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Electron Transport Chain: Complex I and II01:46

Electron Transport Chain: Complex I and II

The mitochondrial electron transport chain (ETC) is the main energy generation system in the eukaryotic cells. However, mitochondria also produce cytotoxic reactive oxygen species (ROS) due to the large electron flow during oxidative phosphorylation. While Complex I is one of the primary sources of superoxide radicals, ROS production by Complex II is uncommon and may only be observed in cancer cells with mutated complexes.
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Understanding the Changes in Mitochondrial Morphology through Dynamic and Three-dimensional Fluorescence Micrographs
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Metformin overdose causes platelet mitochondrial dysfunction in humans.

Alessandro Protti, Anna Lecchi, Francesco Fortunato

    Critical Care (London, England)
    |October 5, 2012
    PubMed
    Summary

    Metformin intoxication causes mitochondrial dysfunction and lactate overproduction in human platelets. This study investigated these effects in vitro and in patients with metformin overdose.

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    LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism
    06:04

    LC-MS Analysis of Human Platelets as a Platform for Studying Mitochondrial Metabolism

    Published on: April 4, 2016

    Area of Science:

    • Biochemistry
    • Pharmacology
    • Toxicology

    Background:

    • Metformin is a common medication for type 2 diabetes.
    • Metformin intoxication can lead to serious adverse effects, including lactic acidosis.
    • Previous studies indicated metformin-induced mitochondrial dysfunction in porcine platelets.

    Purpose of the Study:

    • To investigate the effects of metformin on human platelet mitochondrial function.
    • To determine if metformin causes lactate overproduction in human platelets.
    • To assess mitochondrial function in platelets from patients with metformin intoxication.

    Main Methods:

    • Human platelets were incubated with metformin in vitro.
    • Lactate production, mitochondrial respiration, and membrane potential were measured.
    • Platelets from metformin-intoxicated patients and healthy controls were analyzed ex vivo.

    Main Results:

    • In vitro, metformin increased lactate production and decreased mitochondrial function in a dose-dependent manner.
    • Platelets from intoxicated patients showed significantly reduced activity of respiratory chain complexes I and IV.
    • Metformin impaired mitochondrial membrane potential and oxygen consumption in human platelets.

    Conclusions:

    • Metformin can induce mitochondrial dysfunction and lactate overproduction in human platelets.
    • These effects were observed both in vitro and in patients with metformin intoxication.
    • Platelet mitochondrial dysfunction may contribute to the toxicity of metformin overdose.