Abstract
Melatonin (MLT) is highly protective against cardiotoxicity caused by doxorubicin (DOX). DOX induces cardiac damage via production of reactive oxygen species. This study tests the hypothesis that oxygen radicals generated by DOX disrupt mitochondrial membrane potential (Δψm) prior to severe cell injury. Myocytes were incubated with 20 μmol/l DOX for 24 h. Myocyte damage was estimated by lactate dehydrogenase (LDH) release. Mitochondrial membrane potential was determined by staining myocytes with 5, 5′, 6, 6′-tetrachloro-1, 1′, 3, 3′-tetraethylbenzimidazolcarbocyanine iodide (JC-1) using confocal microscope. A significant amount of LDH was observed after 24 h of treatment with DOX, Mitochondria in DOX-treated myocytes exhibited a collapse of Δπm. Pretreatment with melatonin (1 mmol/l) for one hour prevented the release of LDH and restored Δπm. The data support the hypothesis that DOX induces damage to mitochondria through radicals, and this is reflected in depolarization of Δπm, which was prevented by melatonin.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 75-79 |
| Number of pages | 5 |
| Journal | Journal of molecular and cellular cardiology |
| Volume | 34 |
| Issue number | 1 |
| DOIs | |
| State | Published - Jan 1 2002 |
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Keywords
- Doxorubicin
- Melatonin
- Mitochondrial Membrane Potential
- Myocyte
ASJC Scopus subject areas
- Molecular Biology
- Cardiology and Cardiovascular Medicine
Cite this
Melatonin protection against lethal myocyte injury induced by doxorubicin as reflected by effects on mitochondrial membrane potential. / Xu, Meifeng; Ashraf, Muhammad.
In: Journal of molecular and cellular cardiology, Vol. 34, No. 1, 01.01.2002, p. 75-79.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Melatonin protection against lethal myocyte injury induced by doxorubicin as reflected by effects on mitochondrial membrane potential
AU - Xu, Meifeng
AU - Ashraf, Muhammad
PY - 2002/1/1
Y1 - 2002/1/1
N2 - Melatonin (MLT) is highly protective against cardiotoxicity caused by doxorubicin (DOX). DOX induces cardiac damage via production of reactive oxygen species. This study tests the hypothesis that oxygen radicals generated by DOX disrupt mitochondrial membrane potential (Δψm) prior to severe cell injury. Myocytes were incubated with 20 μmol/l DOX for 24 h. Myocyte damage was estimated by lactate dehydrogenase (LDH) release. Mitochondrial membrane potential was determined by staining myocytes with 5, 5′, 6, 6′-tetrachloro-1, 1′, 3, 3′-tetraethylbenzimidazolcarbocyanine iodide (JC-1) using confocal microscope. A significant amount of LDH was observed after 24 h of treatment with DOX, Mitochondria in DOX-treated myocytes exhibited a collapse of Δπm. Pretreatment with melatonin (1 mmol/l) for one hour prevented the release of LDH and restored Δπm. The data support the hypothesis that DOX induces damage to mitochondria through radicals, and this is reflected in depolarization of Δπm, which was prevented by melatonin.
AB - Melatonin (MLT) is highly protective against cardiotoxicity caused by doxorubicin (DOX). DOX induces cardiac damage via production of reactive oxygen species. This study tests the hypothesis that oxygen radicals generated by DOX disrupt mitochondrial membrane potential (Δψm) prior to severe cell injury. Myocytes were incubated with 20 μmol/l DOX for 24 h. Myocyte damage was estimated by lactate dehydrogenase (LDH) release. Mitochondrial membrane potential was determined by staining myocytes with 5, 5′, 6, 6′-tetrachloro-1, 1′, 3, 3′-tetraethylbenzimidazolcarbocyanine iodide (JC-1) using confocal microscope. A significant amount of LDH was observed after 24 h of treatment with DOX, Mitochondria in DOX-treated myocytes exhibited a collapse of Δπm. Pretreatment with melatonin (1 mmol/l) for one hour prevented the release of LDH and restored Δπm. The data support the hypothesis that DOX induces damage to mitochondria through radicals, and this is reflected in depolarization of Δπm, which was prevented by melatonin.
KW - Doxorubicin
KW - Melatonin
KW - Mitochondrial Membrane Potential
KW - Myocyte
UR - http://www.scopus.com/inward/record.url?scp=0036171091&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0036171091&partnerID=8YFLogxK
U2 - 10.1006/jmcc.2001.1485
DO - 10.1006/jmcc.2001.1485
M3 - Article
C2 - 11812166
AN - SCOPUS:0036171091
VL - 34
SP - 75
EP - 79
JO - Journal of Molecular and Cellular Cardiology
JF - Journal of Molecular and Cellular Cardiology
SN - 0022-2828
IS - 1
ER -