scholarly journals Roles of Thyroid Hormone-Associated microRNAs Affecting Oxidative Stress in Human Hepatocellular Carcinoma

2019 ◽  
Vol 20 (20) ◽  
pp. 5220 ◽  
Author(s):  
Po-Shuan Huang ◽  
Chia-Siu Wang ◽  
Chau-Ting Yeh ◽  
Kwang-Huei Lin
Keyword(s):  
Oxidative Stress ◽  
Thyroid Hormone ◽  
Liver Cancer ◽  
Negative Impact ◽  
Animal Experiments ◽  
Supporting Evidence ◽  
Antioxidant Genes ◽  
Physiological Processes ◽  
Cellular Components ◽  
And Oxidative Stress

Oxidative stress occurs as a result of imbalance between the generation of reactive oxygen species (ROS) and antioxidant genes in cells, causing damage to lipids, proteins, and DNA. Accumulating damage of cellular components can trigger various diseases, including metabolic syndrome and cancer. Over the past few years, the physiological significance of microRNAs (miRNA) in cancer has been a focus of comprehensive research. In view of the extensive level of miRNA interference in biological processes, the roles of miRNAs in oxidative stress and their relevance in physiological processes have recently become a subject of interest. In-depth research is underway to specifically address the direct or indirect relationships of oxidative stress-induced miRNAs in liver cancer and the potential involvement of the thyroid hormone in these processes. While studies on thyroid hormone in liver cancer are abundantly documented, no conclusive information on the potential relationships among thyroid hormone, specific miRNAs, and oxidative stress in liver cancer is available. In this review, we discuss the effects of thyroid hormone on oxidative stress-related miRNAs that potentially have a positive or negative impact on liver cancer. Additionally, supporting evidence from clinical and animal experiments is provided.

scholarly journals Nitric Oxide Prevents Fe Deficiency-Induced Photosynthetic Disturbance, and Oxidative Stress in Alfalfa by Regulating Fe Acquisition and Antioxidant Defense

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1556
Author(s):  
Md Atikur Rahman ◽  
Ahmad Humayan Kabir ◽  
Yowook Song ◽  
Sang-Hoon Lee ◽  
Mirza Hasanuzzaman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Antioxidant Defense ◽  
Fe Deficiency ◽  
Negative Effects ◽  
No Donor ◽  
Antioxidant Genes ◽  
H2o2 Accumulation ◽  
Fe Homeostasis ◽  
And Oxidative Stress

Iron (Fe) deficiency impairs photosynthetic efficiency, plant growth and biomass yield. This study aimed to reveal the role of nitric oxide (NO) in restoring Fe-homeostasis and oxidative status in Fe-deficient alfalfa. In alfalfa, a shortage of Fe negatively affected the efficiency of root andshoot length, leaf greenness, maximum quantum yield PSII (Fv/Fm), Fe, S, and Zn accumulation, as well as an increase in H2O2 accumulation. In contrast, in the presence of sodium nitroprusside (SNP), a NO donor, these negative effects of Fe deficiency were largely reversed. In response to the SNP, the expression of Fe transporters (IRT1, NRAMP1) and S transporter (SULTR1;2) genes increased in alfalfa. Additionally, the detection of NO generation using fluorescence microscope revealed that SNP treatment increased the level of NO signal, indicating that NO may act as regulatory signal in response to SNP in plants. Interestingly, the increase of antioxidant genes and their related enzymes (Fe-SOD, APX) in response to SNP treatment suggests that Fe-SOD and APX are key contributors to reducing ROS (H2O2) accumulation and oxidative stress in alfalfa. Furthermore, the elevation of Ascorbate-glutathione (AsA-GSH) pathway-related genes (GR and MDAR) Fe-deficiency with SNP implies that the presence of NO relates to enhanced antioxidant defense against Fe-deficiency stress.

Biosorption of copper by immobilized biomass of Aspergillus australensis. Effect of metal on the viability, cellular components, polyhydroxyalkanoates production, and oxidative stress

2020 ◽  
Vol 27 (23) ◽  
pp. 28545-28560 ◽  
Author(s):  
Ana Gabriela Contreras-Cortés ◽  
Francisco Javier Almendariz-Tapia ◽  
Mario Onofre Cortez-Rocha ◽  
Armando Burgos-Hernández ◽  
Ema Carina Rosas-Burgos ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Immobilized Biomass ◽  
Cellular Components ◽  
And Oxidative Stress

scholarly journals TrxR1, Gsr, and oxidative stress determine hepatocellular carcinoma malignancy

2019 ◽  
Vol 116 (23) ◽  
pp. 11408-11417 ◽  
Author(s):  
Michael R. McLoughlin ◽  
David J. Orlicky ◽  
Justin R. Prigge ◽  
Pushya Krishna ◽  
Emily A. Talago ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Standard Care ◽  
Antioxidant Systems ◽  
Null Mouse ◽  
Dependent Manner ◽  
Damage Indices ◽  
And Oxidative Stress

Thioredoxin reductase-1 (TrxR1)-, glutathione reductase (Gsr)-, and Nrf2 transcription factor-driven antioxidant systems form an integrated network that combats potentially carcinogenic oxidative damage yet also protects cancer cells from oxidative death. Here we show that although unchallenged wild-type (WT), TrxR1-null, or Gsr-null mouse livers exhibited similarly low DNA damage indices, these were 100-fold higher in unchallenged TrxR1/Gsr–double-null livers. Notwithstanding, spontaneous cancer rates remained surprisingly low in TrxR1/Gsr-null livers. All genotypes, including TrxR1/Gsr-null, were susceptible to N-diethylnitrosamine (DEN)-induced liver cancer, indicating that loss of these antioxidant systems did not prevent cancer cell survival. Interestingly, however, following DEN treatment, TrxR1-null livers developed threefold fewer tumors compared with WT livers. Disruption of TrxR1 in a marked subset of DEN-initiated cancer cells had no effect on their subsequent contributions to tumors, suggesting that TrxR1-disruption does not affect cancer progression under normal care, but does decrease the frequency of DEN-induced cancer initiation. Consistent with this idea, TrxR1-null livers showed altered basal and DEN-exposed metabolomic profiles compared with WT livers. To examine how oxidative stress influenced cancer progression, we compared DEN-induced cancer malignancy under chronically low oxidative stress (TrxR1-null, standard care) vs. elevated oxidative stress (TrxR1/Gsr-null livers, standard care or phenobarbital-exposed TrxR1-null livers). In both cases, elevated oxidative stress was correlated with significantly increased malignancy. Finally, although TrxR1-null and TrxR1/Gsr-null livers showed strong Nrf2 activity in noncancerous hepatocytes, there was no correlation between malignancy and Nrf2 expression within tumors across genotypes. We conclude that TrxR1, Gsr, Nrf2, and oxidative stress are major determinants of liver cancer but in a complex, context-dependent manner.

scholarly journals Buprenorphine Alters Inflammatory and Oxidative Stress Molecular Markers in Arthritis

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Mahadevappa Hemshekhar ◽  
Vidyanand Anaparti ◽  
Carol Hitchon ◽  
Neeloffer Mookherjee
Keyword(s):  
Oxidative Stress ◽  
Molecular Markers ◽  
Murine Model ◽  
Animal Experiments ◽  
Response To Therapy ◽  
Prediction Of Response ◽  
Stress Markers ◽  
Oxidative Markers ◽  
Pain Scores ◽  
And Oxidative Stress

Buprenorphine is recommended for use as an analgesic in animal models including in murine models of collagen-induced arthritis (CIA). However, the effect of buprenorphine on the expression of disease-associated biomarkers is not well defined. We examined the effect of buprenorphine administration on disease progression and the expression of inflammatory and oxidative stress markers, in a murine model of CIA. Buprenorphine administration altered the expression of cytokines, IFN-γ, IL-6, and MMP-3, and oxidative markers, for example, iNOS, superoxide dismutase (SOD1), and catalase (CAT), in the CIA mice. As buprenorphine is an analgesic, we further monitored the association of expression of these biomarkers with pain scores in a human cohort of early rheumatoid arthritis (RA). Serum MMP-3 levels and blood mRNA expression of antioxidants sod1 and cat correlated with pain scores in the RA cohort. We have demonstrated that administration of buprenorphine alters the expression of inflammatory and oxidative stress-related molecular markers in a murine model of CIA. This caveat needs to be considered in animal experiments using buprenorphine as an analgesic, as it can be a confounding factor in murine studies used for prediction of response to therapy. Furthermore, the antioxidant enzymes that showed an association with pain scores in the human cohort may be explored as biomarkers for pain in future studies.

scholarly journals NUPR1: A Critical Regulator of the Antioxidant System

Cancers ◽  
2021 ◽  
Vol 13 (15) ◽  
pp. 3670
Author(s):  
Can Huang ◽  
Patricia Santofimia-Castaño ◽  
Juan Iovanna
Keyword(s):  
Oxidative Stress ◽  
Antioxidant System ◽  
Mitochondrial Function ◽  
Therapeutic Potential ◽  
Current Knowledge ◽  
Redox Homeostasis ◽  
Antioxidant Genes ◽  
Intrinsically Disordered ◽  
And Oxidative Stress

Nuclear protein 1 (NUPR1) is a small intrinsically disordered protein (IDP) activated in response to various types of cellular stress, including endoplasmic reticulum (ER) stress and oxidative stress. Reactive oxygen species (ROS) are mainly produced during mitochondrial oxidative metabolism, and directly impact redox homeostasis and oxidative stress. Ferroptosis is a ROS-dependent programmed cell death driven by an iron-mediated redox reaction. Substantial evidence supports a maintenance role of the stress-inducible protein NUPR1 on cancer cell metabolism that confers chemotherapeutic resistance by upregulating mitochondrial function-associated genes and various antioxidant genes in cancer cells. NUPR1, identified as an antagonist of ferroptosis, plays an important role in redox reactions. This review summarizes the current knowledge on the mechanism behind the observed impact of NUPR1 on mitochondrial function, energy metabolism, iron metabolism, and the antioxidant system. The therapeutic potential of genetic or pharmacological inhibition of NUPR1 in cancer is also discussed. Understanding the role of NUPR1 in the antioxidant system and the mechanisms behind its regulation of ferroptosis may promote the development of more efficacious strategies for cancer therapy.

scholarly journals Mitochondrial and Organellar Crosstalk in Parkinson’s Disease

ASN NEURO ◽  
2021 ◽  
Vol 13 ◽  
pp. 175909142110283
Author(s):  
Bipul Ray ◽  
Abid Bhat ◽  
Arehally Marappa Mahalakshmi ◽  
Sunanda Tuladhar ◽  
Muhammed Bishir ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Mitochondrial Dysfunction ◽  
Protein Misfolding ◽  
Contact Sites ◽  
Physiological Processes ◽  
Pathological Conditions ◽  
And Oxidative Stress ◽  
Pathological Event

Mitochondrial dysfunction is a well-established pathological event in Parkinson’s disease (PD). Proteins misfolding and its impaired cellular clearance due to altered autophagy/mitophagy/pexophagy contribute to PD progression. It has been shown that mitochondria have contact sites with endoplasmic reticulum (ER), peroxisomes and lysosomes that are involved in regulating various physiological processes. In pathological conditions, the crosstalk at the contact sites initiates alterations in intracellular vesicular transport, calcium homeostasis and causes activation of proteases, protein misfolding and impairment of autophagy. Apart from the well-reported molecular changes like mitochondrial dysfunction, impaired autophagy/mitophagy and oxidative stress in PD, here we have summarized the recent scientific reports to provide the mechanistic insights on the altered communications between ER, peroxisomes, and lysosomes at mitochondrial contact sites. Furthermore, the manuscript elaborates on the contributions of mitochondrial contact sites and organelles dysfunction to the pathogenesis of PD and suggests potential therapeutic targets.

scholarly journals Ginsenoside Rg1 attenuates arsenic-induced mice nephrotoxicity via the activated HO-1/mTOR-associated apoptosis or autophagy signaling

2021 ◽  
Author(s):  
yuan yang
Keyword(s):  
Oxidative Stress ◽  
Sodium Arsenite ◽  
Animal Experiments ◽  
Arsenic Exposure ◽  
Pharmacological Effects ◽  
Ginsenoside Rg1 ◽  
Sequestosome 1 ◽  
Bioactive Product ◽  
Apoptotic Effects ◽  
And Oxidative Stress

Nephrotoxicity attributed to environmental arsenic exposure, has been recognized by animal experiments and populational survey over 30 years in China, given a significance of public health by preventing from the disorder of renal function and hispathological abnormality. Here, Ginsenoside Rg1 (Rg1) as the commercial bioactive product of ginseng, play a beneficial role via antioxidant, anti-inflammatory and anti-apoptotic effects, which is poorly understood in arsenic-induced nephrotoxicity. The present study applied animal experiments to explore the pharmacological effects of Rg1 on sodium arsenite (SA)-induced nephrotoxicity in mice. Results showed that SA exposure led to renal pathological damage, and induced renal oxidative stress and the elevated levels of apoptosis or autophagy-associated indices in kidney. Further, western-blotting results confirmed the upregulations of pro-apoptotic Bax or autophagic unc-51-like kinase-1 (ULK1) or LC3-B signal, and the downregulations of HO-1 or mTOR signal and autophagy substrate sequestosome 1 (p62/SQSTM1) in kidney. Significantly, the intervention with Rg1 alleviated arsenic-induced renal pathological damage and oxidative stress, and upregulated the levels of HO-1, mTOR and p62, while the levels of Bax, ULK1 or LC3-B downregulated in kidney. In conclusion, the intervention with Rg1 relieves arsenic-induced mice nephrotoxicity maybe involved in the regulation of HO-1/mTOR-related apoptotic or autophagic signaling.

scholarly journals Nephroprotective Effects of Synthetic Flavonoid Hidrosmin in Experimental Diabetic Nephropathy

Antioxidants ◽  
2021 ◽  
Vol 10 (12) ◽  
pp. 1920
Author(s):  
Luna Jiménez-Castilla ◽  
Gema Marín-Royo ◽  
Macarena Orejudo ◽  
Lucas Opazo-Ríos ◽  
Teresa Caro-Ordieres ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetic Nephropathy ◽  
Kidney Injury ◽  
Redox Balance ◽  
Protective Effects ◽  
Chronic Complications ◽  
Antioxidant Genes ◽  
Cytokines And Chemokines ◽  
And Oxidative Stress

Diabetes mellitus (DM) is a high-impact disease commonly characterized by hyperglycemia, inflammation, and oxidative stress. Diabetic nephropathy (DN) is a common diabetic microvascular complication and the leading cause of chronic kidney disease worldwide. This study investigates the protective effects of the synthetic flavonoid hidrosmin (5-O-(beta-hydroxyethyl) diosmin) in experimental DN induced by streptozotocin injection in apolipoprotein E deficient mice. Oral administration of hidrosmin (300 mg/kg/day, n = 11) to diabetic mice for 7 weeks markedly reduced albuminuria (albumin-to-creatinine ratio: 47 ± 11% vs. control) and ameliorated renal pathological damage and expression of kidney injury markers. Kidneys of hidrosmin-treated mice exhibited lower content of macrophages and T cells, reduced expression of cytokines and chemokines, and attenuated inflammatory signaling pathways. Hidrosmin treatment improved the redox balance by reducing prooxidant enzymes and enhancing antioxidant genes, and also decreased senescence markers in diabetic kidneys. In vitro, hidrosmin dose-dependently reduced the expression of inflammatory and oxidative genes in tubuloepithelial cells exposed to either high-glucose or cytokines, with no evidence of cytotoxicity at effective concentrations. In conclusion, the synthetic flavonoid hidrosmin exerts a beneficial effect against DN by reducing inflammation, oxidative stress, and senescence pathways. Hidrosmin could have a potential role as a coadjutant therapy for the chronic complications of DM.

Abstract 80: Modulating the Vascular Healing Response via SIRT1 Transgene Delivery

2014 ◽  
Vol 34 (suppl_1) ◽  
Author(s):  
Michele C Jen ◽  
Vincent Y Chen ◽  
Lonnie D Shea ◽  
Guillermo A Ameer
Keyword(s):  
Oxidative Stress ◽  
Intimal Hyperplasia ◽  
Cytokine Expression ◽  
Sirtuin 1 ◽  
Antioxidant Genes ◽  
Healing Response ◽  
Adventitial Fibroblasts ◽  
Transgene Delivery ◽  
And Oxidative Stress

Bypass graft procedures are commonly performed to treat narrowing or blocked vessels. However, damage to the vascular wall from the surgical intervention can lead to pro-inflammatory events and oxidative stress that promote intimal hyperplasia and may eventually lead to restenosis. Therefore, strategies that seek to reduce inflammation and oxidative stress during the initial stages of wound healing at the graft anastomoses are expected to inhibit intimal hyperplasia and reduce graft failure rates. Sirtuin-1 (Sirt1), an NAD+-dependent lysine deacetylase, protects against inflammation and oxidative stress by deacetylating the RelA/p65 subunit of NF-kB and FOXO transcription factors. We hypothesize that the localized overexpression of Sirt1 at the perivascular wall via lentivirus entrapped in a thermoresponsive gel referred to as nanonets will lead to an improved vascular healing response at the graft anastomoses and attenuate intimal hyperplasia via reduced tissue inflammation and oxidative stress. Human aortic adventitial fibroblasts (AoAFs) were transduced with lentiviruses encoding for Sirt1 and assessed for NF-kB activity, cytokine expression, senescence, and upregulation of antioxidant genes. To assess perivascular transgene delivery, nanonets containing lentiviruses encoding GFP were applied perivascularly around the aortas of rats. After one week of in vivo transduction, aortas were explanted and probed for GFP positive cells. Upon TNFα stimulation, NF-kB activity and cytokine expression levels were decreased when compared to non-transduced and empty vector-transduced AoAFs. Furthermore, Sirt1-overexpression prevented cellular senescence and protected against oxidative stress. Nanonets containing lentiviruses effectively transduced adventitial fibroblasts in vivo. In conclusion, Sirt1 overexpression in AoAFs may be protective against inflammation and oxidative stress.

scholarly journals Role of Peroxisome Proliferator-Activated Receptorγin Ocular Diseases

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Su Zhang ◽  
Hongwei Gu ◽  
Nan Hu
Keyword(s):  
Oxidative Stress ◽  
Eye Diseases ◽  
Age Related Macular Degeneration ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Physiological Processes ◽  
Age Related ◽  
Potential Benefits ◽  
And Oxidative Stress

Peroxisome proliferator-activated receptorγ(PPARγ), a member of the nuclear receptor superfamily, is a ligand-activated transcription factor that plays an important role in the control of a variety of physiological processes. The last decade has witnessed an increasing interest for the role played by the agonists of PPARγin antiangiogenesis, antifibrosis, anti-inflammation effects and in controlling oxidative stress response in various organs. As the pathologic mechanisms of major blinding diseases, such as age-related macular degeneration (AMD), diabetic retinopathy (DR), keratitis, and optic neuropathy, often involve neoangiogenesis and inflammation- and oxidative stress-mediated cell death, evidences are accumulating on the potential benefits of PPARγto improve or prevent these vision threatening eye diseases. In this paper we describe what is known about the role of PPARγin the ocular pathophysiological processes and PPARγagonists as novel adjuvants in the treatment of eye diseases.

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