Effects of acute administration of mazindol on brain energy metabolism in adult mice

Gonçalves, Cinara L.; Scaini, Giselli; Rezin, Gislaine T.; Jeremias, Isabela C.; Bez, Gisele Daiane; Daufenbach, Juliana F.; Gomes, Lara M.; Ferreira, Gabriela K.; Zugno, Alexandra I.; Streck, Emílio L.

doi:10.1017/neu.2013.43

Cited by 5 publications

(2 citation statements)

References 59 publications

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“…The increase in the activity of CS reinforces the hypothesis that mitochondrial biogenesis is induced in VLCAD-deficient cells. An increase in this Krebs cycle enzyme that provides additional reducing equivalents for the ETC may also be a compensatory mechanism for the bioenergetics failure in the FAO pathway and the ETC as suggested by the reduced oxygen consumption in VLCAD-deficient cells (43,44).…”

Section: Discussionmentioning

confidence: 99%

Mitochondrial energetics is impaired in very long-chain acyl-CoA dehydrogenase deficiency and can be rescued by treatment with mitochondria-targeted electron scavengers

Seminotti

Leipnitz

Karunanidhi

et al. 2018

Human Molecular Genetics

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Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is the most common defect of mitochondrial long-chain fatty acid -oxidation. Patients present with heterogeneous clinical phenotypes affecting heart, liver and skeletal muscle predominantly. The full pathophysiology of the disease is unclear and patient response to current therapeutic regimens is incomplete. To identify additional cellular alterations and explore more effective therapies, mitochondrial bioenergetics and redox homeostasis were assessed in VLCAD-deficient fibroblasts, and several protective compounds were evaluated. The results revealed cellular and tissue changes, including decreased respiratory chain (RC) function, increased reactive oxygen species (ROS) production and altered mitochondrial function and signaling pathways in a variety of VLCAD-deficient fibroblasts. The mitochondrially enriched electron and free radical scavengers JP4-039 and XJB-5-131 improved RC function and decreased ROS production significantly, suggesting that they are viable candidate compounds to further develop to treat VLCAD-deficient patients.

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Section: Discussionmentioning

confidence: 99%

Mitochondrial energetics is impaired in very long-chain acyl-CoA dehydrogenase deficiency and can be rescued by treatment with mitochondria-targeted electron scavengers

Seminotti

Leipnitz

Karunanidhi

et al. 2018

Human Molecular Genetics

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“…PGC1‐ α, a transcriptional coactivator, is a key inducer of mitochondrial biogenesis in cells (Austin and St‐Pierre, 2012). Although mitochondria morphology in fatty liver did not vary much from normal liver, its function was impaired (Bruguera et al, ; Yang et al, ; Gonçalves et al, ). Adiponectin has been shown to promote mitochondrial biogenesis and enhance oxidative capacity in the skeletal muscles using adiponectin gene knocked out and transgenic mouse models (Civitarese et al, ; Iwabu et al, ; Qiao et al, ).…”

mentioning

confidence: 99%

Adiponectin Prevents Reduction of Lipid‐Induced Mitochondrial Biogenesis via AMPK/ACC2 Pathway in Chicken Adipocyte

Gan

Yan

Liu

et al. 2015

J of Cellular Biochemistry

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Adiponectin (APN) stimulates mitochondrial biogenesis and reduces lipid content in human and animal adipocytes. However, the mechanism of adiponectin in regulating mitochondrial biogenesis in chicken adipocytes has never been reported. The objective of this study is to examine the mechanism that adiponectin plays in lipid-induced mitochondrial biogenesis and mitochondrial function in chicken adipocytes. We found that the overexpression of adiponectin reduced the membrane DAG content and elevated the membrane translocation of PKCθ. In contrast to control groups, the overexpression of adiponectin increased mitochondrial density and mitochondrial DNA contents and peroxisome proliferator-activated receptor αcoactivator 1α (PGC1-α) expression. Mitochondrial membrane potential and cytochrome C (Cyt C) content were detected by JC-1 fluorescent staining and immunofluorescence which indicated that overexpression of adiponectin enhanced mitochondrial ATP synthesis. Moreover, AMPK/ACC2 signaling pathway was activated along with the elevation of PGC1-α and TFAM by the overexpression of adiponectin, meanwhile the lipid transcription marker genes were down-regulated. This effect was alleviated by reducing adiponectin and a specific inhibitor of AMPK pathway. We concluded that adiponectin could prevent reduction of lipid-induced mitochondrial biogenesis via AMPK/ACC2 pathway in chicken adipocytes.

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Pulmonary Arterial Hypertension Secondary to Drugs and Toxins

Ramírez

Pienkos

Perez

et al. 2021

Clinics in Chest Medicine

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Effects of acute administration of mazindol on brain energy metabolism in adult mice

Abstract: We suggest that the inhibition of complex I in the hippocampus only and activation of complex IV, citrate synthase and creatine kinase occurs because of a stimulus effect of mazindol in the central nervous system, which causes a direct impairment on energy metabolism.

Cited by 5 publications

References 59 publications

Mitochondrial energetics is impaired in very long-chain acyl-CoA dehydrogenase deficiency and can be rescued by treatment with mitochondria-targeted electron scavengers

Mitochondrial energetics is impaired in very long-chain acyl-CoA dehydrogenase deficiency and can be rescued by treatment with mitochondria-targeted electron scavengers

Adiponectin Prevents Reduction of Lipid‐Induced Mitochondrial Biogenesis via AMPK/ACC2 Pathway in Chicken Adipocyte

Pulmonary Arterial Hypertension Secondary to Drugs and Toxins

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