کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
8545976 | 1561686 | 2018 | 32 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Acetyl-l-carnitine attenuates arsenic-induced liver injury by abrogation of mitochondrial dysfunction, inflammation, and apoptosis in rats
ترجمه فارسی عنوان
استیل-ال-کارنیتین آسیب کبدی ناشی از آرسنیک را با حذف اختلال عملکرد میتوکندریال، التهاب و آپوپتوز در موش صحرایی کاهش می دهد
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کلمات کلیدی
آرسنیک، استیل ال-کارنیتین، سمیت میتوکندری کبدی، استرس اکسیداتیو، التهاب
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی
Industrial and agricultural developments in recent years have resulted in the excessive discharge of arsenic into the environment, making arsenic toxicity a major worldwide concern. Oxidative stress is considered the primary mechanism for arsenic toxicity. The main objective of this study was to evaluate acetyl-l-carnitine's (ALC) protective ability against the arsenic-induced hepatotoxicity. For this purpose, male Wistar rats were distributed randomly into 5 groups of 8 rats each: control, arsenic (5â¯mg/kg) and arsenic plus ALC (5â¯mg/kg; 100, 200, 300â¯mg/kg). The animals were gavaged for 21 consecutive days. Liver tissue samples were extracted 24â¯h after the last treatment and were later analyzed for biochemical and histological alterations. The arsenic-induced oxidative damage was confirmed by elevation of malondialdehyde (MDA), a lipid peroxidation byproduct, as well as depletion in physiological antioxidant content such as superoxide dismutase (SOD) and catalase (CAT). Furthermore, alterations in mitochondrial functions including a significant decrease of mitochondrial outer membrane potential and reactive oxygen species (ROS) generation increase, mitochondrial swelling, release of cytochrome c and consequent activation of caspase-3 and caspase-9 and initiation of apoptosis, was observed following arsenic administration. Moreover, the inflammation was confirmed by the overexpression of inflammatory mediators such as NF-ĸB and IL-1 and IL-6. The present study demonstrated that ALC ameliorates arsenic-induced oxidative damage, mitochondrial dysfunction, apoptosis, inflammation and histological damage. ALC's protective features against arsenic hepatotoxicity may be due to this agent's antioxidant and anti-inflammatory properties as well as its stabilizing effects on mitochondrial function.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Environmental Toxicology and Pharmacology - Volume 58, March 2018, Pages 11-20
Journal: Environmental Toxicology and Pharmacology - Volume 58, March 2018, Pages 11-20
نویسندگان
Vida Bodaghi-Namileh, Mohammad Reza Sepand, Ameneh Omidi, Mehdi Aghsami, Seyed Afshin Seyednejad, Sara Kasirzadeh, Omid Sabzevari,