Design of a Practical Fluorescent Probe for Superoxide Based on Protection–Deprotection Chemistry of Fluoresceins with Benzenesulfonyl Protecting Groups

Maeda, Hatsuo; Yamamoto, Keijiro; Kohno, Iho; Hafsi, Leila; Itoh, Norio; Nakagawa, Shinsaku; Kanagawa, Naoko; Suzuki, Keiichiro; Uno, Tadayuki

doi:10.1002/chem.200600522

Cited by 81 publications

(61 citation statements)

References 48 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Other commonly used fluorescent dyes are based on rhodamine, ethidine and the phenoxazine backbones, well known examples include Amplex Red and Amplex Ultra Red which are based on phenoxazine (resourfin). Commonly used chemiluminescent based indicators include lucigenin as a specific detector for O 2¯• while luminol has mostly been used as an indicator for general ROS production.Based on redox active substituents in the benzene ring and using the nucleophilic character of some reactive species, the development of a new generation of dyes with potentially improved characteristics has been described [31][32][33][34][35][36][37][38][39][40].Because of the quite complex chemistry of all of these dyes, great care has to be taken in designing biological experiments and in their interpretation. For example, there is evidence that DCF may produce secondary radicals induced by its own oxidation [41].…”

Section: Dyesmentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

View full text Add to dashboard Cite

a b s t r a c tReactive oxygen species (ROS) are increasingly recognized as second messengers in many cellular processes. While high concentrations of oxidants damage proteins, lipids and DNA, ultimately resulting in cell death, selective and reversible oxidation of key residues in proteins is a physiological mechanism that can transiently alter their activity and function. Defects in ROS producing enzymes cause disturbed immune response and disease.Changes in the intracellular free Ca 2+ concentration are key triggers for diverse cellular functions. Ca 2+ homeostasis thus needs to be precisely tuned by channels, pumps, transporters and cellular buffering systems. Alterations of these key regulatory proteins by reversible or irreversible oxidation alter the physiological outcome following cell stimulation. It is therefore necessary to understand which proteins are regulated and if this regulation is relevant in a physiological-and/or pathophysiological context. Because ROS are inherently difficult to identify and to measure, we first review basic oxygen redox chemistry and methods of ROS detection with special emphasis on electron paramagnetic resonance (EPR) spectroscopy. We then focus on the present knowledge of redox regulation of Ca 2+ permeable ion channels such as voltage-gated (CaV) Ca 2+ channels, transient receptor potential (TRP) channels and Orai channels.© 2011 Elsevier Ltd. All rights reserved. Basic redox chemistry of oxygenMany chemical processes are linked to the exchange of electrons between two or more molecular entities. The transfer of one (or more) electron(s) is associated with oxidation (loss of electron) and reduction (gain of electron) of the components. Such reactions are also known as redox reactions. The processes of reactive oxygen species (ROS) formation and elimination are exclusively of redox nature.Molecular oxygen is the precursor of all ROS. It contains two unpaired electrons in separate (antibonding) orbitals in its outer electron sphere and is thus, by definition, a radical. Radicals have at least one unpaired electron in their orbital system and usually show high reactivity; transition metal ions also may have unpaired electrons, but are not called radicals. Although having radical character, molecular oxygen is chemically rather inert (luckily!), because high * Corresponding authors at: Institut für Biophysik, Gebäude 58, Universität des Saarlandes, D-66421 Homburg/Saar, Germany. Tel.: +49 6841 1626453; fax: +49 6841 1626060.E-mail addresses: ivan.bogeski@uks.eu (I. Bogeski), barbara.niemeyer@uks.eu (B.A. Niemeyer).

show abstract

Section: Dyesmentioning

confidence: 99%

Redox regulation of calcium ion channels: Chemical and physiological aspects

et al. 2011

View full text Add to dashboard Cite

show abstract

“…Cell Death-Involvement of ROS in the ␣-ESA-mediated apoptotic cell death was next investigated using fluorescent probes, CM-5-(and-6)-chloromethyl-2Ј,7Ј-dichlorodihydrofluorescein diacetate for total ROS and BESSo-AM (35,36) and MitoSOX Red for superoxide anion radicals. Intracellular ROS was observed in the ␣-ESA-treated cells.…”

Section: Involvement Of Superoxide Anion Radicals and Mitochondrial Mmentioning

confidence: 99%

Poly(ADP-ribose) Polymerase (PARP)-1-independent Apoptosis-inducing Factor (AIF) Release and Cell Death Are Induced by Eleostearic Acid and Blocked by α-Tocopherol and MEK Inhibition

Kondo

Obitsu

Ohta

et al. 2010

Journal of Biological Chemistry

View full text Add to dashboard Cite

Poly(ADP-ribose)polymerase-1 (PARP-1) is thought to be required for apoptosis-inducing factor (AIF) release from mitochondria in caspase-independent apoptosis. The mechanism by which AIF is released through PARP-1 remains unclear. Here, we provide evidence that PARP-1-independent AIF release and cell death are induced by a trienoic fatty acid, ␣-eleostearic acid (␣-ESA). ␣-ESA induced the caspase-independent and AIF-initiated apoptotic death of neuronal cell lines, independently of PARP-1 activation. The cell death was inhibited by the MEK inhibitor U0126 and by knockdown of MEK using small interfering RNA. However, inhibitors for JNK, p38 inhibitors, calpain, phospholipase A 2 , and phosphatidylinositol 3-kinase, did not block cell death. AIF was translocated to the nucleus after the induction of apoptosis by ␣-ESA in differentiated PC12 cells without activating caspase-3 and PARP-1. The ␣-ESA-mediated cell death was not inhibited by PARP inhibitor 3,4-dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinoline and by knockdown of PARP-1 using small interfering RNA. Unlike N-methyl-N-nitro-N-nitrosoguanidine treatment, histonephosphorylated histone 2AX was not phosphorylated by ␣-ESA, which suggests no DNA damage. Overexpression of Bcl-2 did not inhibit the cell death. ␣-ESA caused a small quantity of superoxide production in the mitochondria, resulting in the reduction of mitochondrial membrane potential, both of which were blocked by a trace amount of ␣-tocopherol localized in the mitochondria. Our results demonstrate that ␣-ESA induces PARP-1-independent AIF release and cell death without activating Bax, cytochrome c, and caspase-3. MEK is also a key molecule, although the link between ERK, AIF release, and cell death remains unknown. Finding molecules that regulate AIF release may be an important therapeutic target for the treatment of neuronal injury.Apoptosis is a mode of programmed cell death that is used by multicellular organisms to remove surplus and unwanted cells in the immune and nervous systems (1-5). Apoptosis is characterized by cell detachment, cell shrinkage, chromatin condensation, DNA degradation, and plasma membrane blebbing (5-7). The surplus cells are removed by caspases, which are key effector molecules of apoptotic cell death. Apoptosis is activated through two main pathways as follows: the extrinsic pathway, which originates from the activation of cell-surface death receptors, such as Fas and tumor necrosis factor-receptor 1, and results in the activation of caspase-8; and the intrinsic pathway, which originates from the mitochondrial release of cytochrome c and results in the activation of caspase-9 through the Cyt-c 2 /apoptotic protease-activating factor-1/procaspase-9 heptamer (5, 8, 9). Most apoptotic stimuli use a mitochondriondependent process such as membrane potential shutdown and outer membrane permeabilization controlled by Bax and Bak, which are pro-apoptotic members of the Bcl-2 family (6 -9). This results in the release of the pro-apoptotic protein Cyt-c, which triggers caspa...

show abstract

“…14) A superoxide anion (O 2 Ϫ )-specific probe (4,5-dimethoxy-2-nitrobenzenesulfonyl tetrafluorofluorescein (BES-So)) was purchased from Wako Pure Chemicals. 15) Since it was supplied as an acetoxymethyl ester of BES-So (inactive) to improve cell permeability, this part was removed by esterase (1 U/ml) before use. KO 2 was dissolved in a mixture of anhydrous DMSO and DMF (2 : 1) containing 8% 18-crown-6-ether, and this was used as a positive control for O 2 Ϫ .…”

Section: )mentioning

confidence: 99%

“…The reaction mixture was incubated in a quartz cell (1 cmϫ1 cm) with gentle stirring (excitation/emissionϭ490/515 nm for APF and HPF, 504/ 525 nm for SOSGR, 505/544 nm for BES-So). 10,12,15) ) has been described in detail elsewhere. 19) (2) Lacunary-Substituted P/SiW 11 : Structurally, monovacant Keggin (undeca)heteropolytungstates such as P/SiW 11 have a "pit" in their molecules (known as a "lacunary hole"), which allows them to retain another molecule (especially a metal ion (X nϩ )) in the lacunary hole, like porphyllins can, forming a new compound known as a "lacunary-substituted" heteropolytungstate ([P/SiW 11 O 39 X] (7/8Ϫn)Ϫ , P/SiW 11 X).…”

Section: ؊mentioning

confidence: 99%