کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
8554089 1562698 2018 45 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
ROS-mediated oligomerization of VDAC2 is associated with quinocetone-induced apoptotic cell death
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
ROS-mediated oligomerization of VDAC2 is associated with quinocetone-induced apoptotic cell death
چکیده انگلیسی
Quinocetone (QCT) has been approved and widely used as an animal feed additive in China since 2003. However, investigations indicate that QCT shows potential toxicity both in vitro and in vivo. Although voltage dependent anion channel 1 (VDAC1) involved in regulating QCT-induced apoptotic cell death has been established, the role of voltage dependent anion channel 2 (VDAC2) in QCT-induced toxicity remains unclear. In this study, we showed that QCT-induced cell death was coupled to VDAC2 oligomerization. Moreover, VDAC inhibitor 4, 4′-diisothiocyano stilbene-2, 2′-disulfonic acid (DIDS) alleviated QCT-induced cell death and VDAC2 oligomerization. Meanwhile, overexpression VDAC2 aggravated QCT-induced VDAC2 oligomerization. In addition, caspase inhibitor Z-VAD-FMK and reactive oxidative species (ROS) scavenger N-acetyl-l-cysteine (NAC) apparently blocked QCT-induced cell death and VDAC2 oligomerization. Finally, overexpression N-terminal truncated VDAC2 attenuated QCT-induced VDAC2 oligomerization but had no influence on its localization to mitochondria when comparing to the full length of VDAC2. Taken together, our results reveal that ROS-mediated VDAC2 oligomerization is associated with QCT-induced apoptotic cell death. The N-terminal region of VDAC2 is required for QCT-induced VDAC2 oligomerization.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology in Vitro - Volume 47, March 2018, Pages 195-206
نویسندگان
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