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Related Concept Videos

Electron Transport Chain: Complex III and IV01:43

Electron Transport Chain: Complex III and IV

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 oxidation of an organic compound in the presence of air or oxygen is called autoxidation. For example, cumene reacts with oxygen to form hydroperoxide. Autoxidation involves initiation, propagation, and termination steps. Many organic compounds are susceptible to autoxidation—especially ethers in the presence of oxygen, which form hydroperoxides. Even though this reaction is slow, old ether bottles contain small amounts of peroxide, which leads to laboratory explosions during ether...

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Related Experiment Video

Updated: May 23, 2026

Measurement of Carotenoids in Perifovea using the Macular Pigment Reflectometer
09:35

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Published on: January 29, 2020

How does the macula protect itself from oxidative stress?

James T Handa1

  • 1Wilmer Eye Institute, Johns Hopkins School of Medicine, Baltimore, MD, USA. jthanda@jhmi.edu

Molecular Aspects of Medicine
|April 17, 2012
PubMed
Summary
This summary is machine-generated.

Oxidative stress contributes to age-related macular degeneration (AMD) by damaging retinal cells. Strategies to regulate reactive oxygen species (ROS) and oxidation specific epitopes (OSEs) may offer new treatments for early AMD.

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Published on: December 11, 2020

Area of Science:

  • Ophthalmology
  • Immunology
  • Cell Biology

Background:

  • Age-related macular degeneration (AMD) is a leading cause of blindness with no early treatment.
  • Oxidative stress, driven by reactive oxygen species (ROS), plays a key role in RPE cell dysfunction in AMD.
  • The Nrf2 antioxidant system protects RPE cells, but its impairment can lead to damage and immune activation.

Purpose of the Study:

  • To explore the role of oxidative stress and oxidation specific epitopes (OSEs) in AMD pathogenesis.
  • To investigate the potential of modulating antioxidant systems and immune responses for AMD treatment.

Main Methods:

  • Review of existing research on oxidative stress, ROS, Nrf2 signaling, and OSEs in AMD.
  • Analysis of mouse models simulating AMD features through environmental stressors or genetic modifications.
  • Examination of OSE accumulation and innate immune activation in the macula.

Main Results:

  • Impaired Nrf2 signaling leads to oxidative damage and RPE apoptosis, characteristic of AMD.
  • Long-lived OSEs, such as carboxyethylpyrrole, can chronically activate the innate immune system.
  • Immune activation by OSEs, like carboxyethylpyrrole, can induce AMD-like features in mice.

Conclusions:

  • Modulating RPE antioxidant systems is a potential strategy to manage ROS levels.
  • Neutralizing OSEs via the innate immune system offers a therapeutic avenue for early AMD prevention or treatment.