Characterization of a Cell-Lethal Product from the Photooxidation of Tryptophan: Hydrogen Peroxide

McCormick, John; Fischer, Monika; PACHLATKO, J. P.; Eisenstark, A.

doi:10.1126/science.1108203

Cited by 182 publications

(31 citation statements)

References 10 publications

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“…Since light can generate hydrogen peroxide (H 2 O 2 ) in solution (Richardson, 1893; Bedford, 1927; Blum, 1932), especially in the presence of biological photosensitizers such as riboflavin, tryptophan and tyrosine (McCormick et al, 1976; Wang and Nixon, 1978), and since LITE-1 and GUR-3 are members of a gustatory receptor family, we hypothesized that C. elegans might be responding to the hydrogen peroxide generated by bright light. Using a hydrogen peroxide-sensitive electrode, we observed that light could generate hydrogen peroxide in solution that included riboflavin (Figure 5A).…”

Section: Resultsmentioning

confidence: 99%

Light and Hydrogen Peroxide Inhibit C. elegans Feeding through Gustatory Receptor Orthologs and Pharyngeal Neurons

Bhatla

Horvitz

2015

Neuron

133

245

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SUMMARY While gustatory sensing of the five primary flavors (sweet, salty, sour, bitter, and savory) has been extensively studied, pathways that detect non-canonical taste stimuli remain relatively unexplored. In particular, while reactive oxygen species cause generalized damage to biological systems, no gustatory mechanism to prevent ingestion of such material has been identified in any organism. We observed that light inhibits C. elegans feeding and used light as a tool to uncover molecular and neural mechanisms for gustation. Light can generate hydrogen peroxide, and we discovered that hydrogen peroxide similarly inhibits feeding. The gustatory receptor family members LITE-1 and GUR-3 are required for the inhibition of feeding by light and hydrogen peroxide. The I2 pharyngeal neurons increase calcium in response to light and hydrogen peroxide, and these responses require GUR-3 and a conserved antioxidant enzyme peroxiredoxin PRDX-2. Our results demonstrate a gustatory mechanism that mediates the detection and blocks ingestion of a non-canonical taste stimulus, hydrogen peroxide.

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Section: Resultsmentioning

confidence: 99%

Light and Hydrogen Peroxide Inhibit C. elegans Feeding through Gustatory Receptor Orthologs and Pharyngeal Neurons

Bhatla

Horvitz

2015

Neuron

133

245

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“…H 2 O 2 was chosen due to its capability to react with DCFH and to penetrate easily into bacteria cells35. Furthermore, H 2 O 2 is commonly accepted as one of the ROS that are generated inside bacteria under light stress36. Reaction between 10 μM DCFH and H 2 O 2 at different concentrations (0.01 to 1 mM) was done in the absence of bacteria in dark.…”

Section: Resultsmentioning

confidence: 99%

Intracellular mechanisms of solar water disinfection

Castro-Alférez

Polo-López

Fernández‐Ibáñez³

2016

Sci Rep

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Solar water disinfection (SODIS) is a zero-cost intervention measure to disinfect drinking water in areas of poor access to improved water sources, used by more than 6 million people in the world. The bactericidal action of solar radiation in water has been widely proven, nevertheless the causes for this remain still unclear. Scientific literature points out that generation of reactive oxygen species (ROS) inside microorganisms promoted by solar light absorption is the main reason. For the first time, this work reports on the experimental measurement of accumulated intracellular ROS in E. coli during solar irradiation. For this experimental achievement, a modified protocol based on the fluorescent probe dichlorodihydrofluorescein diacetate (DCFH-DA), widely used for oxidative stress in eukaryotic cells, has been tested and validated for E. coli. Our results demonstrate that ROS and their accumulated oxidative damages at intracellular level are key in solar water disinfection.

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“…Irradiation by UV light generates ROS, including H 2 O 2 and superoxide ions [16, 63], which in turn induces various cellular responses in eukaryotes, including damage to DNA and proteins [64, 65], triggering of signal transduction pathways [66–68], and activation of gene expression [66, 68–71]. UV-B triggers the apoptotic pathway during irradiation, although the actual apoptotic process occurs later [10].…”

Section: Discussionmentioning

confidence: 99%

The role of Prdx6 in the protection of cells of the crystalline lens from oxidative stress induced by UV exposure

Shibata

et al. 2016

Jpn J Ophthalmol

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Purpose The immediate aim of this study was to investigate alterations in peroxiredoxin (Prdx) 6 at posttranslational levels, and the levels of protein oxidation, lipid peroxidation, and reactive oxygen species (ROS) in lens epithelial cells (LECs) after exposure to severe oxidative stress, such as ultraviolet-B (UV-B). Our ultimate aim was to provide new information on antioxidant defenses in the lens and their regulation, thereby broadening existing knowledge of the role of Prdx6 in lens physiology and pathophysiology. Methods The expression of the hyperoxidized form of Prdx6 and oxidation of protein were analyzed by western blotting and the OxyBlot assay in human LECs (hLECs). ROS levels were quantified using DCFH-DA dye, and cell viability was quantified by the MTS and TUNEL assays. To evaluate the protective effect of Prdx6, we cultured lenses with or without the TAT transduction domain (TAT-HA-Prdx6) and observed (and photographed) the cultures at specified time-points after the exposure to UV-B for the development of opacity. Results Prdx6 in hLECs was hyperoxidized after exposure to high amounts of UV-B. UV-B treatment of hLECs increased the levels of cell death, protein oxidation, and ROS. hLECs exposed to UV-B showed higher levels of ROS, which could be reduced by the application of extrinsic TAT-HA-Prdx6, attenuating UV-B-induced lens opacity and apoptotic cell death. Conclusion Excessive oxidative stress induces the hyperoxidation of Prdx6 and may reduce the ability of Prdx6 to protect LECs against ROS or stresses. Because extrinsic Prdx6 could attenuate UV-B-induced abuse, this molecule may have a potential in preventing cataractogenesis.

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Characterization of a Cell-Lethal Product from the Photooxidation of Tryptophan: Hydrogen Peroxide

Cited by 182 publications

References 10 publications

Light and Hydrogen Peroxide Inhibit C. elegans Feeding through Gustatory Receptor Orthologs and Pharyngeal Neurons

Light and Hydrogen Peroxide Inhibit C. elegans Feeding through Gustatory Receptor Orthologs and Pharyngeal Neurons

Intracellular mechanisms of solar water disinfection

The role of Prdx6 in the protection of cells of the crystalline lens from oxidative stress induced by UV exposure

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