Elsevier

Biochemical Pharmacology

Volume 34, Issue 9, 1 May 1985, Pages 1588-1590
Biochemical Pharmacology

Short communication
Properties of mitochondria treated with 1-chloro-2,4-dinitrobenzene

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    This indicates that the inhibition of the GSH-dependent pathway is best explained by GSH depletion. More aggressive treatment of liver mitochondria with CDNB (>35 µM), even with a wash to remove unreacted CDNB, has been shown to affect isocitrate oxidation [54]. Because the NADP+-specific IDH may conceivably contribute to the NADPH pool used by the reductases of the respiration-dependent peroxidation pathways, we validated here that the 35 µM CDNB pre-treatment protocol does not affect its activity (Table 3).

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    2010, Journal of Biological Chemistry
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    FCCP was used to titrate Ψm in order to compare H2O2 emission at different Ψm. Depletion of GSH, using CDNB (49, 50), enabled significant ROS generation with oxidation of an NADH-linked substrate. l-Carnitine addition to mitochondria oxidizing PCarn results in higher Ψm and O2 consumption (see below) and thus allowed comparison of H2O2 emission over a wider range of Ψm than could otherwise be achieved.

  • Fatty acids decrease mitochondrial generation of reactive oxygen species at the reverse electron transport but increase it at the forward transport

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    With this in mind, we examined whether depletion of glutathione could affect ROS generation by FFA. Glutathione was depleted by 1-chloro-2,4-dinitrobenzene (CDNB) [45]. It was found that such treatment of heart mitochondria strongly increased ROS generation and, when Phyt or AA was added, a further increase of ROS generation was found (Fig. 4, panel A).

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