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Depleted uranium causes renal mitochondrial dysfunction through the ETHE1/Nrf2 pathway.

Suiyi Liu1, Shuang Wang1, Yazhen Zhao1

  • 1State Key Laboratory of Trauma, Burns and Combined Injury, Institute of Combined Injury, Chongqing Engineering Research Center for Nanomedicine, College of Preventive Medicine, Army Medical University, Chongqing, 400038, China.

Chemico-Biological Interactions
|January 21, 2023
PubMed
Summary

Depleted uranium (DU) causes kidney damage by inducing mitochondrial dysfunction and oxidative stress. Melatonin and ethylmalonic encephalopathy 1 (ETHE1) show protective effects, highlighting the ETHE1/Nrf2 pathway

Keywords:
Depleted uraniumEthylmalonic encephalopathy 1NF-E2-related factor 2Renal mitochondria dysfunction

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Area of Science:

  • Toxicology
  • Mitochondrial Biology
  • Renal Physiology

Background:

  • Depleted uranium (DU) exposure primarily targets the kidney, leading to nephrotoxicity through complex mechanisms.
  • Mitochondrial dysfunction is implicated in DU-induced kidney damage, but the precise pathways require further elucidation.
  • Understanding these mechanisms is crucial for developing effective countermeasures against DU toxicity.

Purpose of the Study:

  • To investigate the role of mitochondrial dysfunction in depleted uranium (DU) nephrotoxicity.
  • To explore the underlying molecular mechanisms, including the involvement of the ETHE1/Nrf2 pathway.
  • To assess the potential protective effects of melatonin against DU-induced kidney injury.

Main Methods:

  • Administration of varying doses of DU (2.5-10 mg/kg) to male rats.
  • Assessment of mitochondrial function, including ATP content and membrane potential.
  • Evaluation of oxidative stress markers and the expression of key proteins (ETHE1, Nrf2, HO-1, NQO1).
  • Inclusion of melatonin treatment (20 mg/kg) and ETHE1 knockdown/overexpression experiments.

Main Results:

  • DU exposure significantly impaired kidney mitochondrial function, decreased ATP levels, and reduced mitochondrial membrane potential.
  • Melatonin treatment attenuated DU-induced oxidative stress and mitochondrial dysfunction, mitigating kidney damage.
  • ETHE1 knockdown exacerbated DU-induced renal injury, oxidative stress, and mitochondrial dysfunction, while exogenous ETHE1 offered protection.
  • ETHE1 knockdown upregulated Nrf2 and its downstream targets; Nrf2 knockout worsened DU nephrotoxicity.

Conclusions:

  • Mitochondrial dysfunction is a critical mediator of depleted uranium (DU) nephrotoxicity.
  • The ETHE1/Nrf2 pathway plays a significant role in regulating antioxidant defense and mitigating DU-induced renal damage.
  • Targeting the ETHE1/Nrf2 pathway and enhancing antioxidant capacity may offer therapeutic strategies against DU nephrotoxicity.