Lithium increases leukocyte mitochondrial complex I activity in bipolar disorder during depressive episodes
Rationale Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or duri...
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| Published in | Psychopharmacology Vol. 232; no. 1; pp. 245 - 250 |
|---|---|
| Main Authors | , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
Berlin/Heidelberg
Springer Berlin Heidelberg
01.01.2015
Springer Springer Nature B.V |
| Subjects | |
| Online Access | Get full text |
| ISSN | 0033-3158 1432-2072 1432-2072 |
| DOI | 10.1007/s00213-014-3655-6 |
Cover
| Abstract | Rationale
Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium’s direct effects on ETC activity in vivo.
Objectives
This study aims to evaluate leukocyte ETC complexes I–IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity.
Methods
Subjects with short-term BD during a depressive episode (
n
= 25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I–IV activities were evaluated and compared to age-matched healthy controls (
n
= 24).
Results
Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (
p
= 0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (
p
= 0.003). Mitochondrial complexes I–IV activities did not differ during depressive episodes in BD compared to healthy controls.
Conclusions
Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. |
|---|---|
| AbstractList | Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo. This study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity. Subjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24). Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (p=0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls. Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development.[PUBLICATION ABSTRACT] Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo. This study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity. Subjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24). Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (p=0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls. Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. Rationale: Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo. Objectives: This study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity. Methods: Subjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24). Results: Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (p=0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls. Conclusions: Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. Rationale Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo. Objectives This study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity. Methods Subjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24). Results Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (p = 0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls. Conclusions Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. Keywords Complex I * Mitochondria * Electron transport chain * Lithium * Bipolar disorder * Depression * Treatment Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo.RATIONALEDifferent lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium's direct effects on ETC activity in vivo.This study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity.OBJECTIVESThis study aims to evaluate leukocyte ETC complexes I-IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity.Subjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24).METHODSSubjects with short-term BD during a depressive episode (n=25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I-IV activities were evaluated and compared to age-matched healthy controls (n=24).Lithium significantly increased mitochondrial complex I activity from baseline to endpoint (p=0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls.RESULTSLithium significantly increased mitochondrial complex I activity from baseline to endpoint (p=0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment (p=0.003). Mitochondrial complexes I-IV activities did not differ during depressive episodes in BD compared to healthy controls.Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development.CONCLUSIONSOur findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. Rationale Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport chain (ETC) is a key target to evaluate mitochondrial function, but its activity has never been assessed in unmedicated BD or during mood episodes. Also, lithium has been shown to increase ETC gene expression/activity in preclinical models and in postmortem brains of BD subjects, but to date, no study has evaluated lithium’s direct effects on ETC activity in vivo. Objectives This study aims to evaluate leukocyte ETC complexes I–IV activities in acute depressive episode in BD (compared to controls) and the effect of lithium treatment on ETC activity. Methods Subjects with short-term BD during a depressive episode ( n = 25) were treated for 6 weeks with lithium. Leukocytes were collected at baseline and endpoint and mitochondrial ETC complexes I–IV activities were evaluated and compared to age-matched healthy controls ( n = 24). Results Lithium significantly increased mitochondrial complex I activity from baseline to endpoint ( p = 0.02), with no changes in other complexes after 6 weeks. Also, plasma lithium levels were significantly correlated to mitochondrial complex I activity after treatment ( p = 0.003). Mitochondrial complexes I–IV activities did not differ during depressive episodes in BD compared to healthy controls. Conclusions Our findings demonstrate for the first time an increase in mitochondrial ETC complex I activity in vivo after lithium treatment in BD, which was positively associated with plasma lithium levels. Further studies are warranted to clarify the potential role of this target in neuroprotection-related drug development. |
| Audience | Academic |
| Author | Brunoni, Andre R. Machado-Vieira, Rodrigo Streck, Emilio L. Diniz, Breno S. Gattaz, Wagner F. de Sousa, Rafael T. Ferreira, Gabriela K. Busatto, Geraldo F. Zanetti, Marcus V. |
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Scand. 2012 Nov;126(5):332-41 – reference: 22972949 - J Med Genet. 2012 Sep;49(9):578-90 – reference: 19624390 - Bipolar Disord. 2009 Aug;11(5):515-22 – reference: 17548157 - Neurosci Lett. 2007 Jun 21;421(1):33-6 – reference: 18539338 - J Affect Disord. 2008 Dec;111(2-3):135-44 – reference: 20368511 - Arch Gen Psychiatry. 2010 Apr;67(4):360-8 – reference: 17622937 - Pharmacogenet Genomics. 2007 Aug;17(8):605-17 – reference: 22200861 - Mol Med Rep. 2012 Mar;5(3):680-2 – reference: 324690 - Clin Pharmacokinet. 1977 Mar-Apr;2(2):73-92 – reference: 8645009 - Arch Biochem Biophys. 1996 Apr 15;328(2):309-16 – reference: 18061150 - Brain Res. 2008 Jan 16;1189:215-8 – reference: 19538689 - Bipolar Disord. 2009 Jun;11 Suppl 2:92-109 – reference: 7955428 - Clin Chim Acta. 1994 Jul;228(1):35-51 – reference: 3000647 - Clin Chim Acta. 1985 Nov 29;153(1):23-36 – reference: 23228201 - Bipolar Disord. 2013 Feb;15(1):100-9 – reference: 23870796 - J Psychiatr Res. 2013 Oct;47(10):1396-402 – reference: 6046425 - Can Vet J. 1967 May;8(5):110-1 |
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Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron... Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron transport... Rationale Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial electron... Rationale: Different lines of evidence suggest that mitochondrial dysfunction may be implicated in bipolar disorder (BD) pathophysiology. Mitochondrial... |
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| SubjectTerms | Adult Antidepressive Agents - pharmacology Antidepressive Agents - therapeutic use Biomedical and Life Sciences Biomedicine Bipolar disorder Bipolar Disorder - blood Bipolar Disorder - drug therapy Bipolar Disorder - psychology Depression (Mood disorder) Depression - blood Depression - drug therapy Depression - psychology Dosage and administration Drug therapy Electron Transport Complex I - blood Female Health aspects Humans Leukocytes - drug effects Leukocytes - metabolism Lithium Lithium Carbonate - pharmacology Lithium Carbonate - therapeutic use Lithium drugs Male Mental depression Mitochondria Mitochondria - drug effects Mitochondria - metabolism Neurosciences Original Investigation Patient outcomes Pharmacology/Toxicology Psychiatry Psychopharmacology White blood cells Young Adult |
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| Title | Lithium increases leukocyte mitochondrial complex I activity in bipolar disorder during depressive episodes |
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