Brain energy metabolism is increased by chronic administration of bupropion

Ferreira, Gabriela K.; Rezin, Gislaine T.; Cardoso, Mariane R.; Gonçalves, Cinara L.; Borges, Lislaine S.; Vieira, Júlia S.; Gomes, Lara M.; Zugno, Alexandra I.; Quevedo, Joao L De; Streck, Emílio L.

doi:10.1111/j.1601-5215.2011.00597.x

Cited by 6 publications

(4 citation statements)

References 46 publications

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“…Drugs used to treat major depression could boost energy metabolism and thus reduce damage caused by oxidative stress . In this context, several studies have shown that some antidepressants may improve energy metabolism . Assis et al .…”

Section: Discussionmentioning

confidence: 99%

“…demonstrated that paroxetine, nortriptyline and venlafaxine caused an increase in activity of some complexes of the mitochondrial respiratory chain in the brains of rats. Ferreira et al . showed that bupropion increased some enzymes of brain energy metabolism in rats.…”

Section: Discussionmentioning

confidence: 99%

“…Hereupon, it is suggested that the impairment of energy metabolism and oxidative stress could participate in the therapeutic or side‐effects of antidepressants . In this sense, it has already been shown that some antidepressants can increase energy metabolism and reduce damage caused by oxidative stress …”

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confidence: 99%

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Effect of subchronic administration of agomelatine on brain energy metabolism and oxidative stress parameters in rats

Mello

Souza

Cereja

et al. 2015

Psychiatry Clin Neurosci

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Aims:The aim of this study was to investigate the effect of subchronic administration of agomelatine on energy metabolism, oxidative stress markers and antioxidant defense in the brains of rats. Methods:The animals received daily intraperitoneal injections of agomelatine (10, 30 or 50 mg/kg) or saline for 14 days. The prefrontal cortex, cerebellum, hippocampus, striatum and posterior cortex were analyzed. Results:The findings showed that complex I was activated in the prefrontal cortex, cerebellum and striatum and inhibited in the posterior cortex at the 10-mg/kg dose, and inhibited in all brain areas analyzed at the 30-mg/kg and 50-mg/kg doses. Complex II was activated in the posterior cortex at the 50-mg/kg dose. Complex IV was inhibited in the striatum and posterior cortex at the 10-mg/kg dose, inhibited in the striatum at the 30-mg/kg dose and activated in the hippocampus at the 50-mg/kg dose.Creatine kinase activity was inhibited in the striatum at the 10-mg/kg and 30-mg/kg doses. Lipid peroxidation and protein carbonylation levels were not changed after the administration of agomelatine. Superoxide dismutase activity was increased in the striatum at the 10-mg/kg dose, and catalase activity was inhibited in the cerebellum at the 10-mg/kg dose and increased in the posterior cortex at the 30-mg/kg dose. Conclusions:Our results are consistent with other studies showing that some antidepressants may influence brain energy metabolism and oxidative stress parameters and expand knowledge about the effects of agomelatine in biochemical parameters in the brains of rats.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Effect of subchronic administration of agomelatine on brain energy metabolism and oxidative stress parameters in rats

Mello

Souza

Cereja

et al. 2015

Psychiatry Clin Neurosci

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“…Finally, in complex V (CV), also known as ATP synthase, the electrochemical gradient is used to catalyze the production of ATP from ADP. B Summary of the global effect of the investigated antidepressants and their effect on each complex of the ETC[22] based on preclinical studies[55][56][57][58][59]: A green box with an upward arrow indicates an increase in the activity of the specific complex after exposure to an antidepressant, a blue box with a downward arrow indicates a decrease in the activity of the specific complex after exposure to an antidepressant and a yellow box with a "~" sign indicates no effect observed. Abbreviations: CI Complex I, NADH:ubiquinone oxidoreductase, NADH reduced nictotinamide adenine dinucleotide, NAD + nictotinamide adenine dinucleotide, CII Complex II, succinate-coenzyme Q reductase, CoQ coenzyme Q, FADH reduced flavin adenine dinucleotide, FAD flavin adenine dinucleotide, CIII Complex III, coenzyme Qcytochrome c reductase, Cyt C cytochrome C, CIV Complex IV, cytochrome C oxidase, CV Complex V, ATP synthase, ADP adenosine diphosphate, ATP adenosine triphosphate.…”

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Antidepressants that increase mitochondrial energetics may elevate risk of treatment-emergent mania

et al. 2022

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Preclinical evidence suggests that antidepressants (ADs) may differentially influence mitochondrial energetics. This study was conducted to investigate the relationship between mitochondrial function and illness vulnerability in bipolar disorder (BD), specifically risk of treatment-emergent mania (TEM). Participants with BD already clinically phenotyped as TEM+ (n = 176) or TEM− (n = 516) were further classified whether the TEM associated AD, based on preclinical studies, increased (Mito+, n = 600) or decreased (Mito−, n = 289) mitochondrial electron transport chain (ETC) activity. Comparison of TEM+ rates between Mito+ and Mito− ADs was performed using generalized estimating equations to account for participants exposed to multiple ADs while adjusting for sex, age at time of enrollment into the biobank and BD type (BD-I/schizoaffective vs. BD-II). A total of 692 subjects (62.7% female, 91.4% White, mean age 43.0 ± 14.0 years) including 176 cases (25.3%) of TEM+ and 516 cases (74.7%) of TEM- with previous exposure to Mito+ and/or Mito- antidepressants were identified. Adjusting for age, sex and BD subtype, TEM+ was more frequent with antidepressants that increased (24.7%), versus decreased (13.5%) mitochondrial energetics (OR = 2.21; p = 0.000009). Our preliminary retrospective data suggests there may be merit in reconceptualizing AD classification, not solely based on monoaminergic conventional drug mechanism of action, but additionally based on mitochondrial energetics. Future prospective clinical studies on specific antidepressants and mitochondrial activity are encouraged. Recognizing pharmacogenomic investigation of drug response may extend or overlap to genomics of disease risk, future studies should investigate potential interactions between mitochondrial mechanisms of disease risk and drug response.

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Antidepressants, mood-stabilizing drugs, and mitochondrial functions: For better or for worse

Preston

Sabbagh

Emmerzaal

et al. 2023

Mitochondrial Intoxication

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Brain energy metabolism is increased by chronic administration of bupropion

Cited by 6 publications

References 46 publications

Effect of subchronic administration of agomelatine on brain energy metabolism and oxidative stress parameters in rats

Effect of subchronic administration of agomelatine on brain energy metabolism and oxidative stress parameters in rats

Antidepressants that increase mitochondrial energetics may elevate risk of treatment-emergent mania

Antidepressants, mood-stabilizing drugs, and mitochondrial functions: For better or for worse

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