Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1470
T. Patrice, B. Rozec, A. Sidoroff, Y. Blanloeil, P. Despins, C. Perrigaud
Oxidative stress (OS) had been evaluated in NSCLC using photoproduced singlet oxygen (1O2) deactivating by oxydizing its targets directly or through secondary reactive oxygen species (SOS) production. Either experimentally (orthotopic grafts in mice) or clinically OS changed non linearly with progression. At time of cachexia OS dramatically increased when at a resectable stage in was lower than in controls. In both cases it correlated with a worse prognosis. Vit C or Vit C+GSH have nearly no effect in resectable NSCLC patients but a negative one in controls. Vit E or Vit E + Vit C have a stronger protective effect in NSCLC, dose dependent but not related to the pathology. There was a trend to an inverse relationship OS/Vit D. An eventual adjuvant supplementation during cancers should by controlled on a per-patient basis.
在非小细胞肺癌中，氧化应激(OS)通过直接氧化其靶细胞或通过产生次级活性氧(SOS)来实现光产生单线态氧(1O2)失活。无论是实验(小鼠原位移植物)还是临床，OS都随进展呈非线性变化。恶病质期OS显著增加，可切除期OS低于对照组。在这两种情况下，它都与较差的预后相关。Vit C或Vit C+GSH在可切除的非小细胞肺癌患者中几乎没有影响，但在对照组中为阴性。Vit E或Vit E + Vit C对NSCLC具有较强的保护作用，其剂量依赖性与病理无关。OS/Vit d呈反比关系，癌症期间的最终辅助补充应以每位患者为基础进行控制。
{"title":"SECONDARY REACTIVE OXYGEN SPECIES PRODUCTION IN SERA OF PATIENTS WITH RESPECTABLE NON-SQUAMOUS CELL LUNG CANCERS","authors":"T. Patrice, B. Rozec, A. Sidoroff, Y. Blanloeil, P. Despins, C. Perrigaud","doi":"10.18143/JISANH_V3I3_1470","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1470","url":null,"abstract":"Oxidative stress (OS) had been evaluated in NSCLC using photoproduced singlet oxygen (1O2) deactivating by oxydizing its targets directly or through secondary reactive oxygen species (SOS) production. Either experimentally (orthotopic grafts in mice) or clinically OS changed non linearly with progression. At time of cachexia OS dramatically increased when at a resectable stage in was lower than in controls.\u0000In both cases it correlated with a worse prognosis. Vit C or Vit C+GSH have nearly no effect in resectable NSCLC patients but a negative one in controls. Vit E or Vit E + Vit C have a stronger protective effect in NSCLC, dose dependent but not related to the pathology. There was a trend to an inverse relationship OS/Vit D. An eventual adjuvant supplementation during cancers should by controlled on a per-patient basis.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"87 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85937108","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1472
Aurélien Ducat, C. Chéreau, L. Châtre, M. Ricchetti, F. Batteux, Daniel Vaiman
Preeclampsia is one of the major diseases of pregnancy, and a major concern for Gynecologists and Obstetricians throughout the World (6). It affects ~5% of pregnancies and is characterized by a pregnancy- induced hypertension accompanied by proteinuria, occurring from the second trimester of gestation. A large corpus of scientific literature connects preeclampsia with oxidative stress (4,5). Free oxygen species combine with Nitric Oxide to generate peroxinitrite ions (ONOO.), which will nitrate proteins. Treating rats with (L-NAME) triggers preeclamptic symptoms, showing the importance of NO as an endothelium protector able to alleviate preeclampsia (8). Preeclampsia has a genetic basis, as shown by epidemiological studies (1), and in 2005, the first gene variants causing preeclampsia were found in Dutch familial forms of preeclampsia in the transcription factor STOX1 (7). In 2013 we have shown that placental overexpression of STOX1 triggers preeclamptic symptoms in pregnant mice (3). A transcriptome study of transgenic and non-transgenic placentas revealed a massive deregulation of genes involved in mitochondrial function and oxidative stress (2) with a massive production of nitrated protein products of nitrosative stress in the transgenic placentas. These results were substantiated by a thorough analysis of mitochondrial physiology in human trophoblast cell models (JEG-3) overexpressing STOX1 or controls. In the present study, we measured by fluorescent markers four molecules involved in oxidative stress: NO, O2., H2O2 and GSH using Diaminofluorescein-2 Diacetate, Dihydroethidium, 2’,7’ Dichlorodihydrofluorescein diacetate, and Monochlorobimane, respectively. The analysis was performed on two control cell lines, a cell line overexpressing STOX1A (AA6) and one overexpressing STOX1B (B10). In addition, twelve drugs were used in order to selectively block specific mitochondrial and oxidative stress pathways. More specifically, O2. production was quenched using Allopurinol (inhibitor of xanthin oxidases), DPI (Inhibitor of NADPH oxidases), rotenone and antimycin (to block the mitochondrial respiratory chain). To evaluate the management of the oxidative stress at later stages, CDD (inhibitor of MnSOD), ATZ (inhibitor of catalase) and BSO (inhibitor of GSH) were used. MnTBAP (simulating MnSOD action), CuDIPS (simulating Cu/ZN SOD action), Catalase, Glutathion (GSH) and NAC were also added before monitoring the four outcomes. Finally the effects of ‘pseudo-hypoxia’ were evaluated by cultivating cells in the presence and in the absence of CoCl2. Basically, when no drug was added to the culture, STOX1A overexpression increased the production of NO, O2. and H2O2, whereas STOX1B decreased the production of O2. and GSH. The same tendencies were observed after CoCl2 treatment, but at a minor extent. The overproduction of NO and O2. is compatible with the increase of nitrosative stress that we observed in transgenic placentas. Amongst various observations,
{"title":"DECIPHERING THE FUNCTION OF THE STOX1 PROTEIN IN THE MANAGEMENT OF OXIDATIVE STRESS IN TROPHOBLAST CELLS","authors":"Aurélien Ducat, C. Chéreau, L. Châtre, M. Ricchetti, F. Batteux, Daniel Vaiman","doi":"10.18143/JISANH_V3I3_1472","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1472","url":null,"abstract":"Preeclampsia is one of the major diseases of pregnancy, and a major concern for Gynecologists and Obstetricians throughout the World (6). It affects ~5% of pregnancies and is characterized by a pregnancy- induced hypertension accompanied by proteinuria, occurring from the second trimester of gestation. A large corpus of scientific literature connects preeclampsia with oxidative stress (4,5). Free oxygen species combine with Nitric Oxide to generate peroxinitrite ions (ONOO.), which will nitrate proteins. Treating rats with (L-NAME) triggers preeclamptic symptoms, showing the importance of NO as an endothelium protector able to alleviate preeclampsia (8). Preeclampsia has a genetic basis, as shown by epidemiological studies (1), and in 2005, the first gene variants causing preeclampsia were found in Dutch familial forms of preeclampsia in the transcription factor STOX1 (7). In 2013 we have shown that placental overexpression of STOX1 triggers preeclamptic symptoms in pregnant mice (3). A transcriptome study of transgenic and non-transgenic placentas revealed a massive deregulation of genes involved in mitochondrial function and oxidative stress (2) with a massive production of nitrated protein products of nitrosative stress in the transgenic placentas. These results were substantiated by a thorough analysis of mitochondrial physiology in human trophoblast cell models (JEG-3) overexpressing STOX1 or controls. In the present study, we measured by fluorescent markers four molecules involved in oxidative stress: NO, O2., H2O2 and GSH using Diaminofluorescein-2 Diacetate, Dihydroethidium, 2’,7’ Dichlorodihydrofluorescein diacetate, and Monochlorobimane, respectively. The analysis was performed on two control cell lines, a cell line overexpressing STOX1A (AA6) and one overexpressing STOX1B (B10). In addition, twelve drugs were used in order to selectively block specific mitochondrial and oxidative stress pathways. More specifically, O2. production was quenched using Allopurinol (inhibitor of xanthin oxidases), DPI (Inhibitor of NADPH oxidases), rotenone and antimycin (to block the mitochondrial respiratory chain). To evaluate the management of the oxidative stress at later stages, CDD (inhibitor of MnSOD), ATZ (inhibitor of catalase) and BSO (inhibitor of GSH) were used. MnTBAP (simulating MnSOD action), CuDIPS (simulating Cu/ZN SOD action), Catalase, Glutathion (GSH) and NAC were also added before monitoring the four outcomes. Finally the effects of ‘pseudo-hypoxia’ were evaluated by cultivating cells in the presence and in the absence of CoCl2. Basically, when no drug was added to the culture, STOX1A overexpression increased the production of NO, O2. and H2O2, whereas STOX1B decreased the production of O2. and GSH. The same tendencies were observed after CoCl2 treatment, but at a minor extent. The overproduction of NO and O2. is compatible with the increase of nitrosative stress that we observed in transgenic placentas. Amongst various observations, ","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85989762","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1453
T. Brioche
Sarcopenia could be currently defined as a geriatric syndrome initially characterized by a decrease in muscle mass that will get worse causing deterioration in strength and physical performance. A negative protein turnover, impaired mitochondrial dynamics and functions, a decreased muscle regeneration capacity, as well as an exacerbation of apoptosis are usually considered to be cellular mechanisms involved in muscle atrophy leading to sarcopenia. Here, we first present that muscle overproduction of reactive oxygen and nitrogen species (RONS) and oxidative stress observed during aging, are associated with sarcopenia, and then discuss how RONS are involved in redox-sensitive signaling pathways leading to sarcopenia. The identification of cost-effectiveness interventions to maintain muscle mass and physical functions in the elderly is one of the most important public health challenges. Here, we also discuss about the efficiency of different kind of current antioxidant strategies against sarcopenia and future strategies. Since exercise is the best strategy to prevent and reverse sarcopenia, we also highlight that exercise acts as an antioxidant.
{"title":"OXIDATIVE STRESS, SARCOPENIA, ANTIOXIDANT STRATEGIES AND EXERCISE: MOLECULAR ASPECTS","authors":"T. Brioche","doi":"10.18143/JISANH_V3I3_1453","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1453","url":null,"abstract":"Sarcopenia could be currently defined as a geriatric syndrome initially characterized by a decrease in muscle mass that will get worse causing deterioration in strength and physical performance. A negative protein turnover, impaired mitochondrial dynamics and functions, a decreased muscle regeneration capacity, as well as an exacerbation of apoptosis are usually considered to be cellular mechanisms involved in muscle atrophy leading to sarcopenia. Here, we first present that muscle overproduction of reactive oxygen and nitrogen species (RONS) and oxidative stress observed during aging, are associated with sarcopenia, and then discuss how RONS are involved in redox-sensitive signaling pathways leading to sarcopenia. The identification of cost-effectiveness interventions to maintain muscle mass and physical functions in the elderly is one of the most important public health challenges.\u0000Here, we also discuss about the efficiency of different kind of current antioxidant strategies against sarcopenia and future strategies. Since exercise is the best strategy to prevent and reverse sarcopenia, we also highlight that exercise acts as an antioxidant.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"69 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84070833","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1456
N. Kavian
Our team works on systemic sclerosis (SSc), a disease that is characterized by vascular dysfunction, skin and visceral fibrosis, and dysimmunity. Oxidative stress in endothelial cells and fibroblasts is partly responsible for the activation of these cells and the consecutive oxidization of DNA-topoisomerase-1 that leads to the breach of immune tolerance and the production of autoantibodies in SSc patients. Our work regards the mechanisms of spreading and perpetuation of cellular activation and oxidative stress through various tissues and organs such as skin, lungs and kidneys. We report that in vitro and in various relevant mouse models of SSc, pantethine exerts vasculoprotective and anti-fibrotic effects by protecting endothelial cells and fibroblasts from oxidative and nitrosative stresses. These beneficial effects are the consequences of the inhibition of endothelial microparticle shedding and of proper anti- oxidant properties. Pantethine is metabolized by pantetheinase/vanine-1 enzyme into pantothenic acid and cystamine. Therefore, the level of pantethine depends on the enzymatic activity of its metabolizing enzyme pantetheinase/vanin-1. The pantetheinase-vanin-1 activity is significantly increased in the skin and in the blood of mice and of patients with SSc compared to controls. This imbalance favours the conversion of the vasculoprotective pantethine into pantothenic acid and cysteamine that, in sharp contrast with pantethine, act as pro-fibrotic and pro-oxidative agents. Vanin-1-/- animals do not develop fibrosis, vascular dysfunction and autoimmunity when submitted to experimental SSc. Thus, the levels of pantetheinase/vanin-1 activity determine the severity of the disease and this data suggests that the restoration of pantethine levels could treat systemic sclerosis. Altogether, the imbalance in the pantethine/pantetheinase-vanin-1 pathway is a new argument for the role of ROS as a pivotal feature of the pathophysiology of SSc.
{"title":"THE PATHENINE/VANINE PATHWAY CONTROLS ROS-INDUCED SKIN FIBROSIS","authors":"N. Kavian","doi":"10.18143/JISANH_V3I3_1456","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1456","url":null,"abstract":"Our team works on systemic sclerosis (SSc), a disease that is characterized by vascular dysfunction, skin and visceral fibrosis, and dysimmunity. Oxidative stress in endothelial cells and fibroblasts is partly responsible for the activation of these cells and the consecutive oxidization of DNA-topoisomerase-1 that leads to the breach of immune tolerance and the production of autoantibodies in SSc patients. Our work regards the mechanisms of spreading and perpetuation of cellular activation and oxidative stress through various tissues and organs such as skin, lungs and kidneys.\u0000We report that in vitro and in various relevant mouse models of SSc, pantethine exerts vasculoprotective and anti-fibrotic effects by protecting endothelial cells and fibroblasts from oxidative and nitrosative stresses. These beneficial effects are the consequences of the inhibition of endothelial microparticle shedding and of proper anti- oxidant properties. Pantethine is metabolized by pantetheinase/vanine-1 enzyme into pantothenic acid and cystamine. Therefore, the level of pantethine depends on the enzymatic activity of its metabolizing enzyme pantetheinase/vanin-1. The pantetheinase-vanin-1 activity is significantly increased in the skin and in the blood of mice and of patients with SSc compared to controls. This imbalance favours the conversion of the vasculoprotective pantethine into pantothenic acid and cysteamine that, in sharp contrast with pantethine, act as pro-fibrotic and pro-oxidative agents. Vanin-1-/- animals do not develop fibrosis, vascular dysfunction and autoimmunity when submitted to experimental SSc. Thus, the levels of pantetheinase/vanin-1 activity determine the severity of the disease and this data suggests that the restoration of pantethine levels could treat systemic sclerosis. Altogether, the imbalance in the pantethine/pantetheinase-vanin-1 pathway is a new argument for the role of ROS as a pivotal feature of the pathophysiology of SSc.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"34 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91346066","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I2_1434
M. Sternberg, J. M'bemba, P. Urios, A. Borsos, J. Selam, J. Peyroux, G. Slama
We measured pentosidine and fluorescence at 370/440nm in collagen extracted from skin punch-biopsies in 30 patients with diabetes (14 type 1 diabetes and 16 type 2 diabetes) without renal insufficiency, and in age- and gender-matched normoglycemic controls, followed at Hotel-Dieu in Paris. At the time of biopsy, marked increases in pentosidine and fluorescence levels, expressed per collagen hydroxyproline, were found in the patients with diabetes versus normoglcemic controls. Pentosidine and fluorescence were correlated with diabetes duration. Fluorescence was significantly dependent on retinopathy presence and score in type-1 and type-2 diabetes. Fluorescence was correlated with microalbuminuria, only in type-1 diabetes. Already six years after biopsy, retinopathy score progression and creatininemia increase were significantly correlated with initial pentosidine and fluorescence levels.
{"title":"SKIN COLLAGEN PENTOSIDINE AND FLUORESCENCE IN DIABETES ARE PREDICTORS OF CREATININEMIA INCREASE AND RETINOPATHY PROGRESSION ALREADY 6 YEARS AFTER PUNCH-BIOPSY","authors":"M. Sternberg, J. M'bemba, P. Urios, A. Borsos, J. Selam, J. Peyroux, G. Slama","doi":"10.18143/JISANH_V3I2_1434","DOIUrl":"https://doi.org/10.18143/JISANH_V3I2_1434","url":null,"abstract":"We measured pentosidine and fluorescence at 370/440nm in collagen extracted from skin punch-biopsies in 30 patients with diabetes (14 type 1 diabetes and 16 type 2 diabetes) without renal insufficiency, and in age- and gender-matched normoglycemic controls, followed at Hotel-Dieu in Paris. At the time of biopsy, marked increases in pentosidine and fluorescence levels, expressed per collagen hydroxyproline, were found in the patients with diabetes versus normoglcemic controls. Pentosidine and fluorescence were correlated with diabetes duration. Fluorescence was significantly dependent on retinopathy presence and score in type-1 and type-2 diabetes. Fluorescence was correlated with microalbuminuria, only in type-1 diabetes. Already six years after biopsy, retinopathy score progression and creatininemia increase were significantly correlated with initial pentosidine and fluorescence levels.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"12 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78197638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I4_1418
J. Teixeira
Polyphenols are well-known antioxidant molecules, which present different mechanisms at several subcellular compartments. Polyphenols, in its oxidized quinone form, may act as potent regulators of the cellular redox status. Mitochondria, the cell’s powerhouse, adapt to environmental factors by producing effectors that activate multiple pathways related to oxidative stress balance. Targeting mitochondria with therapeutic agents is an effective therapeutic strategy in human health and disease. Re-designing natural products and improving intracellular addressing can be a promising strategy to improve the cellular antioxidant status and contribute to decrease oxidative stress.
{"title":"THE HORMETIC ROLE OF REDOX-ACTIVE POLYPHENOLS IN HUMAN HEALTH AND DISEASE","authors":"J. Teixeira","doi":"10.18143/JISANH_V3I4_1418","DOIUrl":"https://doi.org/10.18143/JISANH_V3I4_1418","url":null,"abstract":"Polyphenols are well-known antioxidant molecules, which present different mechanisms at several subcellular compartments.\u0000Polyphenols, in its oxidized quinone form, may act as potent regulators of the cellular redox status.\u0000Mitochondria, the cell’s powerhouse, adapt to environmental factors by producing effectors that activate multiple pathways related to oxidative stress balance.\u0000Targeting mitochondria with therapeutic agents is an effective therapeutic strategy in human health and disease.\u0000Re-designing natural products and improving intracellular addressing can be a promising strategy to improve the cellular antioxidant status and contribute to decrease oxidative stress.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"6 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79546025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1467
Renata Smulik, Adrianna Mesjasz, J. Adamus, A. Sikora
Nitroxyl (HNO, IUPAC name azanone), being formally the protonated product of one-electron reduction of nitric oxide (NO), is an elusive reactive nitrogen species possessing interesting biological chemistry and high pharmacological importance. 1,2 Thiols, thiol proteins and metaloproteins are the most established biological targets for HNO. 1-3 Contrary to nitric oxide, HNO is a strong electrophile highly reactive towards thiols, phosphines and nitroso compounds. A number of fluorescent probes for HNO detection based on the reaction of HNO with arylphosphines have been developed recently. Here, we present the study on the HNO reactivity towards selected HNO scavengers: thiols, arylphosphines (including profluorescent probe PCM) and nitroso compounds. In this study we applied previously described competition kinetics method 4 based on two parallel, competing HNO reactions – with studied scavenger and with molecular oxygen. The latter, relatively fast reaction (k=(1.8 ± 0.3)10 4 M -1 s -1), results in the formation of peroxynitrite, 4 that can be easily detected fluorometrically with the use of fluorogenic boronate probes. Potential implications for fluorescent imaging of HNO in cells using phosphine-based fluorogenic probes are discussed.
硝基(Nitroxyl, IUPAC名称azanone)是一氧化氮(nitric oxide, NO)单电子还原反应的质子化产物，是一种难以捉摸的活性氮物质，具有有趣的生物化学和很高的药理意义。1,2硫醇、硫醇蛋白和金属蛋白是HNO最确定的生物学靶点。与一氧化氮相反，HNO是一种强亲电试剂，对硫醇、膦和亚硝基化合物反应强烈。近年来，人们开发了许多基于HNO与芳基膦反应的荧光探针来检测HNO。在这里，我们研究了HNO对选定的HNO清除剂的反应性:硫醇、芳基膦(包括前荧光探针PCM)和亚硝基化合物。在这项研究中，我们应用了先前描述的竞争动力学方法4，该方法基于两个平行的竞争HNO反应-与研究的清除剂和与分子氧。后者反应相对较快(k=(1.8±0.3)10.4 M -1 s -1)，生成过氧亚硝酸盐4，使用荧光硼酸探针可以很容易地检测到过氧亚硝酸盐。讨论了基于磷化氢的荧光探针对细胞中HNO荧光成像的潜在影响。
{"title":"WHAT DO WE REALLY KNOW ABOUT HNO REACTIVITY? IMPLICATIONS FOR ITS FLUORESCENCE IMAGING IN VIVO","authors":"Renata Smulik, Adrianna Mesjasz, J. Adamus, A. Sikora","doi":"10.18143/JISANH_V3I3_1467","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1467","url":null,"abstract":"Nitroxyl (HNO, IUPAC name azanone), being formally the protonated product of one-electron reduction of nitric oxide (NO), is an elusive reactive nitrogen species possessing interesting biological chemistry and high pharmacological importance. 1,2 Thiols, thiol proteins and metaloproteins are the most established biological targets for HNO. 1-3 Contrary to nitric oxide, HNO is a strong electrophile highly reactive towards thiols, phosphines and nitroso compounds. A number of fluorescent probes for HNO detection based on the reaction of HNO with arylphosphines have been developed recently. Here, we present the study on the HNO reactivity towards selected HNO scavengers: thiols, arylphosphines (including profluorescent probe PCM) and nitroso compounds. In this study we applied previously described competition kinetics method 4 based on two parallel, competing HNO reactions – with studied scavenger and with molecular oxygen. The latter, relatively fast reaction (k=(1.8 ± 0.3)10 4 M -1 s -1), results in the formation of peroxynitrite, 4 that can be easily detected fluorometrically with the use of fluorogenic boronate probes. Potential implications for fluorescent imaging of HNO in cells using phosphine-based fluorogenic probes are discussed.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"134 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79674654","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I2_1446
I. Zs.-Nagy
This lecture will survey the history of the free-radical research in biological systems starting from the original concept of D. Harman formed during the late fifties. This original concept has undergone a series of misinterpretations during the subsequent decades, leading to a number of contradictions in the theory and the applications if this idea in biology and medicine. At last a tentative explanation will be presented on the basis of the real physicochemical properties of the oxygen free-radicals and the macromolecules involved in the biological functions.
{"title":"CONCEPTS AND MISCONCEPTS REGARDING THE NATURE OF THE OXYGEN FREE-RADICALS IN THE LIVING SYSTEMS","authors":"I. Zs.-Nagy","doi":"10.18143/JISANH_V3I2_1446","DOIUrl":"https://doi.org/10.18143/JISANH_V3I2_1446","url":null,"abstract":"This lecture will survey the history of the free-radical research in biological systems starting from the original concept of D.\u0000Harman formed during the late fifties. This original concept has undergone a series of misinterpretations during the subsequent decades, leading to a number of contradictions in the theory and the applications if this idea in biology and medicine. At last a tentative explanation will be presented on the basis of the real physicochemical properties of the oxygen free-radicals and the macromolecules involved in the biological functions.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"56 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76842070","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I4_1410
E. Richling
Epidemiologic evidence suggests coffee consumption to be associated with reduced risk due to certain diseases, including diabetes type 2, Parkinson, and cardiovascular disease or various types of cancer. In human interventions studies we investigated effects of regular coffee consumption on DNA integrity in peripheral white blood cells (WBC) by the comet assay. During four weeks, volunteers daily ingested three large cups (250 ml) of a specific coffee blend, rich in both, green bean constituents and roast products. Controls received the same volume of water. The results allow the conclusion that regular coffee consumption is associated with markedly reduced DNA strand breaks, reflecting total as well as background DNA damage. In a recently performed short term study, when volunteers consumed four cups of coffee (200 ml) every two hours the results showed a significant reduction of background DNA strand breaks in comparison to baseline. Interestingly, this DNA protective effect was detected already two hours after the first coffee consumption. Taken together, our studies clearly showed that consumption of coffee reduces DNA damage in white blood cells of humans.
{"title":"INFLUENCE OF COFFEE CONSUMPTION ON DNA INTEGRITY IN HUMANS","authors":"E. Richling","doi":"10.18143/JISANH_V3I4_1410","DOIUrl":"https://doi.org/10.18143/JISANH_V3I4_1410","url":null,"abstract":"Epidemiologic evidence suggests coffee consumption to be associated with reduced risk due to certain diseases, including diabetes type 2, Parkinson, and cardiovascular disease or various types of cancer. In human interventions studies we investigated effects of regular coffee consumption on DNA integrity in peripheral white blood cells (WBC) by the comet assay. During four weeks, volunteers daily ingested three large cups (250 ml) of a specific coffee blend, rich in both, green bean constituents and roast products. Controls received the same volume of water. The results allow the conclusion that regular coffee consumption is associated with markedly reduced DNA strand breaks, reflecting total as well as background DNA damage. In a recently performed short term study, when volunteers consumed four cups of coffee (200 ml) every two hours the results showed a significant reduction of background DNA strand breaks in comparison to baseline. Interestingly, this DNA protective effect was detected already two hours after the first coffee consumption.\u0000Taken together, our studies clearly showed that consumption of coffee reduces DNA damage in white blood cells of humans.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76536786","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I3_1449
G. McBean
Astrocytes supply neurons with the antioxidant, glutathione. Cysteine is the precursor of glutathione and is imported as cystine via the plasma-membrane cystine glutamate exchanger. Recent evidence has shown that the transsulphuration pathway that converts methionine to cysteine also contributes to glutathione in astrocytes. Data on the relationship between the cystine glutamate exchanger and the transsulphuration pathway and changes in response to oxidative stress in astrocytes will be presented. The implications of this work for targeting pathways of cysteine metabolism in neurodegenerative disease will be discussed.
{"title":"ANTIOXIDANT SYSTEMS IN BRAIN ASTROCYTES: SOURCES OF CYSTEINE FOR GLUTATHIONE","authors":"G. McBean","doi":"10.18143/JISANH_V3I3_1449","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1449","url":null,"abstract":"Astrocytes supply neurons with the antioxidant, glutathione. Cysteine is the precursor of glutathione and is imported as cystine via the plasma-membrane cystine glutamate exchanger. Recent evidence has shown that the transsulphuration pathway that converts methionine to cysteine also contributes to glutathione in astrocytes. Data on the relationship between the cystine glutamate exchanger and the transsulphuration pathway and changes in response to oxidative stress in astrocytes will be presented. The implications of this work for targeting pathways of cysteine metabolism in neurodegenerative disease will be discussed.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"14 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75364147","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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