CAPTOPRIL INHIBITED METAMPHETAMINE - INDUCED CARDIAC MITOCHONDRIAL DAMAGE IN HYPERTHERMIC CONDITION VIA MODULATION OF BIOCHEMICAL MARKERS

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Shokrzadeh Mohammd; ZAMANI EHSAN; Mollahasani Javad; SHAKI FATEMEH

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Journal: Koomesh Year:2016 | Volume:18 | Issue:1 (61) Page(s): 128-137

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Information Journal Paper

Title

CAPTOPRIL INHIBITED METAMPHETAMINE - INDUCED CARDIAC MITOCHONDRIAL DAMAGE IN HYPERTHERMIC CONDITION VIA MODULATION OF BIOCHEMICAL MARKERS

Author(s)

Shokrzadeh Mohammd | ZAMANI EHSAN | Mollahasani Javad | SHAKI FATEMEH | Issue Writer Certificate

Keywords

CAPTOPRILQ3

METHAMPHETAMINEQ1

CARDIOTOXICITYQ1

MITOCHONDRIA; OXIDATIVE STRESSQ2

RATQ2

Abstract

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, 250mM) and CAPTOPRIL (0, 25, 50, 100, 200, 400 mM) 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.

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References

TOXICITY OF ARSENIC (III) ON ISOLATED LIVER MITOCHONDRIA: A NEW MECHANISTIC APPROACH

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APA: Copy

Shokrzadeh, Mohammd, ZAMANI, EHSAN, Mollahasani, Javad, & SHAKI, FATEMEH. (2016). CAPTOPRIL INHIBITED METAMPHETAMINE - INDUCED CARDIAC MITOCHONDRIAL DAMAGE IN HYPERTHERMIC CONDITION VIA MODULATION OF BIOCHEMICAL MARKERS. KOOMESH, 18(1 (61)), 128-137. SID. https://sid.ir/paper/36985/en

Vancouver: Copy

Shokrzadeh Mohammd, ZAMANI EHSAN, Mollahasani Javad, SHAKI FATEMEH. CAPTOPRIL INHIBITED METAMPHETAMINE - INDUCED CARDIAC MITOCHONDRIAL DAMAGE IN HYPERTHERMIC CONDITION VIA MODULATION OF BIOCHEMICAL MARKERS. KOOMESH[Internet]. 2016;18(1 (61)):128-137. Available from: https://sid.ir/paper/36985/en

IEEE: Copy

Mohammd Shokrzadeh, EHSAN ZAMANI, Javad Mollahasani, and FATEMEH SHAKI, “CAPTOPRIL INHIBITED METAMPHETAMINE - INDUCED CARDIAC MITOCHONDRIAL DAMAGE IN HYPERTHERMIC CONDITION VIA MODULATION OF BIOCHEMICAL MARKERS,” KOOMESH, vol. 18, no. 1 (61), pp. 128–137, 2016, [Online]. Available: https://sid.ir/paper/36985/en

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