Using Reserve Capacity to Screen for Mitochondrial Toxicities and Biogenesis (

In this webinar we will demonstrate:

  1. How metabolic responses reflect cellular health
  2. How metabolic responses can be used for drug screening
  3. How metabolic responses may discriminate different cell types

Most tissues use only a fraction of their mitochondrial ATP-generating capacity to support homeostatic function. Damage to the mitochondria due to disease, toxicants, or drug adverse effects compromises the reserve mitochondrial capacity leading to the potential for loss in organ function.

Agents that protect against loss in capacity, or that induce mitochondrial biogenesis are thought to have the potential for treating numerous pathologies. We adapted primary cultures of renal proximal tubular cells that exhibit in vivo levels of aerobic metabolism, are not glycolytic, and retain higher levels of differentiated functions and used the XF96 Analyzer to measure mitochondrial respiration in real time.

A number of chemical libraries were screened using decreases or increases in FCCP-uncoupled respiration rates as measures of mitochondrial toxicity or biogenesis, respectively. Clustering of hits based on chemical structures has been used to define novel biogenic pharmacophores and toxicophores.

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