We are analyzing https://link.springer.com/article/10.1007/s12272-010-1114-4.

Title:
NecroX as a novel class of mitochondrial reactive oxygen species and ONOO− scavenger | Archives of Pharmacal Research
Description:
Mitochondrial reactive oxygen species and reactive nitrogen species are proven to be major sources of oxidative stress in the cell; they play a prominent role in a wide range of human disorders resulting from nonapoptotic cell death. The aim of this study is to examine the cytoprotective effect of the NecroX series against harmful stresses, including pro-oxidant (tertiarybutylhydroperoxide), doxorubicin, CCl4, and hypoxic injury. In this study, these novel chemical molecules inhibited caspase-independent cell death with necrotic morphology, which is distinctly different from apoptosis, autophagy, and necroptosis. In addition, they displayed strong mitochondrial reactive oxygen species and ONOO− scavenging activity. Further, oral administration of these molecules in C57BL/6 mice attenuated streptozotocin-induced pancreatic islet β-cell destruction as well as CCl4-induced hepatotoxicity in vivo. Taken together, these results demonstrate that the NecroX series are involved in the blockade of nonapoptotic cell death against mitochondrial oxidative stresses. Thus, these chemical molecules are potential therapeutic agents in mitochondria-related human diseases involving necrotic tissue injury.
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article, google, scholar, pubmed, cas, cell, death, mitochondrial, oxidative, reactive, species, stress, biol, park, oxygen, kim, human, apoptosis, access, melatonin, necrosis, chem, disease, privacy, cookies, content, research, necrox, study, necrotic, physiol, liver, pharmacol, free, rev, smith, antioxidant, biochem, sci, function, publish, search, young, nitrogen, role, nonapoptotic, effect, oxide, res, radicals,

Topics {✒️}

month download article/chapter oxidative stress-induced cancer mitochondria-targeted antioxidant mitoq reactive nitrogen species nonapoptotic cell death noninsulin-dependent diabetes mellitus mitochondrial membrane permeabilization ccl4-induced hepatotoxicity nitrosative stress induced mitochondrial oxidative stress full article pdf including pro-oxidant bmc cell biol cell death pathways neuronal cell death mitochondrial permeability transition related subjects pharmacal research aims privacy choices/manage cookies reactive oxygen acute pancreatitis induced mitochondrial oxidative stresses mitochondria-targeted antioxidants cardiac mitochondrial dysfunction human disorders resulting potent electron donors tert-butylhydroperoxide-characterization u937 cells phase ii study structurally-related placebo-controlled study nitrogen species article kim article archives free radical damage european economic area dong ook seo jong heon won hyeon joo yim hyo-shin kwak chul woong chung potential therapeutic agents specific cellular target 3-amino-2-indolylmaleimide derivatives organelle-specific initiation precursor l-tryptophan endogenous indoles act stressful biological situations h9c2 myoblasts exposed impaired antioxidant status

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         description:Mitochondrial reactive oxygen species and reactive nitrogen species are proven to be major sources of oxidative stress in the cell; they play a prominent role in a wide range of human disorders resulting from nonapoptotic cell death. The aim of this study is to examine the cytoprotective effect of the NecroX series against harmful stresses, including pro-oxidant (tertiarybutylhydroperoxide), doxorubicin, CCl4, and hypoxic injury. In this study, these novel chemical molecules inhibited caspase-independent cell death with necrotic morphology, which is distinctly different from apoptosis, autophagy, and necroptosis. In addition, they displayed strong mitochondrial reactive oxygen species and ONOO− scavenging activity. Further, oral administration of these molecules in C57BL/6 mice attenuated streptozotocin-induced pancreatic islet β-cell destruction as well as CCl4-induced hepatotoxicity in vivo. Taken together, these results demonstrate that the NecroX series are involved in the blockade of nonapoptotic cell death against mitochondrial oxidative stresses. Thus, these chemical molecules are potential therapeutic agents in mitochondria-related human diseases involving necrotic tissue injury.
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      description:Mitochondrial reactive oxygen species and reactive nitrogen species are proven to be major sources of oxidative stress in the cell; they play a prominent role in a wide range of human disorders resulting from nonapoptotic cell death. The aim of this study is to examine the cytoprotective effect of the NecroX series against harmful stresses, including pro-oxidant (tertiarybutylhydroperoxide), doxorubicin, CCl4, and hypoxic injury. In this study, these novel chemical molecules inhibited caspase-independent cell death with necrotic morphology, which is distinctly different from apoptosis, autophagy, and necroptosis. In addition, they displayed strong mitochondrial reactive oxygen species and ONOO− scavenging activity. Further, oral administration of these molecules in C57BL/6 mice attenuated streptozotocin-induced pancreatic islet β-cell destruction as well as CCl4-induced hepatotoxicity in vivo. Taken together, these results demonstrate that the NecroX series are involved in the blockade of nonapoptotic cell death against mitochondrial oxidative stresses. Thus, these chemical molecules are potential therapeutic agents in mitochondria-related human diseases involving necrotic tissue injury.
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