scholarly journals Zinc Nutritional Status on Physiological and Nutritional Indicators, Metabolism of Oxidative Stress, Yield and Fruit Quality of Pecan Tree

2018 ◽  
Vol 47 (2) ◽  
pp. 531-537
Author(s):  
Damaris OJEDA-BARRIOS ◽  
Jorge CASTILLO-GONZALEZ ◽  
Adriana HERNANDEZ-RODRIGUEZ ◽  
Javier ABADIA ◽  
Estaban SANCHEZ ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Nutritional Status ◽  
Zinc Deficiency ◽  
Fruit Quality ◽  
Reactive Oxygen ◽  
The United States ◽  
Oxygen Species

In the United States of America and in Mexico, zinc deficiency is a common nutritional disorder in pecan trees [Carya illinoinensis (Wangenh.) C. Koch], especially in calcareous soils. This study in Chihuahua, northern Mexico, analyses the effects of zinc nutritional status on various physiological and nutritional indicators, on the metabolism of oxidative stress, and on the yield and fruit quality of pecan. The aim was to identify possible bioindicators of soil zinc deficiency. The experimental design was completely randomized with four nutritional conditions with respect to zinc: a control and three levels of zinc deficiency - slight, moderate and severe. Zinc deficiency is characterised by small leaves with interveinal necrosis and rippled leaf margins. The lowest values of leaf area, SPAD values, total N and NO3 concentration were observed under conditions of severe zinc deficiency. With worsening zinc deficiency, results indicate an increased enzymatic activity of superoxide dismutase, catalase and glutathione peroxidase. Interestingly, under severe zinc deficiency there are decreases in trunk cross-sectional area growth, in yield and in percentage kernel. Increased activity of superoxide dismutase, catalase and peroxidase enzymes is associated with detoxification of reactive oxygen species. The activity of enzymes detoxifying reactive oxygen species lessens the negative effects of zinc deficiency stress, and may be good bioindicators of zinc deficiency and its visual symptoms on pecan trees.

Detection of oxidative stress induced by calcium phosphate bions in human arterial endothelial cells

2021 ◽  
pp. 70-78
Author(s):  
А.Г. Кутихин ◽  
Д.К. Шишкова ◽  
Р.А. Мухамадияров ◽  
Е.А. Великанова
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Endothelial Cells ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Calcium Phosphate ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Bafilomycin A1 ◽  
Arterial Endothelial Cells

Введение. Кальций-фосфатные бионы (КФБ) формируются в организме человека при перенасыщении сыворотки ионами кальция и фосфора и вызывают дисфункцию эндотелия, однако молекулярные механизмы нарушения функционирования эндотелия при воздействии КФБ не ясны. Цель исследования - выяснение роли кальций-фосфатных бионов различной формы в развитии окислительного стресса в артериальных эндотелиальных клетках (ЭК) человека. Методика. Для детекции окислительного стресса к конфлюэнтным культурам первичных ЭК коронарной и внутренней грудной артерии человека добавляли равные концентрации КФБ сферической или игольчатой формы (СКФБ и ИКФБ соответственно) с последующим культивированием в течение 1 и 4 ч, добавлением флюоресцентных индикаторов окислительного стресса MitoSOX Red и CellROX Green и конфокальной микроскопией. Измеряли концентрацию продуктов перекисного окисления липидов в культуральной жидкости через 24 ч экспозиции эндотелиальных клеток КФБ. Анализ нейтрализации цитотоксических эффектов перекисного окисления липидов проводили путем добавления к ЭК супероксиддисмутазы и каталазы на 4 или 24 ч (одновременно с КФБ). Для сравнения механизмов клеточной гибели при воздействии СКФБ и ИКФБ анализировали цитотоксичность обоих типов бионов при одновременном воздействии лизосомального ингибитора бафиломицина А1. Результаты. Значимого увеличения генерации активных форм кислорода (АФК) в результате экспозиции СКФБ (независимо от линии ЭК и продолжительности экспозиции) не было выявлено. В то же время наблюдалось повышение генерации супероксида через 4 ч, а иных свободных радикалов через 1 ч после добавления ИКФБ к ЭК. Предварительная нейтрализация АФК супероксиддисмутазой и каталазой частично защищала ЭК от индуцируемой ИКФБ гибели. При этом добавление бафиломицина А1 к ЭК частично защищало их от гибели только при воздействии СКФБ, но не ИКФБ. Заключение. Гибель ЭК при воздействии СКФБ происходит в результате первичного повреждения лизосом, а при воздействии ИКФБ - в первую очередь вследствие окислительного стресса. Background. Calcium phosphate bions (CPB) form in the human blood upon its supersaturation with calcium and phosphate and provoke endothelial dysfunction; however, the molecular mechanisms of these pathological processes remain unclear. Aim. To elucidate the role of differently shaped CPBs in induction of oxidative stress in human arterial endothelial cells (Ecs). Methods. For detection of oxidative stress, equal concentrations of spherical CPB (CPB-S) or needle-shaped CPB (CPB-N) were added to confluent cultures of primary human coronary artery and internal thoracic artery ECs for 1 and 4 h; this was followed by MitoSOX Red and CellROX Green staining and subsequent confocal microscopy. Concentration of thiobarbituric acid-reactive substances was measured in the EC culture supernatant at 24 h of the CPB exposure. The lipid peroxidation cytotoxicity was neutralized by adding superoxide dismutase and catalase to ECs for 4 or 24 h. To compare cell death subroutines induced by CPB-S and CPB-N, the effect of bafilomycin A1, a lysosomal inhibitor, on CRB cytotoxicity was studied. Results. No increase in reactive oxygen species generation was observed in the CPB-S exposure, regardless of the EC line and exposure duration. However, addition of CPB-N to ECs increased the production of superoxide and other free radicals after four- and one-hour exposure, respectively. Prior neutralization of reactive oxygen species with superoxide dismutase and catalase partially protected ECs from CPB-N- but not CPB-S-induced death while bafilomycin A1, vice versa, protected ECs from CPB-S- but not CPB-N-induced death. Conclusion. CPB-S cause cell death due to primary damage of lysosomes whereas CPB-N induce apoptosis due to oxidative stress.

184 Effects of cyanidin supplementation on invitro maturation of pig oocytes

2020 ◽  
Vol 32 (2) ◽  
pp. 220
Author(s):  
E. Hicks ◽  
M. Mentler ◽  
B. D. Whitaker
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Oocyte Maturation ◽  
Catalase Activity ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Enzyme Mechanisms ◽  
Maturation Medium

Oxidative stress can have a negative effect on oocyte maturation during invitro production of pig embryos. Imbalance of reactive oxygen species and antioxidant levels can affect the progression of oocyte maturation up to the point of fertilization. Antioxidants are effective in maintaining more ideal reactive oxygen species levels, which help to protect oocytes from potential harmful effects of oxidative stress. Berries from the elder plant (Sambucus sp.) contain high levels of a broad spectrum of antioxidants. One of these antioxidants, cyanidin, when supplemented to maturation medium at 100μM concentrations, reduces reactive oxygen species formation and improves IVF and early embryonic development in pigs. However, changes in the enzyme mechanisms of action during oocyte maturation due to cyanidin supplementation are unknown. Therefore, the objective of this study was to characterise the intracellular oocyte enzyme mechanisms between oocytes supplemented with 100μM cyanidin during 40 to 44h of maturation (n=600) and oocytes without supplementation of cyanidin during maturation (n=558). At the end of maturation, oocytes were evaluated for either glutathione peroxidase (n=300), catalase (n=564), or superoxide dismutase (n=294) activities. Glutathione peroxidase activity was determined by following the rate of NADPH oxidation, catalase activity was determined by following the rate of hydrogen peroxide decomposition, and superoxide dismutase activity was determined by following the reduction rate of cytochrome c, utilising the xanthine-xanthine oxidase system. Data were analysed using ANOVA and Tukey's test. There were no significant differences between oocytes matured with 100μM cyanidin and those that were not when comparing glutathione peroxidase and superoxide dismutase activities. Supplementation of 100μM cyanidin to maturation medium increased (P<0.05) catalase activity in oocytes (0.78±0.15 units/oocyte) compared with no cyanidin supplementation (0.14±0.11 units/oocyte). These results indicate that supplementing 100μM cyanidin to the maturation medium of pig oocytes could reduce the negative effects of oxidative stress by increasing intracellular catalase activity during oocyte maturation.

scholarly journals The effect of acrylamide on sperm oxidative stress, total antioxidant levels, tyrosine phosphorylation, and carboxymethyl-lysine expression: A laboratory study

2021 ◽  
Author(s):  
Mojdeh Hosseinpoor Kashani ◽  
Mina Ramezani ◽  
Zeinab Piravar
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Tyrosine Phosphorylation ◽  
Laboratory Study ◽  
Reactive Oxygen Species Generation ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Total Antioxidant ◽  
Carboxymethyl Lysine

Background: Acrylamide (AA) is a reactive molecule produced during food processing at temperatures above 120°C. Objective: To evaluate the impact of different concentrations of AA on human sperm parameters, oxidative stress and total antioxidant capacity (TAC). Materials and Methods: In this laboratory study, semen samples were obtained from healthy donors referred to the Taleghani Hospital, Tehran, Iran between June and July 2019. Samples were divided into four groups (n = 10/each): one control and three treatment groups (0.5, 1, and 2 mM of AA). After 2 hr of exposure to AA, the superoxide dismutase and malondialdehyde levels were measured based on colorimetric methods. The TAC was determined by the ferric-reducing antioxidant power assay. Flow cytometry was performed to measure the intracellular reactive oxygen species generation. Also, immunohistochemistry was done to determine the effect of AA on tyrosine phosphorylation and carboxymethyl-lysine expression. Results: Results of the study demonstrated that the motility and viability of spermatozoa were significantly decreased after AA exposure (p < 0.001). This decrease was also seen in the TAC and superoxide dismutase activity as well as in the phosphotyrosine percentage compared with the control (p < 0.01). However, the carboxymethyllysine and prooxidant activity including reactive oxygen species generation and lipid peroxidation level increased (p < 0.001). Conclusion: Overall, the results confirmed the detrimental effect of AA on human spermatozoa which may be due to oxidative stress and decreased total antioxidant levels. AA may reduce fertility by reducing sperm capacitation and motility. Key words: Acrylamide, Oxidative stress, Antioxidant, Spermatozoa, Infertility.

scholarly journals Oxymatrine Ameliorates Doxorubicin-Induced Cardiotoxicity in Rats

2017 ◽  
Vol 43 (2) ◽  
pp. 626-635 ◽  
Author(s):  
Yan-Yan Zhang ◽  
Minhan Yi ◽  
Yong-Pan Huang
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
H9c2 Cells ◽  
Western Blots ◽  
Creatine Kinase Mb ◽  
Commercial Kits

Background/Aims: Doxorubicin-induced cardiac toxicity has been a major concern of oncologists and is considered the main restriction on its clinical application. Oxymatrine has shown potent anti-cancer, anti-fibrosis, and anti-oxidative effects. Recently, it has been reported that oxymatrine is protective against some cardiovascular diseases. In this study, we aimed to investigate the effects of oxymatrine on doxorubicin-induced cardiotoxicity in rat hearts and H9c2 cells. Methods: Creatine Kinase - MB (CK-MB) and Lactate Dehydrogenase (LDH) levels were determined using commercial kits. Biochemical indices reflecting oxidative stress, such as catalase (CAT), malonyldialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were also analyzed with commercial kits. Mitochondrial reactive oxygen species (ROS) 2’,7’-dichlorofluorescin diacetate (DCFH-DA) was measured by fluorescence microscopy. Histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. Western blots were used to detect the level of expression of cleaved caspase-3. Results: Doxorubicin treatment significantly increased oxidative stress levels, as indicated by catalase, malonyldialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen species. Doxorubicin also increased pathological damage in myocardial tissue, myocardial ROS levels, and malonyldialdehyde levels, and induced apoptosis in myocardial tissues and H9c2 cells. All of these doxorubicin-induced effects were attenuated by oxymatrine. Conclusion: These in vitro and in vivo findings indicate that oxymatrine may be a promising cardioprotective agent against doxorubicin-induced cardiotoxicity, at least in part mediated through oxymatrine’s inhibition of cardiac apoptosis and oxidative stress.

Comparative effects of pitavastatin and probucol on oxidative stress, Cu/Zn superoxide dismutase, PPAR-γ, and aortic stiffness in hypercholesterolemia

2006 ◽  
Vol 291 (5) ◽  
pp. H2522-H2532 ◽  
Author(s):  
Kyoko Umeji ◽  
Seiji Umemoto ◽  
Shinichi Itoh ◽  
Masakazu Tanaka ◽  
Shinji Kawahara ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Oxidase Activity ◽  
Aortic Stiffness ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Ppar Γ ◽  
Expression And Activity

Reactive oxygen species-scavenging enzyme Cu/Zn superoxide dismutase (SOD) regulated by peroxisome proliferator-activated receptors (PPARs) plays an important role in vascular responsiveness. However, it remains unknown whether statin restores vascular dysfunction through the activation of reactive oxygen species-scavenging enzymes in vivo. We hypothesized that pitavastatin restores vascular function by modulating oxidative stress through the activation of Cu/ZnSOD and PPAR-γ in hypercholesterolemia. New Zealand White male rabbits were fed either normal chow or a 1% cholesterol (CHO) diet for 14 wk. After the first 7 wk, the CHO-fed rabbits were further divided into three groups: those fed with CHO feed only (HC), those additionally given pitavastatin, and those additionally given an antioxidant, probucol. The extent of atherosclerosis was assessed by examining aortic stiffness. When compared with the HC group, both the pitavastatin and probucol groups showed improved aortic stiffness by reducing aortic levels of reactive oxidative stress, nitrotyrosine, and collagen, without affecting serum cholesterol or blood pressure levels. Pitavastatin restored both Cu/ZnSOD activity ( P < 0.005) and PPAR-γ expression and activity ( P < 0.01) and inhibited NAD(P)H oxidase activity ( P < 0.0001) in the aorta, whereas probucol inhibited NAD(P)H oxidase activity more than did pitavastatin ( P < 0.0005) without affecting Cu/ZnSOD activity or PPAR-γ expression and activity. Importantly, Cu/ZnSOD activity was positively correlated with the PPAR-γ activity in the aorta ( P < 0.005), both of which were negatively correlated with aortic stiffness ( P < 0.05). Vascular Cu/ZnSOD and PPAR-γ may play a crucial role in the antiatherogenic effects of pitavastatin in hypercholesterolemia in vivo.

93 EFFECT OF ANTIOXIDANTS SUPPLEMENTATION ON THE QUALITY OF CRYOPRESERVED SPERM OF DOGS

2011 ◽  
Vol 23 (1) ◽  
pp. 152
Author(s):  
C. A. B. Sobrinho ◽  
M. Nichi ◽  
P. A. A. Góes ◽  
A. Dalmazzo ◽  
S. E. Crusco ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Vitamin E ◽  
Reactive Oxygen ◽  
The Other ◽  
Mitochondrial Activity ◽  
Enzymatic Antioxidants ◽  
Oxygen Species ◽  
Intact Membrane

One of the main causes of poor quality of frozen–thawed dog sperm is oxidative stress (i.e. higher production of reactive oxygen species not compensated by improved antioxidant protection). This event is known to impair sperm functionality by attacking plasma membrane, acrosome, mitochondria, and DNA. Spermatozoa are particularly susceptible the oxidative stress, mainly due to the reduced cytoplasm and the high content of polyunsaturated fatty acids (PUFA) in the membrane, which allows the spermatozoa to be motile and confers a higher resistance against the damages caused by cryopreservation, but makes the sperm more susceptible to the attack of the reactive oxygen species (ROS). The present study aimed to evaluate the effects of antioxidant supplementation on semen extender (Tris-egg yolk-citrate-glicerol) with glutathione (GSH) and vitamin E on the quality of cryopreserved dog sperm. Ejaculates of 12 dogs were divided in pools of 3 ejaculates with at least 70% of motility. Each pool was diluted with 7 different extenders for treatment groups as follows: control, vitamin E (1, 5, and 10 mM), and reduced glutathione (GSH; 1, 5, and 10 mM) and submitted to cryopreservation. Samples were thawed (37°C/30′) and evaluated for motility, vigor, percentage of sperm showing intact membrane (eosin/nigrosin), and acrosome (simple stain fast-green and bengal rose), mitochondrial activity (3–3′-diaminobenzidine-DAB), and sperm susceptibility to oxidative stress (TBARS). Statistical analyses were performed using the SAS system for Windows (SAS Institute Inc., Cary, NC, USA; least significant differences test and Spearman correlation; P < 0.05). Samples treated with 1 mM of GSH showed a higher percentage of sperm with intact membrane when compared with the control (11.21 ± 2.84 and 6.21 ± 1.16%, respectively; P < 0.05). On the other hand, treatment with 5 mM of GSH showed better results regarding mitochondrial activity. Vitamin E supplementation also played a protective role on mitochondrial activity; samples treated with 1 mM showed a lower percentage of DAB III sperm (cells with severely compromised mitochondrial activity) when compared with the control group (5.61 ± 0.7 and 8.62 ± 1.05%, respectively; P < 0.05). Both vitamin E and GSH are important non-enzymatic antioxidants responsible for the destruction of the hydroxyl radical. Despite the positive influence of these antioxidants on mitochondrial status, no effect was found on the other variables studied. These results indicate that the action of both antioxidants in dog sperm would be mainly intracellular. Furthermore, other ROS could be responsible for the other damages caused by cryopreservation on the other sperm functionalities (i.e. membrane, acrosome, DNA, oxidative status). Therefore, the use of a combination of enzymatic and non-enzymatic antioxidants could be an alternative to overcome the deleterious influence of oxidative stress in cryopreserved semen of dogs. The authors thank the Brazilian army for the dogs used in this study.

139 Effect of lycopene supplementation in maturation medium on production of reactive oxygen species and post-vitrification quality of bovine blastocysts

2021 ◽  
Vol 33 (2) ◽  
pp. 177
Author(s):  
S. Sidi ◽  
O. B. Pascottini ◽  
D. Angel-Velez ◽  
N. A. Dolatabad ◽  
G. Residiwati ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Oocyte Maturation ◽  
Embryo Quality ◽  
Reactive Oxygen ◽  
Quality Parameters ◽  
Differential Staining ◽  
Oxygen Species ◽  
Fluorescent Intensity

Excessive production and accumulation of reactive oxygen species (ROS) may cause embryo damage associated with oxidative stress. Lycopene, a natural antioxidant, can scavenge singlet oxygen and is one of the most effective antioxidants among carotenoids. We evaluated the effects of supplementation of lycopene (antioxidant), menadione (prooxidant), and their combination during invitro oocyte maturation on ROS generation in matured oocytes and the quality of vitrified-warmed embryos. Cumulus–oocyte complexes, collected from the slaughterhouse, were matured in groups of 60 in 500μL of TCM-199 medium+50mg mL−1 gentamycin+20ng mL−1 epidermal growth factor, for 22h at 38.5°C in 5% CO2 in air and then supplemented with (1) 0.2μM lycopene, (2) 5μM menadione, (3) 0.2μM lycopene+5μM menadione (L+M), or (4) not supplemented (control). Fertilization and embryo culture were performed similarly for all the groups. In the first experiment, ROS measurement (n=236; via fluorescent microscopy) was performed in denuded, matured oocytes incubated in 5μM CellROX® Green (ThermoFisher Scientific) for 1h. Fluorescent intensity was measured in Image-J. In the second experiment, embryos in the blastocyst stage (n=143) were vitrified as previously described by Ortiz-Escribano et al. (2017 Biol. Reprod. 96, 288-301). Vitrified blastocysts were then warmed and washed in decreasing concentrations of sucrose and incubated for 2 days in culture medium [50µL of synthetic oviductal fluid (SOF)+(5g mL−1 insulin, 5g mL−1 transferrin, 5ng mL−1 selenium)]. The quality of vitrified-warmed blastocysts was assessed using a differential staining as described by Wydooghe et al. (2011 Anal. Biochem. 416, 228–230). The effects of pro- and antioxidant supplementation on oocyte fluorescent intensity and embryo quality parameters were fitted in linear mixed-effects models, and results are expressed as least squares means and standard errors. The fluorescent intensity for ROS was lower (P&lt;0.05) in lycopene (10.06±2.92) than in menadione (16.8±2.92). No differences (P&gt;0.05) in ROS intensity values were found among the other groups [control (13.5±2.92) and L+M (13.7±2.90)]. Total cell number (TCN) was similar (P&gt;0.05) in lycopene (153±2.95), L+M (143±4.59), and control (145±3.67) but lower (P&lt;0.05) in menadione (134±6.08). Lesser numbers of apoptotic cells (AC) and AC/TCN values (P&lt;0.05) were recorded in lycopene (4.12±3.07 and 2.71±2.21) compared with control (6.18±3.82 and 4.31±2.75), L+M (6.00±4.79 and 4.22±3.45), and menadione (7.75±6.33 and 5.82±4.56). For the remaining embryo quality parameters, no differences were found (P&gt;0.05). In conclusion, lycopene supplementation during invitro oocyte maturation effectively scavenged free radicals, lowering oxidative stress and improving embryo quality post-vitrification and warming.

Clinical aspects of reactive oxygen and nitrogen species

2004 ◽  
Vol 71 ◽  
pp. 121-133 ◽  
Author(s):  
Ascan Warnholtz ◽  
Maria Wendt ◽  
Michael August ◽  
Thomas Münzel
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Risk Factor ◽  
Endothelial Dysfunction ◽  
Vascular Tissue ◽  
Rapid Development ◽  
Reactive Oxygen ◽  
Clinical Aspects ◽  
No Production ◽  
Oxygen Species

Endothelial dysfunction in the setting of cardiovascular risk factors, such as hypercholesterolaemia, hypertension, diabetes mellitus and chronic smoking, as well as in the setting of heart failure, has been shown to be at least partly dependent on the production of reactive oxygen species in endothelial and/or smooth muscle cells and the adventitia, and the subsequent decrease in vascular bioavailability of NO. Superoxide-producing enzymes involved in increased oxidative stress within vascular tissue include NAD(P)H-oxidase, xanthine oxidase and endothelial nitric oxide synthase in an uncoupled state. Recent studies indicate that endothelial dysfunction of peripheral and coronary resistance and conductance vessels represents a strong and independent risk factor for future cardiovascular events. Ways to reduce endothelial dysfunction include risk-factor modification and treatment with substances that have been shown to reduce oxidative stress and, simultaneously, to stimulate endothelial NO production, such as inhibitors of angiotensin-converting enzyme or the statins. In contrast, in conditions where increased production of reactive oxygen species, such as superoxide, in vascular tissue is established, treatment with NO, e.g. via administration of nitroglycerin, results in a rapid development of endothelial dysfunction, which may worsen the prognosis in patients with established coronary artery disease.

scholarly journals 4-Hydroxychalcone Induces Cell Death via Oxidative Stress in MYCN-Amplified Human Neuroblastoma Cells

2019 ◽  
Vol 2019 ◽  
pp. 1-16 ◽  
Author(s):  
Amnah M. Alshangiti ◽  
Eszter Tuboly ◽  
Shane V. Hegarty ◽  
Cathal M. McCarthy ◽  
Aideen M. Sullivan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Cell Death ◽  
Cytotoxic Effect ◽  
Neuroblastoma Cells ◽  
Reactive Oxygen ◽  
Prognostic Indicator ◽  
Oxygen Species ◽  
Human Neuroblastoma Cells ◽  
Human Neuroblastoma

Neuroblastoma is an embryonal malignancy that arises from cells of sympathoadrenal lineage during the development of the nervous system. It is the most common pediatric extracranial solid tumor and is responsible for 15% of childhood deaths from cancer. Fifty percent of cases are diagnosed as high-risk metastatic disease with a low overall 5-year survival rate. More than half of patients experience disease recurrence that can be refractory to treatment. Amplification of the MYCN gene is an important prognostic indicator that is associated with rapid disease progression and a poor prognosis, highlighting the need for new therapeutic approaches. In recent years, there has been an increasing focus on identifying anticancer properties of naturally occurring chalcones, which are secondary metabolites with variable phenolic structures. Here, we report that 4-hydroxychalcone is a potent cytotoxin for MYCN-amplified IMR-32 and SK-N-BE (2) neuroblastoma cells, when compared to non-MYCN-amplified SH-SY5Y neuroblastoma cells and to the non-neuroblastoma human embryonic kidney cell line, HEK293t. Moreover, 4-hydroxychalcone treatment significantly decreased cellular levels of the antioxidant glutathione and increased cellular reactive oxygen species. In addition, 4-hydroxychalcone treatment led to impairments in mitochondrial respiratory function, compared to controls. In support of this, the cytotoxic effect of 4-hydroxychalcone was prevented by co-treatment with either the antioxidant N-acetyl-L-cysteine, a pharmacological inhibitor of oxidative stress-induced cell death (IM-54) or the mitochondrial reactive oxygen species scavenger, Mito-TEMPO. When combined with the anticancer drugs cisplatin or doxorubicin, 4-hydroxychalcone led to greater reductions in cell viability than was induced by either anti-cancer agent alone. In summary, this study identifies a cytotoxic effect of 4-hydroxychalcone in MYCN-amplified human neuroblastoma cells, which rationalizes its further study in the development of new therapies for pediatric neuroblastoma.

scholarly journals Protective Effects of Gintonin on Reactive Oxygen Species-Induced HT22 Cell Damages: Involvement of LPA1 Receptor-BDNF-AKT Signaling Pathway

Molecules ◽  
2021 ◽  
Vol 26 (14) ◽  
pp. 4138
Author(s):  
Yeon-Jin Cho ◽  
Sun-Hye Choi ◽  
Ra-Mi Lee ◽  
Han-Sung Cho ◽  
Hyewhon Rhim ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Signaling Pathway ◽  
Reactive Oxygen ◽  
Akt Signaling ◽  
Atp Depletion ◽  
Oxygen Species ◽  
Akt Signaling Pathway ◽  
Neuroprotective Effects ◽  
Lpa1 Receptor

Gintonin is a kind of ginseng-derived glycolipoprotein that acts as an exogenous LPA receptor ligand. Gintonin has in vitro and in vivo neuroprotective effects; however, little is known about the cellular mechanisms underlying the neuroprotection. In the present study, we aimed to clarify how gintonin attenuates iodoacetic acid (IAA)-induced oxidative stress. The mouse hippocampal cell line HT22 was used. Gintonin treatment significantly attenuated IAA-induced reactive oxygen species (ROS) overproduction, ATP depletion, and cell death. However, treatment with Ki16425, an LPA1/3 receptor antagonist, suppressed the neuroprotective effects of gintonin. Gintonin elicited [Ca2⁺]i transients in HT22 cells. Gintonin-mediated [Ca2⁺]i transients through the LPA1 receptor-PLC-IP3 signaling pathway were coupled to increase both the expression and release of BDNF. The released BDNF activated the TrkB receptor. Induction of TrkB phosphorylation was further linked to Akt activation. Phosphorylated Akt reduced IAA-induced oxidative stress and increased cell survival. Our results indicate that gintonin attenuated IAA-induced oxidative stress in neuronal cells by activating the LPA1 receptor-BDNF-TrkB-Akt signaling pathway. One of the gintonin-mediated neuroprotective effects may be achieved via anti-oxidative stress in nervous systems.

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