Superoxide dismutase mRNA and protein level in human colorectal cancer

2010 ◽  
Vol 5 (5) ◽  
pp. 590-599 ◽  
Author(s):  
Michał Skrzycki ◽  
Monika Majewska ◽  
Hanna Czeczot
Keyword(s):  
Colorectal Cancer ◽  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Liver Metastases ◽  
Tumor Cells ◽  
Protein Level ◽  
Colorectal Adenocarcinoma ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Colorectal Cancer Liver Metastases

AbstractImpairments of antioxidant enzyme expression are often concomitant with the onset of cancer. Due to epigenetic factors causing an inflammatory state the gastrointestinal tract can become exposed to reactive oxygen species. The purpose of our work was to evaluate mRNA and protein levels of superoxide dismutase isoenzymes in human colorectal adenocarcinoma due to its clinical advancement, and in colorectal cancer liver metastases. Evaluation of SOD expression in regard to CRC advancement, seems useful for clinical applications due to different tumor cells sensitivity to reactive oxygen species based treatment. Studies were conducted on a group of 27 patients: 15 diagnosed with colorectal adenocarcinoma and 12 diagnosed with colorectal cancer liver metastases. The mRNA level was determined by RT-PCR, and protein level by Western blotting. We observed significant (P≤0.05) changes of mRNA and protein level of SOD isoenzymes in subsequent stages of colorectal adenocarcinoma advancement and in colorectal cancer liver metastases. Differences in mRNA and protein level of SOD isoenzymes in colorectal adenocarcinoma and its liver metastases indicates that SOD participate in adaptation of tumor cells to oxidative stress, and maintain certain level of ROS, necessary for appropriate cell proliferation. Expression of superoxide dismutase isoenzymes seems to be regulated not only at transcriptional level, but also posttranscriptional.

The Role of Reactive Oxygen Species in Tumor Treatment and its Impact on Bone Marrow Hematopoiesis

2020 ◽  
Vol 21 (5) ◽  
pp. 477-498
Author(s):  
Yongfeng Chen ◽  
Xingjing Luo ◽  
Zhenyou Zou ◽  
Yong Liang
Keyword(s):  
Reactive Oxygen Species ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Tumor Cells ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Tumor Treatment ◽  
Normal Cells ◽  
Treatment And Prevention

Reactive oxygen species (ROS), an important molecule inducing oxidative stress in organisms, play a key role in tumorigenesis, tumor progression and recurrence. Recent findings on ROS have shown that ROS can be used to treat cancer as they accelerate the death of tumor cells. At present, pro-oxidant drugs that are intended to increase ROS levels of the tumor cells have been widely used in the clinic. However, ROS are a double-edged sword in the treatment of tumors. High levels of ROS induce not only the death of tumor cells but also oxidative damage to normal cells, especially bone marrow hemopoietic cells, which leads to bone marrow suppression and (or) other side effects, weak efficacy of tumor treatment and even threatening patients’ life. How to enhance the killing effect of ROS on tumor cells while avoiding oxidative damage to the normal cells has become an urgent issue. This study is a review of the latest progress in the role of ROS-mediated programmed death in tumor treatment and prevention and treatment of oxidative damage in bone marrow induced by ROS.

Engineering of a novel chimera of superoxide dismutase and Vitreoscilla hemoglobin for rapid detoxification of reactive oxygen species

2010 ◽  
Vol 110 (6) ◽  
pp. 633-637 ◽  
Author(s):  
Chartchalerm Isarankura-Na-Ayudhya ◽  
Sakda Yainoy ◽  
Tanawut Tantimongcolwat ◽  
Leif Bülow ◽  
Virapong Prachayasittikul
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Reactive Oxygen ◽  
Vitreoscilla Hemoglobin ◽  
Oxygen Species

Effects of Superoxide Dismutase Inhibitors and Glucose on Cell Death and Generation of Reactive Oxygen Species in Pea Leaves

2021 ◽  
Vol 86 (7) ◽  
pp. 878-886
Author(s):  
Vitaly D. Samuilov ◽  
Dmitry B. Kiselevsky ◽  
Elena V. Dzyubinskaya ◽  
Olga Yu. Frolova
Keyword(s):  
Reactive Oxygen Species ◽  
Cell Death ◽  
Superoxide Dismutase ◽  
Reactive Oxygen ◽  
Oxygen Species

Identification of the signature genes and network of Reactive Oxygen Species (ROS) related genes and DNA repair genes in Lung Adenocarcinoma (LUAD)

2021 ◽  
Author(s):  
Ye Zhao ◽  
Hai-Ming Feng ◽  
Xiao-Ping Wei ◽  
Wei-Jian Yan ◽  
Bin Li ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Dna Repair ◽  
Tumor Cell ◽  
Lung Adenocarcinoma ◽  
Tumor Cells ◽  
Patient Survival ◽  
Reactive Oxygen ◽  
Dna Repair Genes ◽  
Oxygen Species ◽  
Repair Genes

Abstract Reactive Oxygen Species (ROS) are present in high amount in patients with tumors, and these ROS can kill and destroy tumor cells. Thus, tumor cells upregulate ROS-related genes to protect themselves and reduce their destruction. Cancer cells already damaged by ROS can be repaired by expressing DNA repair genes consequently promoting their proliferation. In this work, lung adenocarcinoma (LUAD) transcriptome data in the TCGA database was analyzed and samples were clustered into 5 ROS-related categories and 6 DNA repair categories. Survival analysis revealed a significant difference in patient survival between the two classification methods. In addition, the samples corresponding to the two categories overlap, thus, the gene expression profile of the same sample with different categories and survival prognosis was further explored, and the connection between ROS-related genes and DNA repair genes was investigated. The interactive sample recombination classification was used, revealing that the patient's prognosis was worse when the ROS-related genes and DNA repair genes were expressed at the same time. The further research on the potential regulatory network of the two categories of genes and the correlation analysis revealed that ROS-related genes and DNA repair genes have a mutual regulatory relationship. The ROS-related genes NQO1, TXNRD1, and PRDX4 could establish links with other DNA repair genes through the DNA repair gene NEIL3, thereby increasing the growth of tumor cells and balancing the level of ROS, leading to tumor cell death and constant damage to the tumor cell repair system, thus prolonging patient survival. Thus, targeting ROS-related genes and DNA repair genes might be a promising strategy in the treatment of LUAD. Finally, a survival prognostic model of ROS-related genes and DNA repair genes was established (TERT, PRKDC, PTTG1, SMUG1, TXNRD1, CAT, H2AFX and PFKP), the risk score might be used as an independent prognostic factor in LUAD patients.

scholarly journals The differential role of reactive oxygen species in early and late stages of cancer

2017 ◽  
Vol 313 (6) ◽  
pp. R646-R653 ◽  
Author(s):  
Mohamad Assi
Keyword(s):  
Reactive Oxygen Species ◽  
Tumor Cells ◽  
Cancer Progression ◽  
Reactive Oxygen ◽  
Pentose Phosphate ◽  
Oxygen Species ◽  
Redox Biology ◽  
Oxidative Damages ◽  
Late Stages

The large doses of vitamins C and E and β-carotene used to reduce reactive oxygen species (ROS) production and oxidative damages in cancerous tissue have produced disappointing and contradictory results. This therapeutic conundrum was attributed to the double-faced role of ROS, notably, their ability to induce either proliferation or apoptosis of cancer cells. However, for a ROS-inhibitory approach to be effective, it must target ROS when they induce proliferation rather than apoptosis. On the basis of recent advances in redox biology, this review underlined a differential regulation of prooxidant and antioxidant system, respective to the stage of cancer. At early precancerous and neoplastic stages, antioxidant activity decreases and ROS appear to promote cancer initiation via inducing oxidative damage and base pair substitution mutations in prooncogenes and tumor suppressor genes, such as RAS and TP53, respectively. Whereas in late stages of cancer progression, tumor cells escape apoptosis by producing high levels of intracellular antioxidants, like NADPH and GSH, via the pentose phosphate pathway to buffer the excessive production of ROS and related intratumor oxidative injuries. Therefore, antioxidants should be prohibited in patients with advanced stages of cancer and/or undergoing anticancer therapies. Interestingly, the biochemical and biophysical properties of some polyphenols allow them to selectively recognize tumor cells. This characteristic was exploited to design and deliver nanoparticles coated with low doses of polyphenols and containing chemotherapeutic drugs into tumor-bearing animals. First results are encouraging, which may revolutionize the conventional use of antioxidants in cancer.

scholarly journals Efek Ekstrak Etanol Daun Gedi Merah (Abelmoschus Manihot (L.) Medik) Terhadap Kadar Superoxide Dismutase Dan Malondialdehyde Jaringan Ginjal Tikus Model Diabetes Melitus Tipe 2

2020 ◽  
Vol 8 (2) ◽  
pp. 83
Author(s):  
Ahmad Fuadi ◽  
Yoyon Arif ◽  
Yudi Purnomo
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Multiple Dose ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Sprague Dawley ◽  
Per Oral ◽  
One Way Anova ◽  
Diabetes Melitus

Hiperglikemia pada Diabetes Melitus (DM) meningkatkan produksi Reactive Oxygen Species (ROS) dan berperan terhadap risiko komplikasi nefropati diabetik. Daun gedi merah (Abelmoschus manihot (L.) Medik) berkhasiat sebagai antidiabetik dan antioksidan tetapi penelitian ekstrak etanol daun gedi merah (EEDGM) untuk mencegah nefropati diabetik belum banyak dilaporkan. Penelitian ini bertujuan untuk mengetahui efek EEDGM terhadap kadar SOD dan MDA ginjal tikus model DM.Metode: Tikus Sprague dawley jantan usia 4-6 minggu dikelompokan menjadi 2 kelompok kontrol dan 3 kelompok perlakuan (n=25 ekor). Tikus DM dibuat dengan diet tinggi lemak-fruktosa (DTLF) dan streptozotocin (STZ) 25 mg/kgBB i.p multiple dose. Ekstrak etanol daun gedi merah (EEDGM) diberikan per oral selama 4 minggu. Kadar SOD dan MDA ginjal diukur menggunakan SOD rat kit dan MDA rat kit. Hasil dianalisa dengan One Way Anova dilanjutkan dengan uji BNT (p<0,05).Hasil: Pemberian EEDGM dosis 800 mg/kgBB menghambat penurunan kadar SOD jaringan ginjal dengan persentase sekitar 60% dibandingkan KDM (p<0,05). Pemberian EEDGM dosis 400 mg/kgBB menghambat peningkatan kadar MDA jaringan ginjal dengan persentase sekitar 20% dibandingkan KDM (p<0,05). Induksi DTLF dan STZ menurunkan kadar SOD jaringan ginjal dengan persentase sekitar 40% dan meningkatkan kadar MDA jaringan ginjal dengan persentase sekitar 30%.Kesimpulan: Pemberian EEDGM dapat menghambat penurunan kadar SOD dan peningkatan kadar MDA jaringan ginjal tikus model DM.

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.

scholarly journals Potentiation of Antibiofilm Activity of Amphotericin B by Superoxide Dismutase Inhibition

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
Katrijn De Brucker ◽  
Anna Bink ◽  
Els Meert ◽  
Bruno P. A. Cammue ◽  
Karin Thevissen
Keyword(s):  
Reactive Oxygen Species ◽  
Superoxide Dismutase ◽  
Candida Albicans ◽  
Amphotericin B ◽  
Reactive Oxygen ◽  
Intracellular Reactive Oxygen Species ◽  
Superoxide Dismutases ◽  
Antibiofilm Activity ◽  
Oxygen Species ◽  
Ammonium Tetrathiomolybdate

This study demonstrates a role for superoxide dismutases (Sods) in governing tolerance ofCandida albicansbiofilms to amphotericin B (AmB). Coincubation ofC. albicansbiofilms with AmB and the Sod inhibitors N,N′-diethyldithiocarbamate (DDC) or ammonium tetrathiomolybdate (ATM) resulted in reduced viable biofilm cells and increased intracellular reactive oxygen species levels as compared to incubation of biofilm cells with AmB, DDC, or ATM alone. Hence, Sod inhibitors can be used to potentiate the activity of AmB againstC. albicansbiofilms.

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