An Adverse Outcome Pathway Linking Organohalogen Exposure to Mitochondrial Disease

We present an Adverse outcome pathways framework that depicts how exposure to organohalogens can lead to mitochondrial disease

Brooke McMinn; Alicia L. Duval; Christie M. Sayes

2019

Scholarcy highlights

  • In the early 1960s, researchers identified mitochondrial disease as a serious clinical condition and have since increased their efforts to identify its etiology
  • Based on well-established knowledge of mitochondrial function, the biological plausibility between increased reactive oxygen species production and mitochondrial disease is strong. This is often associated with mitochondrial electron transport chain disruption or complex I inhibition
  • An Adverse outcome pathways was created to best characterize the pathway-based analysis of organohalogen exposure that results in dysfunction of the mitochondrial electron transport chain in humans
  • For the purposes of this AOP, more emphasis was placed on the front-end of the AOP) than the back-end
  • Its role was previously described in simple terms, such as “mitochondria is the powerhouse of the cell”; new research is emerging that enables our understanding of mitochondria-to-disease pathways
  • With the motivation to reduce the number of animals in experimental designs and to create unprecedented value in the enormous amount of published studies on mitochondrial dysfunction, AOP development has the unique opportunity to serve as a framework for understanding mitochondrial disease
  • The strength of the biological plausibility of our Adverse outcome pathways is strong, the strength of empirical evidence ranges from weak to strong, with the least amount of evidence existing to support the adverse outcome

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