Difference between revisions of "Dinitrochlorobenzene"
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|abbr=DNCB | |abbr=DNCB | ||
|description='''Dinitrochlorobenzene (1-chloro-2,4-dinitrobenzene)''' (DNCB) is a | |description='''Dinitrochlorobenzene (1-chloro-2,4-dinitrobenzene)''' (DNCB) is a glutathione (GSH) inhibitor. | ||
}} | }} | ||
{{MitoPedia concepts}} | {{MitoPedia concepts}} | ||
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= H<sub>2</sub>O<sub>2</sub> production = | = H<sub>2</sub>O<sub>2</sub> production = | ||
[[Oxidative stress]] plays an important role in many pathological conditions, therefore mitochondrial ([[ROS]]) measurements are crucial for understanding a disease and for evaluating specific treatments. Evaluation of [[hydrogen peroxide]] (H<sub>2</sub>O<sub>2</sub>) emission flux by fluorescence can be used to detect H<sub>2</sub>O<sub>2</sub> production in biological samples. Mitochondrial H<sub>2</sub>O<sub>2</sub> emission flux is a balance between H<sub>2</sub>O<sub>2</sub> generation, [[superoxide]] (O2<sup>•-</sup>) dismutation and the H<sub>2</sub>O<sub>2</sub> scavenging. Mitochondrial antioxidant systems (which scavenge ROS) can be stimulated in specific physiopathological conditions masking the real ROS generation. | [[Oxidative stress]] plays an important role in many pathological conditions, therefore mitochondrial ([[ROS]]) measurements are crucial for understanding a disease and for evaluating specific treatments. Evaluation of [[hydrogen peroxide]] (H<sub>2</sub>O<sub>2</sub>) emission flux by fluorescence can be used to detect H<sub>2</sub>O<sub>2</sub> production in biological samples. Mitochondrial H<sub>2</sub>O<sub>2</sub> emission flux is a balance between H<sub>2</sub>O<sub>2</sub> generation, [[superoxide]] (O2<sup>•-</sup>) dismutation and the H<sub>2</sub>O<sub>2</sub> scavenging. Mitochondrial antioxidant systems (which scavenge ROS) can be stimulated in specific physiopathological conditions masking the real ROS generation. | ||
[[Dinitrochlorobenzene]] (DNCB), an inhibitor of GSH can be used to obtain the GSH contribution scavenging H<sub>2</sub>O<sub>2</sub>. Additionally, [[auranofin]] (AF), an inhibitor of | [[Dinitrochlorobenzene]] (DNCB), an inhibitor of GSH can be used to obtain the GSH contribution scavenging H<sub>2</sub>O<sub>2</sub>. Additionally, [[auranofin]] (AF), an inhibitor of thioredoxin reductase (TrxR) can be used to quantified the contribution of the thioredoxin system (Trx)[1]. | ||
== References == | == References == | ||
# Aon MA, Stanley AS, Sivakumaran V, Kembro JM, O´Rourke B, Paolocci N, Cortassa S (2012) Glutathione/thioredoxin sytems modulate mitochondrial H2O2 emission: An experimental-computational study. J Gen Physiol 139(6):479-91. | # Aon MA, Stanley AS, Sivakumaran V, Kembro JM, O´Rourke B, Paolocci N, Cortassa S (2012) Glutathione/thioredoxin sytems modulate mitochondrial H2O2 emission: An experimental-computational study. J Gen Physiol 139(6):479-91. | ||
Revision as of 16:49, 5 April 2017
- high-resolution terminology - matching measurements at high-resolution
Dinitrochlorobenzene
Description
Dinitrochlorobenzene (1-chloro-2,4-dinitrobenzene) (DNCB) is a glutathione (GSH) inhibitor.
Abbreviation: DNCB
MitoPedia topics: Inhibitor
H2O2 production
Oxidative stress plays an important role in many pathological conditions, therefore mitochondrial (ROS) measurements are crucial for understanding a disease and for evaluating specific treatments. Evaluation of hydrogen peroxide (H2O2) emission flux by fluorescence can be used to detect H2O2 production in biological samples. Mitochondrial H2O2 emission flux is a balance between H2O2 generation, superoxide (O2•-) dismutation and the H2O2 scavenging. Mitochondrial antioxidant systems (which scavenge ROS) can be stimulated in specific physiopathological conditions masking the real ROS generation. Dinitrochlorobenzene (DNCB), an inhibitor of GSH can be used to obtain the GSH contribution scavenging H2O2. Additionally, auranofin (AF), an inhibitor of thioredoxin reductase (TrxR) can be used to quantified the contribution of the thioredoxin system (Trx)[1].
References
- Aon MA, Stanley AS, Sivakumaran V, Kembro JM, O´Rourke B, Paolocci N, Cortassa S (2012) Glutathione/thioredoxin sytems modulate mitochondrial H2O2 emission: An experimental-computational study. J Gen Physiol 139(6):479-91.
