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Organochalcogens inhibit mitochondrial complexes I and II in rat brain: possible implications for neurotoxicity

Robson Luiz Puntel1, Daniel Henrique Roos, Rodrigo Lopes Seeger

  • 1Universidade Federal do Pampa, Campus Uruguaiana BR-472 Km 7, Uruguaiana, RS 97500-970, Brazil. robson_puntel@yahoo.com.br

Neurotoxicity Research
|December 11, 2012
PubMed

Insights

Organochalcogens, like organoselenium and organotellurium, inhibit rat brain mitochondrial complexes I and II. This neurotoxicity is linked to thiol oxidation, impacting neurological disorder research.

Area of Science:

  • Biochemistry
  • Neuroscience
  • Toxicology

Background:

  • Organochalcogens (organoselenium, organotellurium) exhibit neurotoxicity in rodents.
  • Mitochondrial dysfunction is a key factor in neurological disorders.

Purpose of the Study:

  • To investigate if rat brain mitochondrial complexes are molecular targets of organochalcogens.
  • To elucidate the mechanism of organochalcogen-induced neurotoxicity.

Main Methods:

  • Assessing the impact of organochalcogens on rat brain mitochondrial complexes I, II, and IV.
  • Investigating the role of NADH and reduced glutathione (GSH) in modulating these effects.

Main Results:

  • Organochalcogens significantly inhibited mitochondrial complex I activity, an effect reversed by NADH and blunted by GSH.
  • Complex II inhibition was observed with Ebs and (PhTe)₂, also blunted by GSH.
  • Mitochondrial complex IV activity remained unaffected by organochalcogens.
  • Organochalcogens were more potent inhibitors of complex I than complex II.

Conclusions:

  • Organochalcogens target mitochondrial complexes I and II, suggesting a mechanism involving thiol oxidation.
  • These findings provide insights into the neurotoxic mechanisms of organochalcogens and their potential role in neurological disorders.

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