Paradoxical Effect of Diphenyleneiodonium in Inducing DNA Damage and Apoptosis

UNCG Author/Contributor (non-UNCG co-authors, if there are any, appear on document)
George Loo, Professor (Creator)
The University of North Carolina at Greensboro (UNCG )
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Abstract: Diphenyleneiodonium (DPI) is often used as a molecular tool in unravelling redox-sensitive cellular events involving NADPH oxidase. However, to better understand unexpected actions of DPI, it was ascertained if DPI affects cellular DNA. DPI induced single-strand breaks in DNA of HCT-116 cells, although this only slightly increased GADD153 expression. Nevertheless, after sustaining DNA damage, the DPI-treated cells subsequently had features characteristic of apoptosis, such as translocated membrane phospholipid and nuclei containing condensed chromatin. Paradoxically, DPI attenuated the DNA damage and overall ROS production caused by sodium deoxycholate (DOC), although DPI did not inhibit DOCinduced generation of mitochondrial O2–. Furthermore, DPI prevented the occurrence of apoptosis caused by DOC. However, other known chemical inhibitors of NADPH oxidase did not produce the same results as DPI in negating the effects of DOC. Collectively, these disparate findings suggest that DPI can act not in accord with conventional wisdom depending on the experimental conditions.

Additional Information

Free Radical Research 42, 533-543.
Language: English
Date: 2008
Apoptosis, Deoxycholate, Diphenyleneiodonium, DNA damage, NADPH oxidase

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