Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers
Introduction: Methamphetamine (METH) is a known abused drug which could induce cardiotoxicity. Captopril is an angiotensin converting enzyme inhibitor that is used in hypertension therapy and has known antioxidant effects. In this study we evaluated the effect of captopril against METH-induced toxic...
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Semnan Univeristy of Medical Sciences
2016-09-01
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doaj-7900853db4b04505abcd2697c73bd8cb2020-11-24T21:06:18ZfasSemnan Univeristy of Medical SciencesMajallah-i ̒Ilmī-i Dānishgāh-i ̒Ulūm-i Pizishkī-i Simnān1608-70462016-09-01181128137Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markersmohammad shokrzadeh0ehsan zamani1javad mollahasani2fatemeh Shaki3 Introduction: Methamphetamine (METH) is a known abused drug which could induce cardiotoxicity. Captopril is an angiotensin converting enzyme inhibitor that is used in hypertension therapy and has known antioxidant effects. In this study we evaluated the effect of captopril against METH-induced toxicity in rat heart isolated mitochondria in hyperthermic condition. Materials and Methods: Mitochondrial fractions were isolated from heart of Wistar rat with different centrifuge technique. Then, heart isolated mitochondrial were exposed to METH (LC50, 250µM) and captopril (0, 25, 50, 100, 200, 400 µM) and incubated at 37 and 41 C. After 1 h incubation, mitochondrial damage was assayed by MTT test. Also, oxidative stress markers were measured. Results: Our results showed that METH significantly induced mitochondrial damage that was more pronounced in hyperthermic condition. Increased oxidative stress markers such as lipid peroxidation, reactive oxygen species formation and glutathione oxidation in the heart isolated mitochondria were observed after METH exposure that was more significant at 41 c than 37 C. Captopril significantly inhibited METH–induced oxidative stress in the heart isolated mitochondria. Also, captopril pretreatment significantly improved mitochondrial function. Mitochondrial swelling also increased after METH exposure, but was significantly decreased with captopril pre-treatment. Conclusion: These results suggested that captopril could ameliorate METH-induced oxidative stress and mitochondrial dysfunction especially in hyperthermic condition. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH cardiotoxicityhttp://koomeshjournal.semums.ac.ir/browse.php?a_code=A-10-2887-2&slc_lang=en&sid=1Captopril Methamphetamine Cardiotoxicity Mitochondria Oxidative Stress Rat |
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DOAJ |
language |
fas |
format |
Article |
sources |
DOAJ |
author |
mohammad shokrzadeh ehsan zamani javad mollahasani fatemeh Shaki |
spellingShingle |
mohammad shokrzadeh ehsan zamani javad mollahasani fatemeh Shaki Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers Majallah-i ̒Ilmī-i Dānishgāh-i ̒Ulūm-i Pizishkī-i Simnān Captopril Methamphetamine Cardiotoxicity Mitochondria Oxidative Stress Rat |
author_facet |
mohammad shokrzadeh ehsan zamani javad mollahasani fatemeh Shaki |
author_sort |
mohammad shokrzadeh |
title |
Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
title_short |
Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
title_full |
Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
title_fullStr |
Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
title_full_unstemmed |
Captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
title_sort |
captopril inhibited metamphetamine - induced cardiac mitochondrial damage in hyperthermic condition via modulation of biochemical markers |
publisher |
Semnan Univeristy of Medical Sciences |
series |
Majallah-i ̒Ilmī-i Dānishgāh-i ̒Ulūm-i Pizishkī-i Simnān |
issn |
1608-7046 |
publishDate |
2016-09-01 |
description |
Introduction: Methamphetamine (METH) is a known abused drug which could induce cardiotoxicity. Captopril is an angiotensin converting enzyme inhibitor that is used in hypertension therapy and has known antioxidant effects. In this study we evaluated the effect of captopril against METH-induced toxicity in rat heart isolated mitochondria in hyperthermic condition.
Materials and Methods: Mitochondrial fractions were isolated from heart of Wistar rat with different centrifuge technique. Then, heart isolated mitochondrial were exposed to METH (LC50, 250µM) and captopril (0, 25, 50, 100, 200, 400 µM) and incubated at 37 and 41 C. After 1 h incubation, mitochondrial damage was assayed by MTT test. Also, oxidative stress markers were measured.
Results: Our results showed that METH significantly induced mitochondrial damage that was more pronounced in hyperthermic condition. Increased oxidative stress markers such as lipid peroxidation, reactive oxygen species formation and glutathione oxidation in the heart isolated mitochondria were observed after METH exposure that was more significant at 41 c than 37 C. Captopril significantly inhibited METH–induced oxidative stress in the heart isolated mitochondria. Also, captopril pretreatment significantly improved mitochondrial function. Mitochondrial swelling also increased after METH exposure, but was significantly decreased with captopril pre-treatment.
Conclusion: These results suggested that captopril could ameliorate METH-induced oxidative stress and mitochondrial dysfunction especially in hyperthermic condition. Therefore, the effectiveness of this antioxidant should be evaluated for the treatment of METH cardiotoxicity |
topic |
Captopril Methamphetamine Cardiotoxicity Mitochondria Oxidative Stress Rat |
url |
http://koomeshjournal.semums.ac.ir/browse.php?a_code=A-10-2887-2&slc_lang=en&sid=1 |
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