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Molybdenum and Cadmium Co-induce Mitochondrial Quality Control Disorder via FUNDC1-Mediated Mitophagy in Sheep Kidney

Yunhui Wu1, Fan Yang1, Guangbin Zhou2

  • 1Jiangxi Provincial Key Laboratory for Animal Health, Institute of Animal Population Health, College of Animal Science and Technology, Jiangxi Agricultural University, Nanchang, China.

Frontiers in Veterinary Science
|February 14, 2022
PubMed

Insights

Molybdenum (Mo) and cadmium (Cd) disrupt mitochondrial quality control in sheep kidneys by impairing FUNDC1-mediated mitophagy. This study reveals how these elements induce kidney damage and alter cellular processes.

Area of Science:

  • Toxicology
  • Animal Science
  • Cellular Biology

Background:

  • Molybdenum (Mo) is an essential trace mineral, but excessive amounts can harm animal health.
  • Cadmium (Cd) is an environmental toxicant with known adverse health effects.
  • The specific mechanisms by which Mo and Cd impact mitochondrial quality control remain unclear.

Purpose of the Study:

  • To investigate the effects of Mo and Cd exposure on mitochondrial quality control in sheep kidneys.
  • To explore the role of mitophagy, specifically FUNDC1-mediated mitophagy, in response to Mo and Cd.
  • To elucidate the molecular mechanisms underlying Mo and Cd-induced kidney damage.

Main Methods:

  • Forty-eight sheep were divided into four groups: control, Mo-only, Cd-only, and combined Mo+Cd exposure for 50 days.
  • Kidney tissues were analyzed for trace mineral balance, cellular damage, mitophagy markers (mitophagosomes, LC3 puncta), oxidative stress (MDA, H2O2), ATP levels, and gene/protein expression.
  • Key genes and proteins involved in mitochondrial dynamics and mitophagy (e.g., FUNDC1, LC3, DRP1, MFN1/2, OPA1) were quantified.

Main Results:

  • Mo and/or Cd exposure led to imbalances in trace minerals and vacuolar/granular degeneration in renal tubular epithelial cells.
  • Increased markers of mitophagy (mitophagosomes, LC3 puncta) and oxidative stress (MDA, H2O2), along with decreased ATP content, were observed.
  • Mo and Cd upregulated mitophagy-related genes/proteins (e.g., FUNDC1, LC3, DRP1) and downregulated mitochondrial fusion/biogenesis markers (e.g., MFN1/2, OPA1, PGC-1α).
  • Combined Mo and Cd exposure resulted in more pronounced effects than individual exposures.

Conclusions:

  • Mo and Cd exposure induces mitochondrial quality control disorder in sheep kidneys.
  • The findings suggest that FUNDC1-mediated mitophagy is a key pathway affected by Mo and Cd.
  • Co-exposure to Mo and Cd exacerbates kidney damage through impaired mitochondrial quality control.
Keywords:
cadmiumkidneymitochondrial quality controlmitophagymolybdenumsheep

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