کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
2579870 1561589 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Hydrogen sulfide modulates sub-cellular susceptibility to oxidative stress induced by myocardial ischemic reperfusion injury
ترجمه فارسی عنوان
سولفید هیدروژن باعث کاهش حساسیت زیر سلولی به استرس اکسیداتیو ناشی از آسیب مجدد ایسکمیک میوکارد
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
چکیده انگلیسی


• Cardiac mitochondria account for the major oxidative stress during reperfusion.
• Response towards H2S conditioning is unequal among the subcellular organelle.
• SSM play prominent role in the reduction of oxidative stress mediated by H2S.

In this study, we compared the impact of H2S pre (HIPC) and post-conditioning (HPOC) on oxidative stress, the prime reason for myocardial ischemia reperfusion injury (I/R), in different compartments of the myocardium, such as the mitochondria beside its subpopulations (interfibrillar (IFM) and subsarcolemmal (SSM) mitochondria) and microsomal fractions in I/R injured rat heart. The results demonstrated that compared to I/R rat heart, HIPC and HPOC treated hearts shows reduced myocardial injury, enhanced antioxidant enzyme activities and reduced the level of TBARS in different cellular compartments. The extent of recovery (measured by TBARS and GSH levels) in subcellular fractions, were in the following descending order: microsome > SSM > IFM in both HIPC and HPOC. In summary, oxidative stress mediated mitochondrial dysfunction, one of the primary causes for I/R injury, was partly recovered by HIPC and HPOC treatment, with significant improvement in SSM fraction compared to the IFM.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 252, 25 May 2016, Pages 28–35
نویسندگان
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