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In mouse adipocyte 3T3-L1 cells, it was shown that an ≈25–50% decrease of mitochondrial CoQ 9 , due to treatment with 4-NB or knockdown of the CoQ biosynthetic gene Coq7 or Coq9 , led to increased mitochondrial peroxiredoxin (PRDX) dimerization, which was used as an indicator of H 2 O 2 burden, as well as increased concentration of mito-2-hydroxyethidium, an O 2 •– -specific oxidation product of MitoSOX (338)
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