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Activating PPARβ/δ-Mediated Fatty Acid β-Oxidation Mitigates Mitochondrial Dysfunction Co-induced by Environmentally Relevant Levels of Molybdenum and Cadmium in Duck Kidneys

  • 0Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, Jiangxi, China.
Biological Trace Element Research +

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November 15, 2024

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November 15, 2024

View abstract on PubMed

Summary

This summary is machine-generated.

Cadmium and molybdenum exposure damages duck kidneys by disrupting fatty acid metabolism and mitochondrial function. Activating peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) can mitigate this damage.

Area Of Science

  • Environmental Toxicology
  • Biochemistry
  • Cell Biology

Background

  • Cadmium (Cd) and molybdenum (Mo) are environmental contaminants with known adverse health effects.
  • Prior research links Mo and Cd exposure to kidney damage in ducks, but the role of fatty acid metabolism remains under-explored.

Purpose Of The Study

  • To investigate the impact of Cd and Mo exposure on fatty acid metabolism and mitochondrial function in duck kidneys.
  • To elucidate the role of peroxisome proliferator-activated receptor beta/delta (PPARβ/δ) in Cd- and Mo-induced kidney damage.

Main Methods

  • In vivo study: Ducks were fed diets containing Cd, Mo, or both.
  • In vitro study: Duck renal tubular epithelial cells were exposed to Cd, Mo, and a PPARβ/δ agonist (GW0742).
  • Analysis of mitochondrial fatty acid β-oxidation, mitochondrial dynamics, and PPARβ/δ protein levels.

Main Results

  • Cd and/or Mo exposure inhibited mitochondrial fatty acid β-oxidation and disrupted mitochondrial dynamics in duck kidneys.
  • PPARβ/δ protein levels were significantly suppressed by Cd and/or Mo exposure.
  • In vitro results confirmed fatty acid oxidation deficiency and mitochondrial dysfunction induced by Cd and Mo, with PPARβ/δ involvement.

Conclusions

  • Cd and Mo co-induce kidney damage through impaired fatty acid β-oxidation and mitochondrial dysfunction.
  • PPARβ/δ plays a crucial role in mitigating Cd- and Mo-induced mitochondrial dysfunction.
  • Activating PPARβ/δ-mediated fatty acid β-oxidation offers a potential therapeutic strategy against heavy metal-induced kidney injury.

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