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Related Concept Videos

Redox Reactions01:27

Redox Reactions

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Redox reactions are vital biochemical processes that underpin energy metabolism in cells. These reactions involve the transfer of electrons between molecules, occurring in tandem as oxidation and reduction. Oxidation refers to the loss of electrons, while reduction denotes their gain. This coupling ensures the seamless flow of electrons through metabolic pathways. For example, in bacterial metabolism, glucose undergoes oxidation to carbon dioxide, while oxygen is simultaneously reduced to...
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Electron Transport Chain: Complex III and IV01:43

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During the electron transport chain, electrons from NADH and FADH2 are first transferred to complexes I and II, respectively. These two complexes then transfer the electrons to ubiquinol, which carries them further to complex III. Complex III passes the electrons across the intermembrane space to Cyt c, which carries them further to complex IV. Complex IV donates electrons to oxygen and reduces it to water. As electrons pass through complexes I, III, and IV, the energy released aids the pumping...
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The Supercomplexes in the Crista Membrane01:41

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The mitochondrial cristae membrane is the primary site for the oxidative phosphorylation (OXPHOS) process of energy conversion mediated through respiratory complexes I to V. These complexes have been widely studied for decades, and it has been proven that they form supramolecular structures called respiratory supercomplexes (SC). These higher-order complexes may be crucial in maintaining the biochemical structure and improving the physiological activity of the individual complexes while...
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Electron Transport Chain Components01:29

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The electron transport chain (ETC) is a crucial metabolic pathway that facilitates energy conversion in prokaryotic and eukaryotic cells. In eukaryotes, the ETC comprises four membrane-associated protein complexes in the inner mitochondrial membrane. In prokaryotes, the ETC in the plasma membrane can vary in composition, with fewer or different complexes depending on the organism and environmental conditions. These complexes transfer electrons from electron donors, such as NADH and FADH2, to...
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Peroxisomes01:24

Peroxisomes

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Peroxisomes are specialized organelles present in fungi, plant, and animal cells. It can vary in number, size, morphology, and activity depending on the type of tissue and the nutritional state of the cell. For example, cells with active lipid metabolism, such as adipocytes, neurons, and hepatocytes, have more peroxisomes than other cells in the body. Besides their primary role in breaking down complex organic molecules, peroxisomes can also synthesize specific macromolecules and participate in...
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Electron Transport Chain: Complex I and II01:46

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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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Related Experiment Video

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Use of Animal Model of Sepsis to Evaluate Novel Herbal Therapies
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HMGB1 redox during sepsis.

Wasan Abdulmahdi1, Devika Patel2, May M Rabadi2

  • 1Department of Physiology, Renal Research Institute, New York Medical College, Valhalla, NY, United States.

Redox Biology
|August 15, 2017
PubMed
Summary
This summary is machine-generated.

Sepsis increases reactive oxygen species (ROS) and high-mobility group box 1 (HMGB1) oxidation in kidney cells, enhancing inflammation. Glutathione and thioredoxin systems help maintain HMGB1 in a reduced state.

Keywords:
CytokinesHMGB1Oxidative stressRedoxSepsis

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Area of Science:

  • Cellular Biology
  • Immunology
  • Nephrology

Background:

  • Sepsis causes multi-organ damage, with kidneys being particularly vulnerable.
  • High-mobility group box 1 (HMGB1) is a key inflammatory mediator released during sepsis.
  • The pro-inflammatory activity of HMGB1 is linked to its redox state.

Purpose of the Study:

  • To investigate the redox state of HMGB1 in kidney cells during sepsis.
  • To understand the role of reactive oxygen species (ROS) in HMGB1 oxidation during sepsis.
  • To explore the impact of HMGB1 oxidation on kidney inflammation and function.

Main Methods:

  • Intravital microscopy and CellROX/MitoSOX labeling in live mice to assess ROS generation.
  • Thiol assay and liquid chromatography-tandem mass spectrometry (LC-MS/MS) to quantify HMGB1 oxidation.
  • Luminex Multiplex assay for cytokine/chemokine release and ATP detection assay for mitochondrial function.

Main Results:

  • LPS-induced sepsis increased ROS generation in kidney perivascular endothelium and tubules.
  • HMGB1 oxidation in kidney cells correlated with sepsis severity and enhanced pro-inflammatory signaling.
  • Inhibitors of glutathione and thioredoxin systems increased HMGB1 oxidation in sepsis models.

Conclusions:

  • Increased ROS generation and HMGB1 oxidation in kidney cells exacerbate sepsis-induced inflammation.
  • The glutathione and thioredoxin systems play a protective role by maintaining HMGB1 in a reduced state.
  • Targeting HMGB1 redox state may offer a therapeutic strategy for sepsis-related kidney injury.