AI Article Synopsis
- A study demonstrates a new interaction between deoxyhemoglobin, nitrite, and RRx-001 that boosts nitric oxide (NO) production in blood.
- RRx-001 significantly speeds up the nitrite reduction process by deoxyhemoglobin, enhancing NO generation compared to nitrite reduction alone.
- The findings suggest that RRx-001 could help release NO specifically in low-oxygen tumor areas, potentially contributing to its tumor-killing effects by inhibiting mitochondrial respiration.
Article Abstract
This study reveals a novel interaction between deoxyhemoglobin, nitrite and the non-toxic compound, RRx-001, to generate supraphysiologic levels of nitric oxide (NO) in blood. We characterize the nitrite reductase activity of deoxyhemoglobin, which in the presence of bound RRx-001 reduces nitrite at a much faster rate, leading to markedly increased NO generation. These data expand on the paradigm that hemoglobin generates NO via nitrite reduction during hypoxia and ischemia when nitric oxide synthase (NOS) function is limited. Here, we demonstrate that RRx-001 greatly enhances NO generation from nitrite reduction. RRx-001 is thus the first example of a functional superagonist for nitrite reductase. We hypothesize that physiologically this reaction releases the potentially cytotoxic effector NO selectively in hypoxic tumor regions. It may be that a binary NO-H2O2 trigger is indirectly responsible for the observed tumoricidal activity of RRx-001 since NO is known to inhibit mitochondrial respiration.
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| http://dx.doi.org/10.1007/s12032-016-0798-9 | DOI Listing |
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