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CoQ10 Deficiency May Indicate Mitochondrial Dysfunction in Cr(VI) Toxicity.

Xiali Zhong1,2, Xing Yi3, Rita de Cássia da Silveira E Sá4

  • 1Department of Health Toxicology, School of Public Health, Central South University, Changsha 410008, China. xializhong87@sina.com.

International Journal of Molecular Sciences
|April 27, 2017
PubMed
Summary

Hexavalent chromium (Cr(VI)) exposure damages mitochondria by causing Coenzyme 10 (CoQ10) deficiency. Supplementing with CoQ10 may protect liver cells from Cr(VI) toxicity.

Keywords:
L-02 hepatocytesapoptosiscoenzyme Q10hexavalent chromium Cr(VI)mitochondrial membrane potential (MMP)reactive oxygen species (ROS)

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Area of Science:

  • Toxicology
  • Cell Biology
  • Biochemistry

Background:

  • Hexavalent chromium (Cr(VI)) is a toxic environmental pollutant.
  • Cr(VI) exposure can lead to significant cellular damage and organ toxicity, particularly in the liver.
  • Understanding the precise mechanisms of Cr(VI) toxicity is crucial for developing effective treatments.

Purpose of the Study:

  • To elucidate the toxic mechanism of Cr(VI) focusing on mitochondrial dysfunction.
  • To investigate the potential of Coenzyme 10 (CoQ10) as an antidote for Cr(VI)-induced cytotoxicity.
  • To identify potential biomarkers for Cr(VI) poisoning.

Main Methods:

  • Investigated Cr(VI) effects on gene expression, specifically electron transfer flavoprotein dehydrogenase (ETFDH).
  • Assessed changes in Coenzyme 10 (CoQ10) levels, mitochondrial biogenesis, and markers of oxidative stress (ROS, MDA, SOD).
  • Evaluated indicators of apoptosis, including caspase activation, ATP production, mitochondrial membrane potential, and protein expression (Bcl-2, Bax).
  • Examined the protective effects of CoQ10 pretreatment in L-02 hepatocytes exposed to Cr(VI).

Main Results:

  • Cr(VI) exposure significantly downregulated ETFDH gene expression and reduced CoQ10 levels and mitochondrial biogenesis.
  • Cr(VI) induced mitochondrial damage, characterized by increased ROS and MDA, decreased SOD and ATP, and mitochondrial membrane depolarization.
  • Cr(VI) triggered apoptosis via caspase activation, Ca2+ influx, Cyt c release, and altered Bcl-2/Bax expression.
  • CoQ10 pretreatment attenuated Cr(VI)-induced mitochondrial damage and apoptosis in L-02 hepatocytes.

Conclusions:

  • Cr(VI) induces hepatotoxicity primarily through mitochondrial dysfunction and CoQ10 deficiency.
  • Reduced CoQ10 levels in hepatocytes serve as a potential biomarker for Cr(VI) poisoning.
  • Exogenous CoQ10 administration shows promise in restoring mitochondrial function and protecting the liver against Cr(VI) exposure.