Flow cytometric analysis of peroxidative activity in granulocytes from coronary and peripheral blood in acute myocardial ischemia and reperfusion in dogs: Protective effect of methionine

Such, Luis; O’Connor, José-Enrique; Sáez, Guillermo T.; Gil, Francisco Manuel Tortosa; Beltrán, Juan F.; Moya, Amparo Ayuso; Alberola, Arcadio García

doi:10.1002/(sici)1097-0320(19991001)37:2<140::aid-cyto7>3.0.co;2-7

Cited by 7 publications

(4 citation statements)

References 40 publications

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“…It is a non‐fluorescent membrane‐permeable dye that can be oxidized directly to the red fluorescent ethidium bromide by O 2 generated inside the cells after different treatments. DHR 123 is a dye freely diffusing into cells, oxidized primarily by H 2 O 2 in a myeloperoxidase dependent reaction to green fluorescence [17]. As DHR 123 is accumulated by mitochondria, we excluded possible interference in ROS evaluation by using carbonyl cyanide p ‐(trifluoro‐methoxy) phenylhydrazone (FCCP, 20 μM Sigma) a protonophore able to depolarize mitochondrial membrane, as previously described [18].…”

Section: Methodsmentioning

confidence: 99%

Galectin‐3 overexpression protects from cell damage and death by influencing mitochondrial homeostasis

et al. 2000

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Galectins are a family of proteins involved in several cell processes, including their survival and death. Galectin-3 has in particular been described as an anti-apoptotic molecule entangled with a number of subcellular activities including anoikis resistance. In this work we partially address the mechanisms underlying this activity pointing at two key factors in injury progression: the alteration of mitochondrial membrane potential and the formation of reactive oxygen species. Overexpression of galectin-3 appears in fact to exert a protective effect towards both these events. On the basis of these data, we propose a reappraisal of the role of galectin-3 as a regulator of mitochondrial homeostasis.z 2000 Federation of European Biochemical Societies.

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Section: Methodsmentioning

confidence: 99%

Galectin‐3 overexpression protects from cell damage and death by influencing mitochondrial homeostasis

et al. 2000

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“…DHR 123 is a dye freely diffusing into cells and oxidized primarily by H 2 O 2 in a myeloperoxidase-dependent reaction to green fluorescence. 41 As DHR 123 is accumulated by mitochondria, it is possible to detect ROS production at mitochondrial levels. 42 …”

Section: Flow Cytometrymentioning

confidence: 99%

Type I Interferon Gene Transfer Sensitizes Melanoma Cells to Apoptosis via a Target Activity on Mitochondrial Function

Matarrese

Biase

Santodonato

et al. 2002

The American Journal of Pathology

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Our previous article reported that retroviral transduction of human type I consensus interferon-coding sequence into two human melanoma cells increased their susceptibility to cisplatin-induced apoptosis. Importantly, primary melanoma cells were significantly more sensitive to cisplatin-induced apoptosis with respect to metastatic melanoma cells. The aim of this study was to elucidate the subcellular mechanisms involved in this interferon-induced apoptotic proneness. Our results indicate that 1) cisplatin-induced apoptosis can be referred to as the type II apoptosis, ie, to the mitochondrially driven cascade; 2) treatment of interferon-producing melanoma cells with other type II apoptotic stimuli, such as radiation or staurosporine, also resulted in massive apoptosis, whereas type I stimuli, ie, anti-Fas, were ineffective; 3) interferon sensitization involved the caspase cascade in primary melanoma cells and the alternative pathway represented by cathepsin-mediated apoptosis in metastatic melanoma cells; 4) interferon production sensitizes cells to apoptosis by inducing, as the earliest event, mitochondrial membrane hyperpolarization. These results suggest that constitutive production of type I interferon by melanoma cells can act as an intracellular booster capable of increasing cell proneness to apoptosis by specifically modifying mitochondrial homeostasis and independently from the apoptotic cascade involved. (Am J Pathol 2002,

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“…Additionally, Met (35) oxidized Aβ is both soluble and toxic to neuronal cells [17] and may prove to play an important role in AD. Methionine also has been reported to protect other residues from MCO [45]. Hence, investigation of MCO of methionine is important, as is the identification of stable and suitable MCO methionine products that may be used as a biomarker for MCO of proteins and peptides in biological systems.…”

Section: Introductionmentioning

confidence: 99%

Methionine regulates copper/hydrogen peroxide oxidation products of Aβ

et al. 2005

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Metal-catalysed oxidation (MCO) may play a causative role in the pathogenesis of Alzheimer's disease (AD). Amyloid beta peptide (Abeta), the major biomarker of AD, in the presence of copper ions reduces Cu(2+) to Cu(+) and catalyses the formation of H(2)O(2) that subsequently induces radicals through Fenton chemistry. Abeta is also subject to attack by free radicals, where the presence of Cu(2+) in conjunction with H(2)O(2) catalyses oxygenation, primarily at the methionine sulfur atom. This work investigates MCO of Abeta, to gain further insight into the role of oxidative stress in AD. By combining a fluorescence assay with gel electrophoresis to monitor MCO reactions of Abeta (1-28) in the presence and absence of methionine it was determined that methionine can both protect some residues against MCO and promote the oxidation of Tyr(10) specifically. Electrospray ionization mass spectrometric analysis of methionine MCO products indicated the formation of methionine sulfoxide, methionine sulfone and related hydroxylated products. Similar products could be formed from the oxidation of Met(35) of Abeta and may relate to changes in properties of the peptide following MCO.

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Flow cytometric analysis of peroxidative activity in granulocytes from coronary and peripheral blood in acute myocardial ischemia and reperfusion in dogs: Protective effect of methionine

Cited by 7 publications

References 40 publications

Galectin‐3 overexpression protects from cell damage and death by influencing mitochondrial homeostasis

Galectin‐3 overexpression protects from cell damage and death by influencing mitochondrial homeostasis

Type I Interferon Gene Transfer Sensitizes Melanoma Cells to Apoptosis via a Target Activity on Mitochondrial Function

Methionine regulates copper/hydrogen peroxide oxidation products of Aβ

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