Superoxide reacts with hydroethidine but forms a fluorescent product that is distinctly different from ethidium: potential implications in intracellular fluorescence detection of superoxide.

By Hongtao Zhao, S. Kalivendi, Hao Zhang, J. Joseph, K. Nithipatikom, J. Vasquez-Vivar, B. Kalyanaraman. Free Radical Biology & Medicine, 2003

779 citations recorded by the source corpus.

Subfields: Biophysics, Electrical and Electronic Engineering, Physiology

View Paper: https://www.semanticscholar.org/paper/92848b71a8b50b0bf8330e14f9aebd1006ddd015

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Biophysics

1. Barry Halliwell
2. A. Gomes
3. Eduarda Fernandes
4. J. Lima

In Physiology

1. Barry Halliwell
2. K. Davies
3. M. Whiteman
4. B. Kalyanaraman
5. S. Biswas
6. P. Wardman

Citations in the corpus

• Oxidants, antioxidants and the ischemic brain (2004, background): “The brain has potent defenses against superoxide including dietary free-radical scavengers (ascorbate, α-tocopherol), the endogenous tripeptide glutathione, and enzymatic antioxidants.”
• Fluorescence probes used for detection of reactive oxygen species. (2005, background): “[29] have verified that in the presence of other ROS and RNS (ONOO , HO, H2O2) HE does not originate the same oxidation product observed with the O2 ! .”
• Measuring reactive oxygen and nitrogen species with fluorescent probes: challenges and limitations. (2012, background): “HE, or dihydroethidium, is another widely used probe for detecting intracellular O2[26].”
• Measuring reactive species and oxidative damage in vivo and in cell culture: how should you do it and what do the results mean? (2004, background): “Ethidium fluoresces strongly at around 600 nm when excited at 500–530 nm. Recent work, however, suggests that the product is not ethidium (Zhao et al., 2003).”
• Review of Methods to Determine Antioxidant Capacities (2009, neutral): “The oxidation mechanism still remains unclear (Benov et al. 1998; Zhao et al. 2003).”
• Electron transfer between cytochrome c and p66Shc generates reactive oxygen species that trigger mitochondrial apoptosis. (2005, neutral): “To characterize ROS production by p66Shc, we used H2DCFDA or hydroetidine (HE), two fluorescent probes that are oxidized by H2O2 or O2-·, respectively (LeBel et al., 1992; Zhao et al., 2003).”