2018
DOI: 10.1016/j.freeradbiomed.2018.05.064
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H2O2 metabolism in liver and heart mitochondria: Low emitting-high scavenging and high emitting-low scavenging systems

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Cited by 28 publications
(12 citation statements)
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“…Catalase was measured using Purpald (4-amino-3-hydrazino-5-mercapto-1,2,4-triazole) based on [35] as we recently described for fish mitochondria [36]. Briefly catalase reacts with methanol in the presence of hydrogen peroxide to produce formaldehyde which upon binding to Purpald changes from colorless to purple.…”
Section: Methodsmentioning
confidence: 99%
See 1 more Smart Citation
“…Catalase was measured using Purpald (4-amino-3-hydrazino-5-mercapto-1,2,4-triazole) based on [35] as we recently described for fish mitochondria [36]. Briefly catalase reacts with methanol in the presence of hydrogen peroxide to produce formaldehyde which upon binding to Purpald changes from colorless to purple.…”
Section: Methodsmentioning
confidence: 99%
“…For SOD, superoxide anion radical (O 2 •– ) generated by a xanthine oxidase-hypoxanthine system was detected using water-soluble tetrazolium, WST-1 (sodium salt of 4-[3-(4iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate) according to [37] as recently described for fish mitochondria [36]. Here, WST-1 produces a water soluble dye upon reduction of the O 2 •– and the rate of reduction of WST-1 is linear to xanthine oxidase activity and is inhibited by SOD.…”
Section: Methodsmentioning
confidence: 99%
“…In support of this, there is increasing evidence that mitochondria can also act as net sinks of ROS and this is linked to lifespan. For instance mitochondria from the long lived naked mole rat (NMR) produce less ROS than comparable shorter lived animals [ 139 , 140 ]. Furthermore the mitochondria in NMR, and bats, also appear to be able to maintain a depolarisation of the inner membrane for much longer during their life cycle, which is a key mechanism to reduce ROS production during ageing [ 141 ].…”
Section: The Immune System Hormesis and Mitochondriamentioning
confidence: 99%
“…Although mitochondria have long been recognized as one of the many cellular sites of H 2 O 2 formation [15] , [21] , [6] mitochondria also have a substantial capacity to eliminate H 2 O 2 . Indeed, mitochondria from several tissues, including brain, liver, heart and skeletal muscle appear to have far greater maximal capacity to consume H 2 O 2 than to produce it; however, in all tissues other than liver the rate of H 2 O 2 consumption requires respiratory substrate to be maximized [10] , [16] , [24] , [25] , [30] , [32] , [35] . The respiration-dependency of mitochondrial H 2 O 2 consumption comes largely from the GSH-peroxidase and thioredoxin-dependent peroxiredoxin pathways, both of which require a supply of electrons, via NADPH, to remain active [2] .…”
Section: Introductionmentioning
confidence: 99%
“…Although the maximal capacity to consume H 2 O 2 can be much higher in mitochondria than the production rates, the consumption of H 2 O 2 becomes limited as the concentration of H 2 O 2 declines [10] , [16] , [3] , [30] , [32] . Recently Starkov and colleagues [30] combined this concentration-dependent capacity for mitochondrial H 2 O 2 consumption into an elegantly simple model to describe H 2 O 2 metabolism in mouse brain mitochondria.…”
Section: Introductionmentioning
confidence: 99%