scholarly journals Exploring Biologic Correlates of Cancer-Related Fatigue in Men With Prostate Cancer: Cell Damage Pathways and Oxidative Stress

2020 ◽  
Vol 22 (4) ◽  
pp. 514-519
Author(s):  
Kristin Dickinson ◽  
Adam J. Case ◽  
Kevin Kupzyk ◽  
Leorey Saligan
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Potential Role ◽  
Cell Damage ◽  
Cellular Responses ◽  
Preliminary Evidence ◽  
Cancer Related Fatigue ◽  
Targeted Treatments ◽  
And Oxidative Stress

The pathobiology of cancer-related fatigue (CRF) remains elusive, hindering the development of targeted treatments. Radiation therapy (RT), a common treatment for men with prostate cancer, induces cell damage through the generation of free radicals and oxidative stress. We hypothesized that disruption in cellular responses to this surge of nonphysiological oxidative stress might contribute to CRF in men with prostate cancer treated with RT. We evaluated the potential role of three cell damage pathways (apoptosis, autophagy, necrosis) and oxidative stress in CRF in men with prostate cancer receiving RT. Fatigue was measured by the Functional Assessment of Cancer Therapy-Fatigue (FACT-F) questionnaire. Gene expression was measured in whole blood using RT2 profiler™ PCR arrays. Data were collected at two time points: either baseline or Day 1 of treatment (T1) and completion of treatment (T2). Participants were grouped into either the fatigued or nonfatigued phenotype at T2 using the recommended FACT-F cut-off score for clinical significance. We observed significant upregulation of seven genes related to three cell damage pathways in the fatigued group from T1 to T2 and no significant changes in the nonfatigued group. We also observed significant downregulation of two genes related to oxidative stress in the fatigued group compared to the nonfatigued group at T2. These collective results provide preliminary evidence that cell damage might be upregulated in the CRF phenotype. Validation of these findings using a larger and more diverse sample is warranted.

Potential role of pulses in the development of functional foods modulating inflammation and oxidative stress

2022 ◽  
pp. 287-309
Author(s):  
Helena Ferreira ◽  
Elisabete Pinto ◽  
Ana M. Gil ◽  
Marta W. Vasconcelos
Keyword(s):  
Oxidative Stress ◽  
Functional Foods ◽  
Potential Role ◽  
And Oxidative Stress

scholarly journals Potential Role of Cytochrome c and Tryptase in Psoriasis and Psoriatic Arthritis Pathogenesis: Focus on Resistance to Apoptosis and Oxidative Stress

2018 ◽  
Vol 9 ◽  
Author(s):  
Maria Sole Chimenti ◽  
Flavia Sunzini ◽  
Laura Fiorucci ◽  
Elisabetta Botti ◽  
Giulia Lavinia Fonti ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Psoriatic Arthritis ◽  
Cytochrome C ◽  
Potential Role ◽  
And Oxidative Stress

scholarly journals Role of gangliosides in prostate pathology

2016 ◽  
Vol 19 (1) ◽  
pp. 10-15
Author(s):  
Ilinca Nicolae ◽  
◽  
Corina-Daniela Ene ◽  
Simona Roxana Georgescu ◽  
◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Prostate Cancer ◽  
Differential Diagnosis ◽  
Benign Prostatic Hyperplasia ◽  
Molecular Pathology ◽  
Potential Role ◽  
Prostatic Hyperplasia ◽  
Immunologic Markers ◽  
Immunological Interactions

Molecular pathology of benign prostatic hyperplasia is multifactorial and involves endocrine, biochemical, immunological interactions. The mechanisms involved in the onset and progression of benign prostatic hyperplasia are: infections, 50 years of age, hormones and neurotransmitters imbalances, inflammation, oxidative stress. The potential role of glycosylation in the pathogenesis of prostate disease has been neglected. In this study we documented the profile of gangliosides in normal and pathological prostatic tissues together with the pathologic changes seen in the level of extracellular gangliosides in patients with prostate pathology. Analysis of the data in the literature suggests that gangliosides may represent immunologic markers useful in the differential diagnosis between prostate cancer and benign prostatic hyperplasia.

scholarly journals New Insights in the Pathogenesis of HPV Infection and the Associated Carcinogenic Processes: The Role of Chronic Inflammation and Oxidative Stress

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Simona Roxana Georgescu ◽  
Cristina Iulia Mitran ◽  
Madalina Irina Mitran ◽  
Constantin Caruntu ◽  
Maria Isabela Sarbu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Chronic Inflammation ◽  
Cell Damage ◽  
Redox Homeostasis ◽  
Harmful Effect ◽  
Hpv Infection ◽  
Host Cells ◽  
E6 And E7 ◽  
And Oxidative Stress

Human papillomavirus (HPV) is a small double-stranded DNA virus with tropism for epithelial cells. To this date, over 150 genotypes are known and are classified into two major groups, low-risk and high-risk strains, depending on the ability of the virus to induce malignant transformation. The host’s immunity plays a central role in the course of the infection; therefore, it may not be clinically manifest or may produce various benign or malignant lesions. The pathogenic mechanisms are complex and incompletely elucidated. Recent research suggests the role of chronic inflammation and oxidative stress (OS) in the pathogenesis of HPV infection and the associated carcinogenic processes. Chronic inflammation induces OS, which in turn promotes the perpetuation of the inflammatory process resulting in the release of numerous molecules which cause cell damage. Reactive oxygen species exert a harmful effect on proteins, lipids, and nucleic acids. Viral oncogenes E5, E6, and E7 are involved in the development of chronic inflammation through various mechanisms. In addition, HPV may interfere with redox homeostasis of host cells, inducing OS which may be involved in the persistence of the infection and play a certain role in viral integration and promotion of carcinogenesis. Knowledge regarding the interplay between chronic inflammation and OS in the pathogenesis of HPV infection and HPV-induced carcinogenesis has important consequences on the development of new therapeutic strategies.

scholarly journals Effect of Polyaryl Hydrocarbons on Cytotoxicity in Monocytic Cells: Potential Role of Cytochromes P450 and Oxidative Stress Pathways

PLoS ONE ◽  
2016 ◽  
Vol 11 (9) ◽  
pp. e0163827 ◽  
Author(s):  
Sabina Ranjit ◽  
Narasimha M. Midde ◽  
Namita Sinha ◽  
Benjamin J. Patters ◽  
Mohammad A. Rahman ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Potential Role ◽  
Cytochromes P450 ◽  
Monocytic Cells ◽  
And Oxidative Stress

The potential role of Punica granatum treatment on murine malaria-induced hepatic injury and oxidative stress

2015 ◽  
Vol 115 (4) ◽  
pp. 1427-1433 ◽  
Author(s):  
Taghreed A. Hafiz ◽  
Murad A. Mubaraki ◽  
Saleh Al-Quraishy ◽  
Mohamed A. Dkhil
Keyword(s):  
Oxidative Stress ◽  
Hepatic Injury ◽  
Potential Role ◽  
Punica Granatum ◽  
And Oxidative Stress

scholarly journals Inter-Relationship between Platelet-Derived Microparticles and Oxidative Stress in Patients with Venous Thromboembolism

Antioxidants ◽  
2020 ◽  
Vol 9 (12) ◽  
pp. 1217
Author(s):  
Salvatore Santo Signorelli ◽  
Gea Oliveri Conti ◽  
Maria Fiore ◽  
Maria Grazia Elfio ◽  
Antonio Cristaldi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Venous Thromboembolism ◽  
Potential Role ◽  
Thiobarbituric Acid ◽  
Thiobarbituric Acid Reactive Substances ◽  
Circulating Microparticles ◽  
Galectin 3 ◽  
And Oxidative Stress ◽  
Control Study

Background: Hypercoagulative conditions play a key role in venous thromboembolism (VTE). Inflammation is currently linked to VTE, but the potential role of circulating microparticles and oxidative stress (OxS) must be elucidated. The aim of this study was to evaluate platelet-derived microparticles and surrogate OxS biomarkers in patients diagnosed with VTE through a case–control study. Methods: Platelet-derived microparticles (MPs), pro-thrombinase-induced clotting time assay (PiCT), phospholipids (PLPs), malondialdehyde (MDA), 4-hydroxynonenale (4-HNE), thiobarbituric acid reactive substances (TBARs), superoxide dismutase (SOD), and galectin-3 (Gal-3) were measured in VTE patients and in healthy controls. Results: PLPs, 4-HNE, TBARs, and Gal-3 were higher in VTE patients compared to controls; conversely, SOD was lower. A significant non-linear regression between OxS biomarkers and the markers of platelet degranulation was found. Conclusion: Our results suggest that OxS and platelet degranulation are concomitant pathophysiological mechanisms in VTE.

scholarly journals Potential Role of Microfibrillar-Associated Protein 4, Fibrotic Indices and Oxidative Stress in Hepatocellular Carcinoma

2018 ◽  
Vol 86 (4) ◽  
pp. 44 ◽  
Author(s):  
Mohamed Salama ◽  
Manal Nomir ◽  
Maryan Fahmi ◽  
Amal El-Gayar ◽  
Mamdouh El-Shishtawy
Keyword(s):  
Oxidative Stress ◽  
Hepatocellular Carcinoma ◽  
Potential Role ◽  
Control Group ◽  
Significant Elevation ◽  
Cirrhotic Patients ◽  
Mechanisms Of Persistence ◽  
And Oxidative Stress ◽  
Related Mortality

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. In an attempt to understand some potential mechanisms of persistence and oncogenicity of Hepatitis C virus (HCV)-related HCC, microfibrillar-associated protein 4 (MFAP4), fibrotic indices and oxidative status biomarkers were assessed in the sera of 50 patients with HCV-associated HCC, 25 patients with HCV-related liver cirrhosis and 15 healthy individuals. Serum oxidized Coenzyme Q10 (CoQ10) and malondialdehyde showed significant elevation in HCC patients compared to the control group (p < 0.001), as well as cirrhotic patients (p < 0.05 and p < 0.001, respectively), while serum glutathione content and superoxide dismutase activity were significantly decreased in HCC patients compared to the control group (p < 0.001). Serum MFAP4, aspartate aminotransferase to platelet ratio index (APRI), fibrosis index based on the 4 factors (FIB-4) and Forns index showed significant increase in HCC patients compared to the control group (p < 0.001), while only APRI and FIB-4 were significantly different between HCC and cirrhotic patients (p < 0.05), with a sensitivity of 86% and 92%, respectively, at cut off ≥0.7 for APRI and ≥1.57 for FIB-4. Therefore, increasing oxidative stress and fibrosis might mediate HCV induced cirrhosis and HCC. APRI and FIB-4 may be used as a simple non-expensive formula for the screening of HCC rather than MFAP4.

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