed by hematoxylin and eosin staining using light microscopy. results: the results demonstrated that long term exposure to polyethylene terephthalate nanoplastics caused a significant increase in the levels of lactate dehydrogenase and creatine kinase. also, an increase in lipid peroxidation, and a decrement in total antioxidant capacity, catalase activity were observed in the heart tissue of treatment group animals compared to the control group (p value < 0.05). in histological studies, intermuscular edema and degeneration of myofibrils were evident in the group that received nanoplastics. conclusion: long-term exposure to polyethylene terephthalate nanoplastics causes a change in the redox state of the heart tissue of male wistar rats, these nanoparticles cause the cardiac antioxidant enzymatic and non-enzymatic defense mechanisms to be overwhelmed, such as reducing the total antioxidant capacity and catalase.  which has finally led to irreversible damage to the cardiac tissue, which was confirmed by increasing serum levels of creatine kinase and lactate dehydrogenase enzymes and intramuscular edema and degeneration of myofibrils.