Pub Date : 2016-07-08DOI: 10.18143/JISANH_V3I2_1442
B. Sperlágh
Mitochondrial dysfunction, oxidative stress and their interplay are core pathological features of neurodegenerative diseases. In Parkinson's disease (PD), mitochondrial dysfunction and oxidative stress have a supra-additive impact on the pathological, cytoplasmic accumulation of dopamine and its subsequent release. Moreover, dopamine and their metabolites provide an additional source of reactive oxygen species (ROS) during their breakdown by monoamine oxidase or auto-oxidation. Therefore those drugs which simultaneously target mitochondrial dysfunction, oxidative stress and subsequent pathological dopamine release may have disease- modifying potential in addition to symptomatic improvement by the blockade of self-amplifying circuits leading to ROS generation. To fulfill this aim we have developed a novel series of potent and selective MAO-B inhibitory (hetero)arylalkenylpropargylamine compounds having also protective properties against the supra-additive effect of mitochondrial dysfunction and oxidative stress. The compounds were tested in a wide range of in vitro and in vivo toxin-induced animal models of PD. The compounds exhibited consistent protective effects against i) in vitro oxidative stress induced pathological dopamine release and the formation of toxic dopamine quinone in the rat striatum and rescued dopaminergic neurons; ii) in vivo MPTP-induced striatal dopamine depletion and motor dysfunction in mice using acute, subchronic, and chronic protocols. In conclusion the above strategy seems a plausible approach to halt the progressive loss of nigrostriatal dopaminergic neurons and to combat PD.
{"title":"SUPRA-ADDITIVE IMPACT OF MITOCHONDRIAL DYSFUNCTION AND SUBSEQUENT OXIDATIVE STRESS IN CENTRAL NERVOUS SYSTEM PATHOLOGY","authors":"B. Sperlágh","doi":"10.18143/JISANH_V3I2_1442","DOIUrl":"https://doi.org/10.18143/JISANH_V3I2_1442","url":null,"abstract":"Mitochondrial dysfunction, oxidative stress and their interplay are core pathological features of neurodegenerative diseases. In Parkinson's disease (PD), mitochondrial dysfunction and oxidative stress have a supra-additive impact on the pathological, cytoplasmic accumulation of dopamine and its subsequent release. Moreover, dopamine and their metabolites provide an additional source of reactive oxygen species (ROS) during their breakdown by monoamine oxidase or auto-oxidation. Therefore those drugs which simultaneously target mitochondrial dysfunction, oxidative stress and subsequent pathological dopamine release may have disease- modifying potential in addition to symptomatic improvement by the blockade of self-amplifying circuits leading to ROS generation.\u0000To fulfill this aim we have developed a novel series of potent and selective MAO-B inhibitory (hetero)arylalkenylpropargylamine compounds having also protective properties against the supra-additive effect of mitochondrial dysfunction and oxidative stress. The compounds were tested in a wide range of in vitro and in vivo toxin-induced animal models of PD. The compounds exhibited consistent protective effects against i) in vitro oxidative stress induced pathological dopamine release and the formation of toxic dopamine quinone in the rat striatum and rescued dopaminergic neurons; ii) in vivo MPTP-induced striatal dopamine depletion and motor dysfunction in mice using acute, subchronic, and chronic protocols. In conclusion the above strategy seems a plausible approach to halt the progressive loss of nigrostriatal dopaminergic neurons and to combat PD.","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":"86605416","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_1436
F. Rigoldi, A. D. Vedove, S. Vesentini, E. Parisini, A. Gautieri
The progressive accumulation of Advanced Glycation End-product (AGEs) in the human body leads to several deleterious consequences, involving tissues stiffening and pathologies (aterosclerosis, nephropathy, and Alzheimer’s disease). Nowadays there are no effective therapies against AGEs build-up, although a promising strategy is redeglycating enzymes (FAOXs), which are however inactive towards entire proteins due to their buried active site.
{"title":"AMADORIASE ENGINEERED ENZYME FOR PROTEIN DEGLYCATION","authors":"F. Rigoldi, A. D. Vedove, S. Vesentini, E. Parisini, A. Gautieri","doi":"10.18143/JISANH_V3I2_1436","DOIUrl":"https://doi.org/10.18143/JISANH_V3I2_1436","url":null,"abstract":"The progressive accumulation of Advanced Glycation End-product (AGEs) in the human body leads to several deleterious consequences, involving tissues stiffening and pathologies (aterosclerosis, nephropathy, and Alzheimer’s disease). Nowadays there are no effective therapies against AGEs build-up, although a promising strategy is redeglycating enzymes (FAOXs), which are however inactive towards entire proteins due to their buried active site.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"24 1","pages":"1-1"},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89996512","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_1457
Maya Ben-Yehuda Greenwald, S. Sasson, H. Peled, R. Kohen
The skin, functions as a barrier between our body and the environment. Therefore, skin is consistently exposed to physical damages (e.g. wounds, sunburns) and to various exogenous and endogenous sources producing reactive oxygen species (e.g. air pollutants, ionizing and non-ionizing irradiation, toxins, mitochondrial metabolism, enzymes activity, etc.). Although skin has developed an array of counteracting defense mechanisms, augmented or continued reactive oxygen species activity may result in oxidative stress leading to many skin disorder including inflammatory diseases, pigmenting disorders and some types of cutaneous malignancies. The nuclear factor erythroid 2–related factor 2 (Nrf2) is an emerging regulator of cellular resistance and of defensive phase II enzymes. Induction of the Keap1-Nrf2 pathway may have a beneficial effect in treatment of a large number of skin disorders, by stimulating the endogenous defense mechanism. However, sustained and enhanced activation of this pathway is detrimental and limits the therapeutic potential of Keap1-Nrf2 activators. Here, we suggest a novel strategy for maintenance of skin redox homeostasis by modulating the Keap1-Nrf2 pathway using delivery systems.
{"title":"SKIN REDOX BALANCE MAINTENANCE: THE NEED FOR AN NRF2- ACTIVATORS DELIVERY SYSTEM","authors":"Maya Ben-Yehuda Greenwald, S. Sasson, H. Peled, R. Kohen","doi":"10.18143/JISANH_V3I3_1457","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1457","url":null,"abstract":"The skin, functions as a barrier between our body and the environment. Therefore, skin is consistently exposed to physical damages (e.g. wounds, sunburns) and to various exogenous and endogenous sources producing reactive oxygen species (e.g. air pollutants, ionizing and non-ionizing irradiation, toxins, mitochondrial metabolism, enzymes activity, etc.). Although skin has developed an array of counteracting defense mechanisms, augmented or continued reactive oxygen species activity may result in oxidative stress leading to many skin disorder including inflammatory diseases, pigmenting disorders and some types of cutaneous malignancies. The nuclear factor erythroid 2–related factor 2 (Nrf2) is an emerging regulator of cellular resistance and of defensive phase II enzymes. Induction of the Keap1-Nrf2 pathway may have a beneficial effect in treatment of a large number of skin disorders, by stimulating the endogenous defense mechanism. However, sustained and enhanced activation of this pathway is detrimental and limits the therapeutic potential of Keap1-Nrf2 activators.\u0000Here, we suggest a novel strategy for maintenance of skin redox homeostasis by modulating the Keap1-Nrf2 pathway using delivery systems.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"27 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78914328","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_1468
Thong Thua-Huy
Endothelial dysfunction and activation of the immune system are the two major pathophysiological mechanisms responsible for the fibrosis of the skin and internal organs in systemic sclerosis. The diffuse interstitial lung disease (PID) has become the main cause of the disease mortality. Pulmonary inflammation is the result of activation of the immune system, which stimulates the inducible NO synthase and increases cellular production of nitric oxide (NO). Increasing alveolar NO concentration (CANO) was significantly correlated with the severity of the PID in patients with systemic sclerosis. Increased CANO is related to the inducing capacity of serum from patients on lung fibroblast proliferation and their differentiation into myofibroblasts, linking active alveolitis to cell mechanism of pulmonary fibrosis in the disease. Alveolar nitric oxide concentration has a strong predictive value on the deterioration of the PID within a 3-year follow-up. These patients could then receive early appropriate treatment such as immunosuppressive medication.
{"title":"EXHALED NITRIC OXIDE AS PREDICTOR MARKER OF INTERSTITIAL LUNG DISEASE AND FIBROSIS","authors":"Thong Thua-Huy","doi":"10.18143/JISANH_V3I3_1468","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1468","url":null,"abstract":"Endothelial dysfunction and activation of the immune system are the two major pathophysiological mechanisms responsible for the fibrosis of the skin and internal organs in systemic sclerosis. The diffuse interstitial lung disease (PID) has become the main cause of the disease mortality. Pulmonary inflammation is the result of activation of the immune system, which stimulates the inducible NO synthase and increases cellular production of nitric oxide (NO). Increasing alveolar NO concentration (CANO) was significantly correlated with the severity of the PID in patients with systemic sclerosis. Increased CANO is related to the inducing capacity of serum from patients on lung fibroblast proliferation and their differentiation into myofibroblasts, linking active alveolitis to cell mechanism of pulmonary fibrosis in the disease. Alveolar nitric oxide concentration has a strong predictive value on the deterioration of the PID within a 3-year follow-up. These patients could then receive early appropriate treatment such as immunosuppressive medication.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"175 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82972666","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_1450
R. Vlahos
Introduction : Reactive oxygen species (ROS) are a family of highly reactive molecules that are produced by a variety of cell types in the lung in response to chemical and physical agents in the environment. It is well known that ROS are critical in host defence as they kill invading pathogens, but that their excessive accumulation in the lung results in oxidative damage. Oxidative stress, which is defined as the persistent overproduction of ROS that overwhelms endogenous antioxidant defence systems, has been implicated in both acute (e.g respiratory virus infections) and chronic (e.g. COPD) lung diseases. Therefore, targeting oxidative stress may be a novel way to treat these lung diseases. Results : We have shown that targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate influenza A virus (IAV)-induced lung inflammation and pathology, cigarette smoke-induced lung inflammation, acute exacerbations of COPD (AECOPD) and skeletal muscle wasting in mice. Conclusion : Targeting oxidative stress may be a novel strategy to treat both acute and chronic lung diseases.
{"title":"ACUTE, CHRONIC LUNG DISEASES AND OXIDATIVE STRESS:TARGETING RESPIRATORY INFECTIONS, COPD AND VIRAL-INDUCED EXACERBATIONS OF COPD","authors":"R. Vlahos","doi":"10.18143/JISANH_V3I3_1450","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1450","url":null,"abstract":"Introduction : Reactive oxygen species (ROS) are a family of highly reactive molecules that are produced by a variety of cell types in the lung in response to chemical and physical agents in the environment. It is well known that ROS are critical in host defence as they kill invading pathogens, but that their excessive accumulation in the lung results in oxidative damage. Oxidative stress, which is defined as the persistent overproduction of ROS that overwhelms endogenous antioxidant defence systems, has been implicated in both acute (e.g respiratory virus infections) and chronic (e.g. COPD) lung diseases. Therefore, targeting oxidative stress may be a novel way to treat these lung diseases. Results : We have shown that targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate influenza A virus (IAV)-induced lung inflammation and pathology, cigarette smoke-induced lung inflammation, acute exacerbations of COPD (AECOPD) and skeletal muscle wasting in mice. Conclusion : Targeting oxidative stress may be a novel strategy to treat both acute and chronic lung diseases.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"3 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84053816","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_1422
M. Alves, S. Almeida, A. R. Nunes, M. Sousa, P. Moreira, P. Oliveira, B. Silva
Europe has the highest proportion of older persons in the World. As population ages, it is imperative to find new strategies to avoid or counteract the effects of the incurable neurodegenerative diseases, which already represent a great financial and emotional burden for health care systems, patients, and their families. In this talk, Branca Silva (PhD) will discuss whether polyphenols obtained from diet or food supplements constitute an effective and low-cost strategy to prevent or treat neurodegeneration and neurotoxicity. Special focus will be given to the recent works of her research team about the beneficial effects to the brain of the regular consumption of white tea (Camellia sincensis L.) and its polyphenols. She will also highlight the safety, mechanisms of action, and the current and future relevance of polyphenols in the prevention and therapy of neurodegenerative disorders.
{"title":"POLYPHENOLS AS PROTECTIVE AGENTS AGAINST NEUROTOXICITY AND NEURODEGENERATION: THE CASE OF TEA POLYPHENOLS","authors":"M. Alves, S. Almeida, A. R. Nunes, M. Sousa, P. Moreira, P. Oliveira, B. Silva","doi":"10.18143/JISANH_V3I4_1422","DOIUrl":"https://doi.org/10.18143/JISANH_V3I4_1422","url":null,"abstract":"Europe has the highest proportion of older persons in the World. As population ages, it is imperative to find new strategies to avoid or counteract the effects of the incurable neurodegenerative diseases, which already represent a great financial and emotional burden for health care systems, patients, and their families. In this talk, Branca Silva (PhD) will discuss whether polyphenols obtained from diet or food supplements constitute an effective and low-cost strategy to prevent or treat neurodegeneration and neurotoxicity. Special focus will be given to the recent works of her research team about the beneficial effects to the brain of the regular consumption of white tea (Camellia sincensis L.) and its polyphenols. She will also highlight the safety, mechanisms of action, and the current and future relevance of polyphenols in the prevention and therapy of neurodegenerative disorders.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"72 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80189766","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_1464
C. Glorieux, J. M. Sandoval, N. Dejeans, P. Calderon
Alterations in antioxidant enzymes expression are associated with changes in cancer cell sensitivity to chemotherapeutic drugs. We investigated mechanisms of resistance to pro-oxidant drugs by using a model of oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). A genomic gain of the chromosomal band 16q22 was discovered in Resox cells as compared to parental breast cancer MCF-7 cells and normal human mammary epithelial 250MK cells. By using different pharmacological and genetic invalidation strategies we showed that 16q22-associated amplification of NAD(P)H:quinone oxidoreductase 1 (NQO1) gene was critical for Resox oxidative stress-resistance. Considering that NQO1 is frequently modified in tumor, at genomic or transcriptomic levels, we take advantage of this discover to explore NQO1 modulations roles in breast cancer chemosensitivity. Using different cellular models we found that NQO1 overexpression is a main determinant for the classical resistance, such as menadione and doxorubicin. This resistance was associated with an increased -lapachone, and inversely, conditions leading to the decrease of NQO1 activity trigger quinone- based chemotherapies-sensitivity. This places NQO1 modulations as a potential link between redox alterations in cancers and chemoresistance. Furthermore, this study underlines that the copy number alterations of NQO1 could be taken into account to specifically target breast tumors.
{"title":"Role of NAD(P)H:quinone oxidoreductase 1 polymorphism in breast cancer cell sensitivity to quinone-based chemotherapeutic agents","authors":"C. Glorieux, J. M. Sandoval, N. Dejeans, P. Calderon","doi":"10.18143/JISANH_V3I3_1464","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1464","url":null,"abstract":"Alterations in antioxidant enzymes expression are associated with changes in cancer cell sensitivity to chemotherapeutic drugs. We investigated mechanisms of resistance to pro-oxidant drugs by using a model of oxidative stress-resistant MCF-7 breast cancer cells (Resox cells). A genomic gain of the chromosomal band 16q22 was discovered in Resox cells as compared to parental breast cancer MCF-7 cells and normal human mammary epithelial 250MK cells. By using different pharmacological and genetic invalidation strategies we showed that 16q22-associated amplification of NAD(P)H:quinone oxidoreductase 1 (NQO1) gene was critical for Resox oxidative stress-resistance. Considering that NQO1 is frequently modified in tumor, at genomic or transcriptomic levels, we take advantage of this discover to explore NQO1 modulations roles in breast cancer chemosensitivity. Using different cellular models we found that NQO1 overexpression is a main determinant for the classical resistance, such as menadione and doxorubicin. This resistance was associated with an increased -lapachone, and inversely, conditions leading to the decrease of NQO1 activity trigger quinone- based chemotherapies-sensitivity. This places NQO1 modulations as a potential link between redox alterations in cancers and chemoresistance. Furthermore, this study underlines that the copy number alterations of NQO1 could be taken into account to specifically target breast tumors.","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":"78984974","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_1459
L. Châtre, M. Ricchetti
Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) do not just generate molecular stress but are also signalling molecules with regulatory functions. The nitroso-redox balance, which is the balance between ROS and RNS, plays a role in many intracellular functions including metabolism and mitochondrial activity. Antioxidant therapy is increasingly proposed to treat diseases associated with oxidative stress. However, nowadays, side effects of antioxidant treatments force to reconsider the beneficial therapeutic interest of this approach. Here, we show that antioxidant treatment poorly reverts cellular and mitochondrial defects from a human progeroid disease associated with altered nitroso-redox imbalance. Conversely, full reversion of the cellular and mitochondrial defects is achieved by reducing both ROS and RNS levels. Intriguingly, establishment of an appropriate nitroso-redox balance seems to play a major role in the correction of defects in progeroid cells than simply reducing the levels of these molecules. We will discuss the impact of such treatments on overexpression of proteases and impaired mitochondrial function and the opportunity to reconsider the use of different class of antioxidant molecules in the context of a progeroid dysfunction.
{"title":"RESPONSE TO ANTIOXIDANT THERAPY: IMPACT OF THE NITROSO-REDOX BALANCE IN RESTORING PROTEASES AND MITOCHONDRIAL FUNCTION IN A PROGEROID DISEASE","authors":"L. Châtre, M. Ricchetti","doi":"10.18143/JISANH_V3I3_1459","DOIUrl":"https://doi.org/10.18143/JISANH_V3I3_1459","url":null,"abstract":"Reactive Oxygen Species (ROS) and Reactive Nitrogen Species (RNS) do not just generate molecular stress but are also signalling molecules with regulatory functions. The nitroso-redox balance, which is the balance between ROS and RNS, plays a role in many intracellular functions including metabolism and mitochondrial activity. Antioxidant therapy is increasingly proposed to treat diseases associated with oxidative stress. However, nowadays, side effects of antioxidant treatments force to reconsider the beneficial therapeutic interest of this approach. Here, we show that antioxidant treatment poorly reverts cellular and mitochondrial defects from a human progeroid disease associated with altered nitroso-redox imbalance. Conversely, full reversion of the cellular and mitochondrial defects is achieved by reducing both ROS and RNS levels. Intriguingly, establishment of an appropriate nitroso-redox balance seems to play a major role in the correction of defects in progeroid cells than simply reducing the levels of these molecules.\u0000We will discuss the impact of such treatments on overexpression of proteases and impaired mitochondrial function and the opportunity to reconsider the use of different class of antioxidant molecules in the context of a progeroid dysfunction.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80351463","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_1440
G. Balla, László Potor, Z. Horváth, M. Nyitrai, J. Balla
In the pathogenesis of several vascular disorder modified proteins and lipids generated by reactive oxygen species accumulate in the vessel wall resulted in atherosclerosis, calcification, neovascularization. Since transition metals are also accumulating in these pathologies, generating continuous free radical stress. We suggested that the source of iron is heme derived from modified hemoglobin. Using in vitro cell culture models and human vessel samples, we proved, that heme is an efficient free radical catalyst, toxic for cell membranes and lipoproteins leading to vessel injury. Next we tested several heme proteins as potential origins for heme. We proved that the main heme donor is the modified hemoglobin after red blood cell hemolysis. Hemoglobin is not only heme donor, but the modified globin also plays a role in vessel pathologies. We do not know yet whether glycation of hemoglobin has an effect on hemeprotein mediated vessel wall injury.
{"title":"THE ROLE OF HEMOGLOBIN DERIVED HEME IN THE PATHOGENESIS OF VASCULAR DISORDERS","authors":"G. Balla, László Potor, Z. Horváth, M. Nyitrai, J. Balla","doi":"10.18143/JISANH_V3I2_1440","DOIUrl":"https://doi.org/10.18143/JISANH_V3I2_1440","url":null,"abstract":"In the pathogenesis of several vascular disorder modified proteins and lipids generated by reactive oxygen species accumulate in the vessel wall resulted in atherosclerosis, calcification, neovascularization. Since transition metals are also accumulating in these pathologies, generating continuous free radical stress. We suggested that the source of iron is heme derived from modified hemoglobin. Using in vitro cell culture models and human vessel samples, we proved, that heme is an efficient free radical catalyst, toxic for cell membranes and lipoproteins leading to vessel injury. Next we tested several heme proteins as potential origins for heme. We proved that the main heme donor is the modified hemoglobin after red blood cell hemolysis. Hemoglobin is not only heme donor, but the modified globin also plays a role in vessel pathologies. We do not know yet whether glycation of hemoglobin has an effect on hemeprotein mediated vessel wall injury.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86136816","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_1414
P. Porto-Figueira, J. Figueira, P. Jorge, J. Câmara
Polyphenols are widespread constituents of several foods matrices, including fruits, vegetables, cereals, olive and legumes, juices and beverages such as tea, coffee, beer and wine. Despite their wide distribution, the health effects of dietary polyphenols have come to the attention of nutritionists namely in recent years. The preventive effects of these secondary plant metabolites in terms of cardiovascular, neurodegenerative diseases and cancer are deduced from epidemiologic data as well as in vitro and in vivo studies. The selection of the proper analytical strategy for studying phenolics in food matrices depends on the purpose of the study as well as the nature of the sample and the target analyte. Conventional extraction techniques, as solid-phase extraction andor liquid-liquid extraction, represented for long time the gold standard for sample preparation. However, during the last decade, downstream analytical procedures evolved very significantly, making sample preparation a serious bottleneck in the analytical workflow. In this sense, extraction and characterization of dietary polyphenols will be explored as a case study to demonstrate how modern microextraction strategies solutions, as MEPS, m-SPEed and m-QuEChERS, are fostering the whole analytical workflow and performance. The potentialities of new sorbents and nanomaterials tailored for microextration of specific compounds will be also addressed.
{"title":"EXPLORING THE HIGH THROUGHPUT POTENTIAL OF MICROEXTRACTION TECHNIQUES FOR THE ISOLATION OF LOW-MOLECULAR WEIGHT POLYPHENOLS IN DIFFERENT FOOD MATRICES","authors":"P. Porto-Figueira, J. Figueira, P. Jorge, J. Câmara","doi":"10.18143/JISANH_V3I4_1414","DOIUrl":"https://doi.org/10.18143/JISANH_V3I4_1414","url":null,"abstract":"Polyphenols are widespread constituents of several foods matrices, including fruits, vegetables, cereals, olive and legumes, juices and beverages such as tea, coffee, beer and wine. Despite their wide distribution, the health effects of dietary polyphenols have come to the attention of nutritionists namely in recent years. The preventive effects of these secondary plant metabolites in terms of cardiovascular, neurodegenerative diseases and cancer are deduced from epidemiologic data as well as in vitro and in vivo studies.\u0000The selection of the proper analytical strategy for studying phenolics in food matrices depends on the purpose of the study as well as the nature of the sample and the target analyte. Conventional extraction techniques, as solid-phase extraction andor liquid-liquid extraction, represented for long time the gold standard for sample preparation. However, during the last decade, downstream analytical procedures evolved very significantly, making sample preparation a serious bottleneck in the analytical workflow.\u0000In this sense, extraction and characterization of dietary polyphenols will be explored as a case study to demonstrate how modern microextraction strategies solutions, as MEPS, m-SPEed and m-QuEChERS, are fostering the whole analytical workflow and performance. The potentialities of new sorbents and nanomaterials tailored for microextration of specific compounds will be also addressed.","PeriodicalId":17323,"journal":{"name":"Journal of the International Society of Antioxidants in Nutrition & Health","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2016-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75865717","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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