scholarly journals Preparation of yeast mitochondria and in vitro assay of respiratory chain complex activities

2010 ◽  
Author(s):  
Stefania Magri ◽  
Valentina Fracasso ◽  
Marco Rimoldi ◽  
Franco Taroni
Keyword(s):  
Respiratory Chain ◽  
Chain Complex ◽  
In Vitro Assay ◽  
Yeast Mitochondria ◽  
Respiratory Chain Complex ◽  
Vitro Assay ◽  
Complex Activities

Differential inhibitory effects of methylmalonic acid on respiratory chain complex activities in rat tissues

2005 ◽  
Vol 24 (1) ◽  
pp. 45-52 ◽  
Author(s):  
Leticia F. Pettenuzzo ◽  
Gustavo da C. Ferreira ◽  
Anna Laura Schmidt ◽  
Carlos S. Dutra‐Filho ◽  
Angela T.S. Wyse ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Methylmalonic Acid ◽  
Chain Complex ◽  
Rat Tissues ◽  
Respiratory Chain Complex ◽  
Inhibitory Effects ◽  
Complex Activities

scholarly journals AML cells have low spare reserve capacity in their respiratory chain that renders them susceptible to oxidative metabolic stress

Blood ◽  
2015 ◽  
Vol 125 (13) ◽  
pp. 2120-2130 ◽  
Author(s):  
Shrivani Sriskanthadevan ◽  
Danny V. Jeyaraju ◽  
Timothy E. Chung ◽  
Swayam Prabha ◽  
Wei Xu ◽  
...  
Keyword(s):  
Respiratory Chain ◽  
Metabolic Stress ◽  
Chain Complex ◽  
Reserve Capacity ◽  
Respiratory Chain Complex ◽  
Respiratory Chain Complexes ◽  
Mitochondrial Mass ◽  
Chain Complexes ◽  
Key Points ◽  
Complex Activities

Key Points AML cells have increased mitochondrial mass, low respiratory chain complex activities, and low spare reserve capacity compared with normal cells. AML cells have heightened sensitivity to inhibitors of the respiratory chain complexes and oxidative stressors.

Placental respiratory chain complex activities in high risk pregnancies

2017 ◽  
Vol 30 (24) ◽  
pp. 2911-2917 ◽  
Author(s):  
Mojtaba Beyramzadeh ◽  
Zeliha Gunnur Dikmen ◽  
Nergiz K. Erturk ◽  
Zafer Selcuk Tuncer ◽  
Filiz Akbiyik
Keyword(s):  
High Risk ◽  
Respiratory Chain ◽  
Chain Complex ◽  
Respiratory Chain Complex ◽  
Complex Activities

MELAS-associated m.5541C>T mutation caused instability of mitochondrial tRNATrp and remarkable mitochondrial dysfunction

2020 ◽  
pp. jmedgenet-2020-107323
Author(s):  
Kunqian Ji ◽  
Yan Lin ◽  
Xuebi Xu ◽  
Wei Wang ◽  
Dongdong Wang ◽  
...  
Keyword(s):  
Mitochondrial Dysfunction ◽  
Respiratory Chain ◽  
Nuclear Dna ◽  
Chain Complex ◽  
Trna Genes ◽  
Full Potential ◽  
Respiratory Chain Complex ◽  
Mitochondrial Trna ◽  
Taurine Supplementation ◽  
Complex Activities

BackgroundMitochondrial encephalomyopathy with lactic acidosis and stroke-like episode (MELAS) is a group of genetic diseases caused by mutations in mitochondrial DNA and nuclear DNA. The causative mutations of MELAS have drawn much attention, among them, mutations in mitochondrial tRNA genes possessing prominent status. However, the detailed molecular pathogenesis of these tRNA gene mutations remains unclear and there are very few effective therapies available to date.MethodsWe performed muscle histochemistry, genetic analysis, molecular dynamic stimulation and measurement of oxygen consumption rate and respiratory chain complex activities to demonstrate the molecular pathomechanisms of m.5541C>T mutation. Moreover, we use cybrid cells to investigate the potential of taurine to rescue mitochondrial dysfunction caused by this mutation.ResultsWe found a pathogenic m.5541C>T mutation in the tRNATrp gene in a large MELAS family. This mutation first affected the maturation and stability of tRNATrp and impaired mitochondrial respiratory chain complex activities, followed by remarkable mitochondrial dysfunction. Surprisingly, we identified that the supplementation of taurine almost completely restored mitochondrial tRNATrp levels and mitochondrial respiration deficiency at the in vitro cell level.ConclusionThe m.5541C>T mutation disturbed the translation machinery of mitochondrial tRNATrp and taurine supplementation may be a potential treatment for patients with m.5541C>T mutation. Further studies are needed to explore the full potential of taurine supplementation as therapy for patients with this mutation.

In Vitro Assay of Platelet Adhesiveness with Washed and Tanned Human Red Cells

1968 ◽  
Vol 20 (03/04) ◽  
pp. 384-396 ◽  
Author(s):  
G Zbinden ◽  
S Tomlin
Keyword(s):  
Platelet Adhesion ◽  
Sodium Citrate ◽  
Blood Platelets ◽  
In Vitro Assay ◽  
Red Cells ◽  
Platelet Adhesiveness ◽  
Vitro Assay ◽  
In Vitro System ◽  
Human Red Cells

SummaryAn in vitro system is described in which adhesion of blood platelets to washed and tannic acid-treated red cells was assayed quantitatively by microscopic observation. ADP, epinephrine and TAME produced a reversible increase in platelet adhesiveness which was antagonized by AMP. With Evans blue, polyanetholsulfonate, phthalanilide NSC 38280, thrombin and heparin at concentrations above 1-4 u/ml the increase was irreversible. The ADP-induced increase in adhesiveness was inhibited by sodium citrate, EDTA, AMP, ATP and N-ethylmaleimide. EDTA, AMP and the SH-blocker N-ethylmaleimide also reduced spontaneous platelet adhesion to red cells. No significant effects were observed with adenosine, phenprocoumon, 5-HT, phthalanilide NSC 57155, various estrogens, progestogens and fatty acids, acetylsalicylic acid and similarly acting agents, hydroxylamine, glucose and KCN. The method may be useful for the screening of thrombogenic and antithrombotic properties of drugs.

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