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Related Concept Videos

The Inner Mitochondrial Membrane01:28

The Inner Mitochondrial Membrane

The inner mitochondrial membrane is the primary site of ATP synthesis. The inner membrane domain that forms a smooth layer adjacent to the outer membrane is called the inner boundary membrane. This domain contains membrane transporters that drive metabolites in and out of the mitochondria.  In contrast, the inner membrane network that invaginates into the matrix space is called the cristae membrane. This domain accounts for principle mitochondrial function as it accommodates the protein...
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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.
ROS generation is regulated and maintained at moderate levels necessary...
The Electron Transport Chain01:30

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The electron transport chain or oxidative phosphorylation is an exothermic process in which free energy released during electron transfer reactions is coupled to ATP synthesis. This process is a significant source of energy in aerobic cells, and therefore inhibitors of the electron transport chain can be detrimental to the cell's metabolic processes.
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The Supercomplexes in the Crista Membrane01:41

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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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CMIT/MIT produces mitochondrial ROS via inhibiting mitochondrial complex I and II.

Donghyun Kim1, Yusun Shin2, Jong-In Park2

  • 1College of Pharmacy, Institute of Pharmaceutical Science and Technology, Hanyang University, Ansan, 15588, South Korea; College of Pharmacy, Keimyung University, Daegu, 42601, South Korea.

Free Radical Biology & Medicine
|December 25, 2025
PubMed
Summary

5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one (CMIT/MIT) biocide causes lung injury by disrupting mitochondrial function. CMIT/MIT inhibits mitochondrial complexes I and II, leading to oxidative stress and cellular senescence.

Keywords:
CMIT/MITElectron transport systemMitochondriaReactive oxygen species

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Area of Science:

  • Toxicology
  • Mitochondrial Biology
  • Biochemistry

Background:

  • 5-chloro-2-methyl-4-isothiazolin-3-one and 2-methyl-4-isothiazolin-3-one (CMIT/MIT) is a biocide used in consumer products and humidifier disinfectants.
  • CMIT/MIT toxicity, particularly on the respiratory system, is a concern.
  • Oxidative stress is implicated in CMIT/MIT toxicity, but molecular targets remain unclear.

Purpose of the Study:

  • Investigate CMIT/MIT's effect on mitochondrial redox regulation.
  • Identify molecular targets responsible for CMIT/MIT-induced reactive oxygen species (ROS) generation.

Main Methods:

  • In vitro experiments using H441 cells.
  • Assessed mitochondrial Complexes I and II activity.
  • Analyzed CMIT/MIT binding affinity to succinate dehydrogenase complex subunit B (SDHB).
  • Evaluated ROS production and mitochondrial uncoupling effects.

Main Results:

  • CMIT/MIT inhibited mitochondrial Complexes I and II, causing bioenergetic perturbation.
  • CMIT/MIT exhibited high binding affinity for SDHB.
  • Inhibition of succinate dehydrogenase (SDHA) amplified CMIT/MIT-induced ROS production.
  • CMIT/MIT induced mitochondrial dysfunction, altered mitochondrial dynamics, and promoted cellular senescence.

Conclusions:

  • Mitochondrial Complexes I and II are molecular initiating events in CMIT/MIT cytotoxicity.
  • CMIT/MIT-induced mitochondrial dysfunction contributes to lung injury.