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Related Concept Videos

Phosphorylation01:02

Phosphorylation

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The addition or removal of phosphate groups from proteins is the most common chemical modification that regulates cellular processes. These modifications can affect the structure, activity, stability, and localization of proteins within cells as well as their interactions with other proteins.
During phosphorylation, protein kinases transfer the terminal phosphate group of ATP to specific amino acid side chains of substrate proteins. Serine, threonine, and tyrosine are the most commonly...
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Renal dysfunction significantly impairs the renal clearance of drugs, leading to potential complications in drug therapy. Renal failure, which can be caused by various factors, poses a significant challenge in the elimination of drugs from the body.
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Oxidation of Alcohols02:37

Oxidation of Alcohols

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In this lesson, the oxidation of alcohols is discussed in depth. The various reagents used for oxidation of primary and secondary alcohols are detailed, and their mechanism of action is provided.
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Platelet-based Detection of Nitric Oxide in Blood by Measuring VASP Phosphorylation
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Oxidative Phosphorylation Impairment by DDT and DDE.

Sarah E Elmore1, Michele A La Merrill1

  • 1Department of Environmental Toxicology, University of California, Davis, Davis, CA, United States.

Frontiers in Endocrinology
|March 28, 2019
PubMed
Summary

The pesticide DDT and its metabolite DDE act as obesogens, disrupting metabolism by impairing mitochondrial function. This review examines how DDT and DDE damage the electron transport chain, potentially causing obesity and related diseases.

Keywords:
DDEDDTelectron transport chaininsulin resistancemitotoxicityobesitypesticides

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Area of Science:

  • Environmental toxicology
  • Mitochondrial biology
  • Metabolic disease research

Background:

  • DDT and DDE are recognized as obesogens and metabolic disruptors.
  • Mitochondrial dysfunction is linked to metabolic diseases like insulin resistance and obesity.
  • Previous mitotoxicity studies on DDT/DDE predate current understanding of these diseases.

Purpose of the Study:

  • To review the effects of DDT and DDE on mammalian mitochondrial oxidative phosphorylation.
  • To explore mechanistic links between DDT/DDE-induced mitochondrial toxicity and obesity, diabetes, and associated diseases.
  • To re-evaluate the mitotoxicity of DDT and DDE in the context of modern metabolic and neurodegenerative diseases.

Main Methods:

  • Literature review focusing on studies of DDT/DDE effects on mammalian mitochondrial oxidative phosphorylation.
  • Analysis of research investigating mitochondrial defects (e.g., electron transport chain, oxidative phosphorylation) in relation to DDT/DDE exposure.
  • Synthesis of findings on how DDT/DDE impact cellular respiration and energy metabolism.

Main Results:

  • Evidence indicates that both DDT and DDE impair mitochondrial electron transport chain (ETC) function.
  • Studies show that DDT and DDE disrupt oxidative phosphorylation processes.
  • The data suggest specific targeting of mitochondrial complexes and functions by DDT and DDE.

Conclusions:

  • DDT and DDE demonstrably impair mitochondrial oxidative phosphorylation.
  • Mitochondrial insults caused by DDT and DDE may contribute to their role in obesity and diabetes.
  • Further research is warranted to confirm DDT/DDE as causal agents in mitochondria-associated diseases like cancer and Alzheimer's.