Cell death induced by α-terthienyl via reactive oxygen species-mediated mitochondrial dysfunction and oxidative stress in the midgut of Aedes aegypti larvae

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.

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Advanced Glycation End Products and Oxidative Stress in a Hyperglycaemic Environment

10.5772/intechopen.97234 ◽

2021 ◽

Author(s):

Akio Nakamura ◽

Ritsuko Kawahrada

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Advanced Glycation End Products ◽

Reactive Oxygen ◽

Protein Glycation ◽

Oxygen Species ◽

Advanced Glycation ◽

Glycation End Products ◽

End Products ◽

And Oxidative Stress

Protein glycation is the random, nonenzymatic reaction of sugar and protein induced by diabetes and ageing; this process is quite different from glycosylation mediated by the enzymatic reactions catalysed by glycosyltransferases. Schiff bases form advanced glycation end products (AGEs) via intermediates, such as Amadori compounds. Although these AGEs form various molecular species, only a few of their structures have been determined. AGEs bind to different AGE receptors on the cell membrane and transmit signals to the cell. Signal transduction via the receptor of AGEs produces reactive oxygen species in cells, and oxidative stress is responsible for the onset of diabetic complications. This chapter introduces the molecular mechanisms of disease onset due to oxidative stress, including reactive oxygen species, caused by AGEs generated by protein glycation in a hyperglycaemic environment.

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Butin reduces oxidative stress-induced mitochondrial dysfunction via scavenging of reactive oxygen species

Food and Chemical Toxicology ◽

10.1016/j.fct.2010.01.001 ◽

2010 ◽

Vol 48 (3) ◽

pp. 922-927 ◽

Cited By ~ 8

Author(s):

Rui Zhang ◽

Kyoung Ah Kang ◽

Mei Jing Piao ◽

Weon Young Chang ◽

Young Hee Maeng ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Mitochondrial Dysfunction ◽

Reactive Oxygen ◽

Oxygen Species

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

ZHurnal «Patologicheskaia fiziologiia i eksperimental`naia terapiia» ◽

10.25557/0031-2991.2021.01.70-78 ◽

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.

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Underlying mechanisms of reactive oxygen species and oxidative stress photoinduced by graphene and its surface-functionalized derivatives

Environmental Science Nano ◽

10.1039/c9en01295h ◽

2020 ◽

Vol 7 (3) ◽

pp. 782-792 ◽

Cited By ~ 2

Author(s):

Hongye Yao ◽

Yang Huang ◽

Xuan Li ◽

Xuehua Li ◽

Hongbin Xie ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Functional Groups ◽

Reactive Oxygen ◽

Oxygen Species ◽

Underlying Mechanisms ◽

Transformation Processes ◽

And Oxidative Stress

Graphene can be modified by different functional groups through various transformation processes in the environment.

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Effect of Dipyridamole on the Reactive Oxygen Species and Oxidative Stress in Trabecular Meshwork Cells

Journal of the Korean Ophthalmological Society ◽

10.3341/jkos.2013.54.3.496 ◽

2013 ◽

Vol 54 (3) ◽

pp. 496

Author(s):

Keun Woo Lee ◽

Jae Woo Kim

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Trabecular Meshwork ◽

Reactive Oxygen ◽

Oxygen Species ◽

Trabecular Meshwork Cells ◽

And Oxidative Stress

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Redox Regulation and Oxidative Stress: The Particular Case of the Stallion Spermatozoa

Antioxidants ◽

10.3390/antiox8110567 ◽

2019 ◽

Vol 8 (11) ◽

pp. 567 ◽

Cited By ~ 11

Author(s):

Fernando J. Peña ◽

Cristian O’Flaherty ◽

José M. Ortiz Rodríguez ◽

Francisco E. Martín Cano ◽

Gemma L. Gaitskell-Phillips ◽

...

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Redox Regulation ◽

Redox Homeostasis ◽

Reactive Oxygen ◽

Mitochondrial Activity ◽

Oxygen Species ◽

Redox Biology ◽

Major Interest ◽

And Oxidative Stress

Redox regulation and oxidative stress have become areas of major interest in spermatology. Alteration of redox homeostasis is recognized as a significant cause of male factor infertility and is behind the damage that spermatozoa experience after freezing and thawing or conservation in a liquid state. While for a long time, oxidative stress was just considered an overproduction of reactive oxygen species, nowadays it is considered as a consequence of redox deregulation. Many essential aspects of spermatozoa functionality are redox regulated, with reversible oxidation of thiols in cysteine residues of key proteins acting as an “on–off” switch controlling sperm function. However, if deregulation occurs, these residues may experience irreversible oxidation and oxidative stress, leading to malfunction and ultimately death of the spermatozoa. Stallion spermatozoa are “professional producers” of reactive oxygen species due to their intense mitochondrial activity, and thus sophisticated systems to control redox homeostasis are also characteristic of the spermatozoa in the horse. As a result, and combined with the fact that embryos can easily be collected in this species, horses are a good model for the study of redox biology in the spermatozoa and its impact on the embryo.

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Rosmarinic acid induces programmed cell death in Arabidopsis seedlings through reactive oxygen species and mitochondrial dysfunction

PLoS ONE ◽

10.1371/journal.pone.0208802 ◽

2018 ◽

Vol 13 (12) ◽

pp. e0208802 ◽

Cited By ~ 13

Author(s):

Fabrizio Araniti ◽

Aitana Costas-Gil ◽

Luz Cabeiras-Freijanes ◽

Antonio Lupini ◽

Francesco Sunseri ◽

...

Keyword(s):

Reactive Oxygen Species ◽

Cell Death ◽

Programmed Cell Death ◽

Mitochondrial Dysfunction ◽

Rosmarinic Acid ◽

Reactive Oxygen ◽

Oxygen Species

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Arginine Biosynthesis Modulates Pyoverdine Production and Release in Pseudomonas putida as Part of the Mechanism of Adaptation to Oxidative Stress

Journal of Bacteriology ◽

10.1128/jb.00454-19 ◽

2019 ◽

Vol 201 (22) ◽

Cited By ~ 3

Author(s):

Laura Barrientos-Moreno ◽

María Antonia Molina-Henares ◽

Marta Pastor-García ◽

María Isabel Ramos-González ◽

Manuel Espinosa-Urgel

Keyword(s):

Oxidative Stress ◽

Reactive Oxygen Species ◽

Amino Acid ◽

Pseudomonas Putida ◽

Reactive Oxygen ◽

Full Detail ◽

Oxygen Species ◽

Arginine Biosynthesis ◽

Content Type ◽

And Oxidative Stress

ABSTRACT Iron is essential for most life forms. Under iron-limiting conditions, many bacteria produce and release siderophores—molecules with high affinity for iron—which are then transported into the cell in their iron-bound form, allowing incorporation of the metal into a wide range of cellular processes. However, free iron can also be a source of reactive oxygen species that cause DNA, protein, and lipid damage. Not surprisingly, iron capture is finely regulated and linked to oxidative-stress responses. Here, we provide evidence indicating that in the plant-beneficial bacterium Pseudomonas putida KT2440, the amino acid l-arginine is a metabolic connector between iron capture and oxidative stress. Mutants defective in arginine biosynthesis show reduced production and release of the siderophore pyoverdine and altered expression of certain pyoverdine-related genes, resulting in higher sensitivity to iron limitation. Although the amino acid is not part of the siderophore side chain, addition of exogenous l-arginine restores pyoverdine release in the mutants, and increased pyoverdine production is observed in the presence of polyamines (agmatine and spermidine), of which arginine is a precursor. Spermidine also has a protective role against hydrogen peroxide in P. putida, whereas defects in arginine and pyoverdine synthesis result in increased production of reactive oxygen species. IMPORTANCE The results of this study show a previously unidentified connection between arginine metabolism, siderophore turnover, and oxidative stress in Pseudomonas putida. Although the precise molecular mechanisms involved have yet to be characterized in full detail, our data are consistent with a model in which arginine biosynthesis and the derived pathway leading to polyamine production function as a homeostasis mechanism that helps maintain the balance between iron uptake and oxidative-stress response systems.

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