scholarly journals N-acetylcysteine in COPD: why, how, and when?

2016 ◽  
Vol 11 ◽  
Author(s):  
Claudio M. Sanguinetti
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Compounds ◽  
High Dose ◽  
Chinese Populations ◽  
Copd Patients ◽  
Short Period ◽  
Dose Oral ◽  
Low Dosage

Oxidants have long been recognized to have an important role in the pathogenesis of COPD, and in this cigarette smoke has a strong responsibility, because it generates a conspicuous amount of oxidant radicals able to modify the structure of the respiratory tract and to enhance several mechanisms that sustain lung inflammation in COPD. In fact, oxidative stress is highly increased in COPD and natural antioxidant capacities, mainly afforded by reduced glutathione, are often overcome. Thus an exogenous supplementation of antioxidant compounds is mandatory to at least partially counteract the oxidative stress. For this purpose N-acetylcysteine has great potentialities due to its capacity of directly contrasting oxidants with its free thiols, and to the possibility it has of acting as donor of cysteine precursors aimed at glutathione restoration. Many studies in vitro and in vivo have already demonstrated the antioxidant capacity of NAC. Many clinical studies have long been performed to explore the efficacy of NAC in COPD with altern results, especially when the drug was used at very low dosage and/or for a short period of time. More recently, several trials have been conducted to verify the appropriateness of using high-dose NAC in COPD, above all to decrease the exacerbations rate. The results have been encouraging, even if some of the data come from the most widely sized trials that have been conducted in Chinese populations. Although other evidence should be necessary to confirm the results in other populations of patients, high-dose oral NAC nevertheless offers interesting perspectives as add-on therapy for COPD patients.

scholarly journals The Zebrafish Embryo as a Model to Test Protective Effects of Food Antioxidant Compounds

Molecules ◽  
2021 ◽  
Vol 26 (19) ◽  
pp. 5786
Author(s):  
Cristina Arteaga ◽  
Nuria Boix ◽  
Elisabet Teixido ◽  
Fernanda Marizande ◽  
Santiago Cadena ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Zebrafish Embryo ◽  
In Vitro Assays ◽  
Antioxidant Compounds ◽  
Protective Effects ◽  
Tert Butyl Hydroperoxide ◽  
In Vivo Effects ◽  
Β Carotene

The antioxidant activity of food compounds is one of the properties generating the most interest, due to its health benefits and correlation with the prevention of chronic disease. This activity is usually measured using in vitro assays, which cannot predict in vivo effects or mechanisms of action. The objective of this study was to evaluate the in vivo protective effects of six phenolic compounds (naringenin, apigenin, rutin, oleuropein, chlorogenic acid, and curcumin) and three carotenoids (lycopene B, β-carotene, and astaxanthin) naturally present in foods using a zebrafish embryo model. The zebrafish embryo was pretreated with each of the nine antioxidant compounds and then exposed to tert-butyl hydroperoxide (tBOOH), a known inducer of oxidative stress in zebrafish. Significant differences were determined by comparing the concentration-response of the tBOOH induced lethality and dysmorphogenesis against the pretreated embryos with the antioxidant compounds. A protective effect of each compound, except β-carotene, against oxidative-stress-induced lethality was found. Furthermore, apigenin, rutin, and curcumin also showed protective effects against dysmorphogenesis. On the other hand, β-carotene exhibited increased lethality and dysmorphogenesis compared to the tBOOH treatment alone.

Transfer of mouse blastocysts exposed to ambient oxygen levels can lead to impaired lung development and redox balance

2019 ◽  
Vol 25 (11) ◽  
pp. 745-754
Author(s):  
Nedim Karagenç ◽  
Göksel Doğan ◽  
Kerem Esmen ◽  
Bengi Çınar Kul ◽  
Hasan Yeşilkaya ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Lung Development ◽  
Atmospheric Oxygen ◽  
Redox Balance ◽  
Perinatal Period ◽  
Altered Expression ◽  
Short Period

Abstract In vitro culture under atmospheric oxygen puts embryos under oxidative stress and impairs preimplantation development. However, to what extent this process alters the redox balance in the perinatal period remains largely unknown. The aim of the present study was to examine if the redox balance is altered in the lung tissue of fetuses generated through transfer of mouse embryos exposed to atmospheric oxygen at different stages of development and to determine if this has any effect on lung morphogenesis and gene expression. Two experimental groups (EGs) were generated by transferring in vitro- and in vivo-derived blastocysts to pseudo-pregnant females. In vivo-developed fetuses served as control. Enzymatic/nonenzymatic antioxidants, malondialdehyde (MDA) levels, total antioxidant capacity, stage of lung development and gene expression were evaluated on day 18 of pregnancy. Weight of fetuses was significantly less in both experimental cohorts (ANOVA, P < 0.001 versus control), associated with delayed lung development, higher amounts of MDA (ANOVA, P < 0.001 versus control) and altered expression of several genes in oxidative stress/damage pathways. Evidence gathered in the present study indicates that pre-implantation stress caused by culture under atmospheric oxygen, even for a short period of time, leads to fetal growth restriction, impaired lung development and redox balance along with dysregulation of several genes in oxidative stress response. Absence of an EG in which in vitro embryo culture was performed at 5% oxygen and the use of genetically heterogeneous F2 fetuses are the limitations of the study. In any case, the long-term impact of such dramatic changes in the developmental programming of resulting fetuses warrants further investigations.

scholarly journals In vitrofolate supplementation alleviates oxidative stress, mitochondria-associated death signalling and apoptosis induced by 7-ketocholesterol

2004 ◽  
Vol 92 (6) ◽  
pp. 887-894 ◽  
Author(s):  
R.-F. S. Huang ◽  
H.-C. Yaong ◽  
S.-C. Chen ◽  
Y.-F. Lu
Keyword(s):  
Oxidative Stress ◽  
Nuclear Dna ◽  
High Dose ◽  
Protective Effects ◽  
Folate Supplementation ◽  
Mitochondria Membrane Potential ◽  
Induced Apoptosis ◽  
Apoptotic Damage

Folate has recently been proposed as a new antioxidant. Folate supplementation may have a protective effect in counteracting oxidant-induced apoptotic damage. The present studies were undertaken to examine whether there is a direct link between folate levels, antioxidant capability and reduced apoptotic damage. Using anin vitrocellular model of 7-ketocholesterol (KC)-induced apoptosis, U937 cells were pre-cultured with a folate-deficient medium supplemented with various levels of folate (2–1500μmol/l) before treatment with 7-KC. Apoptotic markers, mitochondria-associated death signals and levels of reactive oxygen species were assayed. After treatment with 7-KC for 30h, low and high levels of folate supplementation significantly (P<0.05) reduced nuclear DNA loss. Only high levels of folate supplementation (>1000μmol/l) were effective in counteracting 7-KC-promoted apoptotic membrane phosphatidylserine exposure and DNA laddering. The attenuation of 7-KC-induced apoptotic damage by high-dose folate supplementation coincided with a partial normalization of mitochondria membrane potential dissipation, a suppression of cytochromecrelease and an inhibition of procaspase 3 activation. The prevention of mitochondrial dysfunctions and apoptotic processes was associated with antioxidant actions of high-dose folate by a marked scavenging of intracellular superoxide. Collectively, our present results demonstrate thatin vitrofolate supplementation exerts differentially protective effects against 7-KC-induced damage. High-dose supplementation alleviates oxidative stress, mitochondria-associated death signalling and apoptosis induced by 7-KC. However, thein vivorelevance is not clear and requires further study.

scholarly journals Antioxidant and Neuroprotective Properties of Eugenia dysenterica Leaves

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Douglas Vieira Thomaz ◽  
Luanna Fernandes Peixoto ◽  
Thiago Sardinha de Oliveira ◽  
James Oluwagbamigbe Fajemiroye ◽  
Hiasmin Franciely da Silva Neri ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Neuroprotective Effect ◽  
Antioxidant Properties ◽  
Electrode System ◽  
Antioxidant Compounds ◽  
Hydroalcoholic Extract ◽  
Markers Of Oxidative Stress ◽  
Eugenia Dysenterica

Eugenia dysenterica ex DC Mart. (Myrtaceae), popularly known as “cagaita,” is a Brazilian plant rich in polyphenols and other antioxidant compounds. Aiming to evaluate the potential use of cagaita in pathologies involving oxidative stress, such as neurodegenerative disorders, this study investigated its antioxidant potential and neuroprotective effect. Electrochemical approaches and aluminium-induced neurotoxicity were used to determine respectively in vitro and in vivo antioxidant properties of cagaita. Voltammetric experiments were carried out in a three-electrode system, whose working electrode consisted of glassy carbon. Male Swiss mice were administered with AlCl3 orally at a dose of 100 mg/kg/day and with cagaita leaf hydroalcoholic extract (CHE) at doses of 10, 100, and 300 mg/kg/day. The redox behavior of CHE presented similar features to that of quercetin, a widely known antioxidant standard. CHE prevented mouse memory impairment which resulted from aluminium intake. In addition, biochemical markers of oxidative stress (catalase, superoxide dismutase activity, and lipid peroxidation) were normalized by CHE treatment. The potential of CHE to prevent aluminium-induced neurotoxicity was reflected at the microscopic level, through the decrease of the number of eosinophilic necrosis phenotypes seen in treated groups. Moreover, the protective effect of CHE was similar to that of quercetin, which was taken as the standard. These findings showed that the CHE of cagaita leaves has a potential to protect the brain against oxidative-induced brain damage.

scholarly journals Effect of Nardostachys jatamansi DC. on Apoptosis, Inflammation and Oxidative Stress Induced by Doxorubicin in Wistar Rats

Plants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1579
Author(s):  
Mhaveer Singh ◽  
Mohammad Ahmed Khan ◽  
Kamal Y. T. ◽  
Javed Ahmad ◽  
Usama A. Fahmy ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Protective Action ◽  
Total Phenolic ◽  
High Dose ◽  
Cardiac Tissues ◽  
Nardostachys Jatamansi ◽  
Histopathological Evaluation

The study aimed to investigate the protective action of jatamansi (Nardostachys jatamansi DC.) against doxorubicin cardiotoxicity. Methanolic extract of jatamansi (MEJ) was prepared and standardized using HPTLC fingerprinting, GC-MS chemoprofiling, total phenolic content, and antioxidant activity in vitro. Further in vivo activity was evaluated using rodent model. Animals were divided into five groups (n = 6) namely control (CNT) (Normal saline), toxicant (TOX, without any treatment), MEJ at low dose (JAT1), MEJ at high dose (JAT2), and standard desferrioxamine (STD). All groups except control received doxorubicin 2.5 mg per Kg intra-peritoneally for 3 weeks in twice a week regimen. After 3 weeks, the blood samples and cardiac tissues were collected from all groups for biochemical and histopathological evaluation. Treatment with MEJ at both dose levels exhibited significant reduction (p < 0.001 vs. toxicant) of serum CK-MB (heart creatine kinase), LDH (Lactate dehydrogenase) & HMG-CoA (3-hydroxy-3-methylglutaryl-coenzyme A) levels, and tissue MDA (melondialdehyde) level; insignificant difference was observed (p > 0.05) in TNF-alpha (tumour necrosis factor), IL-6 (interleukine-6) levels and caspase activity as compared to TOX. Histopathological evaluation of cardiac tissues of different treatment groups further reinforced the findings of biochemical estimation. This study concludes that jatamansi can protect cardiac tissues from oxidative stress-induced cell injury and lipid peroxidation as well as against inflammatory and apoptotic effects on cardiac tissues.

scholarly journals N-Acetylcysteine for COVID-19: A Potential Adjuvant Therapy

2021 ◽  
Author(s):  
Mia Elhidsi ◽  
Fanny Fachrucha ◽  
Rizky Yudha Irawan
Keyword(s):  
Oxidative Stress ◽  
Older Patients ◽  
Distress Syndrome ◽  
Viral Infections ◽  
High Dose ◽  
Risk Of Falling ◽  
Early Evidence ◽  
And Oxidative Stress

Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV2) infection or known as coronavirus disease 2019 (COVID-19) is a highly infectious disease that has been declared as a world pandemic by WHO. Although the majority of patients only experience mild symptoms, older patients and those with comorbidities are in the risk of falling into critically ill and even death. This is thought to correlate with systemic inflammatory response and oxidative stress imbalance. N-acetylcysteine (NAC) is recognized as a potent mucolytic, yet its lesser-known function as an antioxidant is a precursor of glutathione. Basic aspects and either in vivo or in vitro studies showed various mechanisms of NAC acting as a counterbalance in viral infections and its role in decreasing inflammation and oxidative stress. High-dose NAC is reported to be effective as an antioxidant in pneumonia, influenza, sepsis, and acute respiratory distress syndrome. Early evidence in COVID-19 patients showed that NAC could be beneficial. This review gives the scientific background in considering NAC as an adjuvant treatment for COVID-19.

Abstract P236: Organofluorine Hydrazones Preventing Oxidant Stress In An In Vitro Model Of Preeclampsia

Hypertension ◽  
2021 ◽  
Vol 78 (Suppl_1) ◽  
Author(s):  
Zsuzsanna K Zsengeller ◽  
Maxim Mastyugin ◽  
Agnes Lo ◽  
Saira Salahuddin ◽  
Ananth Karumanchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Oxidant Stress ◽  
Antioxidant Compounds ◽  
Placental Development ◽  
Human Trophoblast ◽  
Specific Syndrome ◽  
Key Factor

Background: Preeclampsia (PE) is a pregnancy-specific syndrome affecting 5-7% of all pregnant women, and there is no effective treatment available. Early abnormal placental development is associated with oxidative stress and the release of reactive oxygen species in the placenta. This phenomenon leads to downstream signaling and production of anti-angiogenic factors, which cause endothelial and trophoblast dysfunction and the cardinal features of PE, i.e., hypertension, proteinuria, and in severe cases, eclampsia. Our group developed a novel series of mitochondria-targeted antioxidants and sought to test if these compounds can effectively reduce placental oxidative stress and mitigate PE symptoms in vitro. Methods: We induced in vitro oxidant stress in human trophoblast (HTR8/SVneo) cells with hydrogen peroxide (H 2 O 2 ) and assessed whether augmenting cell-redox function with the proposed antioxidant compounds reduced (i) cell injury (cell cytotoxicity assay), (ii) mitochondrial stress (mitochondrial -derived superoxide production, mitochondria dysfunction) (iii) production of the transcription factor HIF1A and (iv) downstream anti-angiogenic responses (sFLT1 production). These effects were compared with the antioxidants - NAC, Vit E and MitoQ. Results: In our cell-based assays, pretreatment with the hydrazone compounds reduced mitochondrial-derived ROS production in H 2 O 2 -exposed trophoblasts cells, indicating that the key factor in the development of PE, the oxidant stress, can be alleviated by the antioxidant hydrazones. The most effective of these compounds, HY12 also reduced HIF-1A expression and sFLT1 protein expression H 2 O 2 -exposed HTR8 cells. Furthermore, the antioxidant hydrazones improved the mitochondrial electron chain enzyme activity in the stressed HTR8 cells, which is another promising characteristic of the applied hydrazones. Conclusion: In reducing placental trophoblast oxidative stress, hydrazone-based antioxidants present a potential novel therapeutic approach for the treatment of preeclampsia. Future investigation is warranted regarding the in vivo use of these compounds.

scholarly journals Dipeptide YA is Responsible for the Positive Effect of Oyster Hydrolysates on Alcohol Metabolism in Single Ethanol Binge Rodent Models

Marine Drugs ◽  
2020 ◽  
Vol 18 (10) ◽  
pp. 512
Author(s):  
Adrian S. Siregar ◽  
Marie Merci Nyiramana ◽  
Eun-Jin Kim ◽  
Eui-Jung Shin ◽  
Min Seok Woo ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Damage ◽  
Inflammatory Mediators ◽  
Liver Toxicity ◽  
High Dose ◽  
Alcohol Metabolism ◽  
Single High Dose ◽  
Anti Inflammatory

Accumulative alcohol hangovers cause liver damage through oxidative and inflammatory stress. Numerous antioxidant and anti-inflammatory reagents have been developed to reduce alcohol hangovers, but these reagents are still insignificant and have limitations in that they can cause liver toxicity. Oyster hydrolysate (OH), another reagent that has antioxidant and anti-inflammatory activity, is a product extracted through an enzymatic hydrolysis process from oysters (Crassostrea gigas), which can be easily eaten in meals. This study was aimed at determining the effects of OH on alcohol metabolism, using a single high dose of ethanol (EtOH) administered to rodents, by monitoring alcohol metabolic enzymes, oxidative stress signals, and inflammatory mediators. The effect of tyrosine-alanine (YA) peptide, a main component of OH, on EtOH metabolism was also identified. In vitro experiments showed that OH pretreatment inhibited EtOH-induced cell death, oxidative stress, and inflammation in liver cells and macrophages. In vivo experiments showed that OH and YA pre-administration increased alcohol dehydrogenase, aldehyde dehydrogenase, and catalase activity in EtOH binge treatment. In addition, OH pre-administration alleviated CYP2E1 activity, ROS production, apoptotic signals, and inflammatory mediators in liver tissues. These results showed that OH and YA enhanced EtOH metabolism and had a protective effect against acute alcohol liver damage. Our findings offer new insights into a single high dose of EtOH drinking and suggest that OH and YA could be used as potential marine functional foods to prevent acute alcohol-induced liver damage.

scholarly journals Modulation and Protection Effects of Antioxidant Compounds against Oxidant Induced Developmental Toxicity in Zebrafish

Antioxidants ◽  
2020 ◽  
Vol 9 (8) ◽  
pp. 721
Author(s):  
Nuria Boix ◽  
Elisabet Teixido ◽  
Ester Pique ◽  
Juan Maria Llobet ◽  
Jesus Gomez-Catalan
Keyword(s):  
Oxidative Stress ◽  
Developmental Toxicity ◽  
Experimental System ◽  
In Vitro Assays ◽  
Antioxidant Compounds ◽  
Protective Effects ◽  
Response Curves ◽  
Zebrafish Model

The antioxidant effect of compounds is regularly evaluated by in vitro assays that do not have the capability to predict in vivo protective activity or to determine their underlying mechanisms of action. The aim of this study was to develop an experimental system to evaluate the in vivo protective effects of different antioxidant compounds, based on the zebrafish embryo test. Zebrafish embryos were exposed to tert-butyl hydroperoxide (tBOOH), tetrachlorohydroquinone (TCHQ) and lipopolysaccharides from Escherichia coli (LPS), chemicals that are known inducers of oxidative stress in zebrafish. The developmental toxic effects (lethality or dysmorphogenesis) induced by these chemicals were modulated with n-acetyl l-cysteine and Nω-nitro l-arginine methyl ester hydrochloride, dimethyl maleate and dl-buthionine sulfoximine in order to validate the oxidant mechanism of oxidative stress inducers. The oxidant effects of tBOOH, TCHQ, and LPS were confirmed by the determination of significant differences in the comparison between the concentration–response curves of the oxidative stress inducers and of the modulators of antioxidant status. This concept was also applied to the study of the effects of well-known antioxidants, such as vitamin E, quercetin, and lipoic acid. Our results confirm the zebrafish model as an in vivo useful tool to test the protective effects of antioxidant compounds.

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