کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5559405 1561582 2016 8 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Mercury and protein thiols: Stimulation of mitochondrial F1FO-ATPase and inhibition of respiration
موضوعات مرتبط
علوم زیستی و بیوفناوری علوم محیط زیست بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
Mercury and protein thiols: Stimulation of mitochondrial F1FO-ATPase and inhibition of respiration
چکیده انگلیسی


- Mercury impact on mitochondrial bioenergetics is still poorly explored.
- Micromolar Hg2+ inhibits the NADH-O2 activity and enhances the F-ATPase activity.
- Hg2+ effects are due to complexation to crucial thiols in the mitochondrial proteins.
- Hg2+ modulation of mitochondrial complexes may counteract membrane depolarization.

In spite of the known widespread toxicity of mercury, its impact on mitochondrial bioenergetics is a still poorly explored topic. Even if many studies have dealt with mercury poisoning of mitochondrial respiration, as far as we are aware Hg2+ effects on individual complexes are not so clear. In the present study changes in swine heart mitochondrial respiration and F1FO-ATPase (F-ATPase) activity promoted by micromolar Hg2+ concentrations were investigated. Hg2+ was found to inhibit the respiration of NADH-energized mitochondria, whereas it was ineffective when the substrate was succinate. Interestingly, the same micromolar Hg2+ doses which inhibited the NADH-O2 activity stimulated the F-ATPase, most likely by interacting with adjacent thiol residues. Accordingly, Hg2+ dose-dependently decreased protein thiols and all the elicited effects on mitochondrial complexes were reversed by the thiol reducing agent DTE. These findings clearly indicate that Hg2+ interacts with Cys residues of these complexes and differently modulate their functionality by modifying the redox state of thiol groups. The results, which cast light on some implications of metal-thiol interactions up to now not fully explored, may contribute to clarify the molecular mechanisms of mercury toxicity to mitochondria.

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ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Chemico-Biological Interactions - Volume 260, 25 December 2016, Pages 42-49
نویسندگان
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