scholarly journals Partial Mitigation of Oxidized Phospholipid-Mediated Mitochondrial Dysfunction in Neuronal Cells by Oxocarotenoids

2020 ◽  
Vol 74 (1) ◽  
pp. 113-126
Author(s):  
Opeyemi S. Ademowo ◽  
Irundika H.K. Dias ◽  
Lorena Diaz-Sanchez ◽  
Lissette Sanchez-Aranguren ◽  
Wilhelm Stahl ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neuronal Cells ◽  
Oxidized Phospholipid

scholarly journals SULT4A1 Protects Against Oxidative-Stress Induced Mitochondrial Dysfunction in Neuronal Cells

2019 ◽  
Vol 47 (9) ◽  
pp. 949-953 ◽  
Author(s):  
Mohammed I. Hossain ◽  
Joshua M. Marcus ◽  
Jun Hee Lee ◽  
Patrick L. Garcia ◽  
Jean-Philippe Gagné ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Neuronal Cells

scholarly journals Synaptosomes: New Vesicles for Neuronal Mitochondrial Transplantation

2020 ◽  
Author(s):  
Pasquale Picone ◽  
Gaetana Porcelli ◽  
Celeste Caruso Bavisotto ◽  
Domenico Nuzzo ◽  
Giacoma Galizzi ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neuronal Cells ◽  
Nile Red ◽  
Critical Factor ◽  
Specific Protein ◽  
Mitochondrial Proteins ◽  
Hexokinase Ii ◽  
Protein Protein Interaction ◽  
First Time ◽  
Fusion Ability

Abstract Background: Mitochondrial dysfunction is a critical factor in the onset and progression of neurodegenerative diseases. Recently, mitochondrial transplantation has been advised as an innovative and attractive strategy to transfer and replace damaged mitochondria. Here we propose, for the first time, to use rat brain extracted synaptosomes, subcellular fraction of isolated synaptic terminal that contain mitochondria, as mitochondrial delivery systems. Results: Synaptosomes preparation was validated by the presence of Synaptophysin and PSD95. Syn aptosomes were characterized in terms of dimension, zeta potential, polydispersity index and number of particles/mL. Nile Red or CTX-FITCH labeled synaptosomes were internalized in LAN5 recipient cells by a mechanism involving specific protein-protein interaction, as demonstrated by loss of fusion ability after trypsin treatment and using different cell lines. The loading and release ability of the synaptosomes was proved by the presence of curcumin both into synaptosomes and LAN5 cells. The vitality of mitochondria transferred by Synaptosomes was demonstrated by the presence of Opa1, Fis1 and TOM40 mitochondrial proteins and JC-1 measurements. Further, synaptosomes deliver vital mitochondria into the cytoplasm of neuronal cells as demonstrated by microscopic images, increase of TOM 40, cytochrome c, Hexokinase II mitochondrial proteins, and presence of rat mitochondrial DNA. Finally, by using synaptosomes as vehicle, healthy mitochondria restored mitochondrial function in cells containing rotenone or CCCp damaged mitochondria. Conclusions: Taken together these results suggest that synaptosomes can be a natural vehicle for the delivery of molecules and organelles to neuronal cells. Further, replacement of affected mitochondria with healthy ones could be a potential therapy for the treatment of neuronal mitochondrial dysfunction-related diseases.

Isoliquiritigenin isolated from Glycyrrhiza uralensis protects neuronal cells against glutamate-induced mitochondrial dysfunction

2012 ◽  
Vol 421 (4) ◽  
pp. 658-664 ◽  
Author(s):  
Eun-Ju Yang ◽  
Ju Sik Min ◽  
Hyun-Yeong Ku ◽  
Hoon-Sung Choi ◽  
Moon-ki Park ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Neuronal Cells ◽  
Glycyrrhiza Uralensis

scholarly journals Diphenyl diselenide protects neuronal cells against oxidative stress and mitochondrial dysfunction: Involvement of the glutathione-dependent antioxidant system

Redox Biology ◽  
2019 ◽  
Vol 20 ◽  
pp. 118-129 ◽  
Author(s):  
Ruth Liliám Quispe ◽  
Michael Lorenz Jaramillo ◽  
Leticia Selinger Galant ◽  
Daiane Engel ◽  
Alcir Luiz Dafre ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Antioxidant System ◽  
Neuronal Cells ◽  
Diphenyl Diselenide

scholarly journals Schisandrin B as a Hormetic Agent for Preventing Age-Related Neurodegenerative Diseases

2012 ◽  
Vol 2012 ◽  
pp. 1-9 ◽  
Author(s):  
Philip Y. Lam ◽  
Kam Ming Ko
Keyword(s):  
Neurodegenerative Diseases ◽  
Mitochondrial Dysfunction ◽  
Clinical Symptoms ◽  
Redox Homeostasis ◽  
Neuronal Cells ◽  
Schisandrin B ◽  
Brain Health ◽  
Age Related ◽  
Oxidative Challenge ◽  
Experimental Findings

Oxidative stress and mitochondrial dysfunction have been implicated in the pathogenesis of neurodegenerative diseases, with the latter preceding the appearance of clinical symptoms. The energy failure resulting from mitochondrial dysfunction further impedes brain function, which demands large amounts of energy. Schisandrin B (Sch B), an active ingredient isolated from Fructus Schisandrae, has been shown to afford generalized tissue protection against oxidative damage in various organs, including the brain, of experimental animals. Recent experimental findings have further demonstrated that Sch B can protect neuronal cells against oxidative challenge, presumably by functioning as a hormetic agent to sustain cellular redox homeostasis and mitoenergetic capacity in neuronal cells. The combined actions of Sch B offer a promising prospect for preventing or possibly delaying the onset of neurodegenerative diseases, as well as enhancing brain health.

Sign in / Sign up

Export Citation Format

Share Document