scholarly journals Cold Atmospheric Plasma: A New Strategy Based Primarily on Oxidative Stress for Osteosarcoma Therapy

2021 ◽  
Vol 10 (4) ◽  
pp. 893
Author(s):  
Miguel Mateu-Sanz ◽  
Juan Tornín ◽  
Maria-Pau Ginebra ◽  
Cristina Canal
Keyword(s):  
Oxidative Stress ◽  
Atmospheric Plasma ◽  
Plasma Therapy ◽  
Primary Bone Tumor ◽  
Current State ◽  
Atmospheric Plasmas ◽  
New Strategy ◽  
Primary Bone ◽  
Stress Dependent ◽  
Review Current

Osteosarcoma is the most common primary bone tumor, and its first line of treatment presents a high failure rate. The 5-year survival for children and teenagers with osteosarcoma is 70% (if diagnosed before it has metastasized) or 20% (if spread at the time of diagnosis), stressing the need for novel therapies. Recently, cold atmospheric plasmas (ionized gases consisting of UV–Vis radiation, electromagnetic fields and a great variety of reactive species) and plasma-treated liquids have been shown to have the potential to selectively eliminate cancer cells in different tumors through an oxidative stress-dependent mechanism. In this work, we review the current state of the art in cold plasma therapy for osteosarcoma. Specifically, we emphasize the mechanisms unveiled thus far regarding the action of plasmas on osteosarcoma. Finally, we review current and potential future approaches, emphasizing the most critical challenges for the development of osteosarcoma therapies based on this emerging technique.

scholarly journals An Old Therapy, Convalescent Plasma, for Coronavirus Disease-19: Do We Have All the Answer?

2020 ◽  
Vol 8 (T1) ◽  
pp. 530-537
Author(s):  
Ahmad Faried ◽  
Wahyu Widowati ◽  
Ruswana Anwar ◽  
Nucki Nursjamsi Hidajat ◽  
Ali Budi Harsono ◽  
...  
Keyword(s):  
Clinical Study ◽  
Healthcare Workers ◽  
Specific Treatment ◽  
Neutralizing Antibody ◽  
Alternative Therapies ◽  
Potential Candidate ◽  
Plasma Therapy ◽  
Current State ◽  
Antibody Titers ◽  
Review Current

BACKGROUND: Coronavirus (CoV) disease (COVID-19) has become a global health pandemic by early 2020; it has pushed the health-care system to its limit. From the initial estimates, 15% of COVID-19 patients caused by severe acute respiratory CoV 2 syndrome present with severe symptoms and requires hospitalization or even intensive care. There is no specific treatment against COVID-19, particularly for those with severe symptoms. Desperation caused by COVID-19 has driven clinicians to try an alternative therapies with little or even no-evidence previously. Convalescent plasma therapy (CPT) has emerged as a promising COVID-19 therapy. AIM: We aimed to review current state of convalescent plasma therapy. METHODS: We summarize the historical CPT, COVID-19 pathology and evaluate potential of CPT for COVID-19; raising the question regarding routinely administrating CPT to the COVID-19 patients, whether it is safe and effective. RESULTS: From cases in Indonesia and other countries, there is bunch of examples that healthcare workers being negatively stigmatized in case of COVID-19. They lost their rights to have a normal life in this pandemic era. A reasonable basis is found in many literatures to advocate the CPT. Convalescent plasma from COVID-19 patients who had been recovered with high neutralizing antibody titers was reported to be effective on transfusion to other COVID-19 patients. CONCLUSION: CPT is one good option to treat COVID-19 patients, but it not without risk; many potential candidate treatment that promising in theory but somehow fall apart when translated into clinical study; only time will tell, including our ongoing CPT clinical study.

scholarly journals Patients with Gaucher disease display systemic oxidative stress dependent on therapy status

2020 ◽  
Vol 25 ◽  
pp. 100667
Author(s):  
Reena V. Kartha ◽  
Marcia R. Terluk ◽  
Roland Brown ◽  
Abigail Travis ◽  
Usha R. Mishra ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gaucher Disease ◽  
Systemic Oxidative Stress ◽  
Stress Dependent

scholarly journals IκBα targeting promotes oxidative stress-dependent cell death

2021 ◽  
Vol 40 (1) ◽  
Author(s):  
Giovanna Carrà ◽  
Giuseppe Ermondi ◽  
Chiara Riganti ◽  
Luisella Righi ◽  
Giulia Caron ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Fate ◽  
Protein Interactions ◽  
In Silico ◽  
Inverse Correlation ◽  
Ros Production ◽  
Gene Encoding ◽  
Specific Expression ◽  
Novel Approach ◽  
Stress Dependent

Abstract Background Oxidative stress is a hallmark of many cancers. The increment in reactive oxygen species (ROS), resulting from an increased mitochondrial respiration, is the major cause of oxidative stress. Cell fate is known to be intricately linked to the amount of ROS produced. The direct generation of ROS is also one of the mechanisms exploited by common anticancer therapies, such as chemotherapy. Methods We assessed the role of NFKBIA with various approaches, including in silico analyses, RNA-silencing and xenotransplantation. Western blot analyses, immunohistochemistry and RT-qPCR were used to detect the expression of specific proteins and genes. Immunoprecipitation and pull-down experiments were used to evaluate protein-protein interactions. Results Here, by using an in silico approach, following the identification of NFKBIA (the gene encoding IκBα) amplification in various cancers, we described an inverse correlation between IκBα, oxidative metabolism, and ROS production in lung cancer. Furthermore, we showed that novel IκBα targeting compounds combined with cisplatin treatment promote an increase in ROS beyond the tolerated threshold, thus causing death by oxytosis. Conclusions NFKBIA amplification and IκBα overexpression identify a unique cancer subtype associated with specific expression profile and metabolic signatures. Through p65-NFKB regulation, IκBα overexpression favors metabolic rewiring of cancer cells and distinct susceptibility to cisplatin. Lastly, we have developed a novel approach to disrupt IκBα/p65 interaction, restoring p65-mediated apoptotic responses to cisplatin due to mitochondria deregulation and ROS-production.

Oxidative stress-dependent contribution of HMGB1 to the interplay between apoptosis and autophagy in diabetic rat liver

2017 ◽  
Vol 73 (4) ◽  
pp. 511-521 ◽  
Author(s):  
Anja Petrović ◽  
Desanka Bogojević ◽  
Aleksandra Korać ◽  
Igor Golić ◽  
Sofija Jovanović-Stojanov ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Rat Liver ◽  
Diabetic Rat ◽  
Stress Dependent

scholarly journals Chondroblastoma: An Update

2017 ◽  
Vol 141 (6) ◽  
pp. 867-871 ◽  
Author(s):  
Wenqian Chen ◽  
Lisa M. DiFrancesco
Keyword(s):  
Aneurysmal Bone Cyst ◽  
Bone Cyst ◽  
Cyst Formation ◽  
Giant Cells ◽  
Lytic Lesion ◽  
Primary Bone Tumor ◽  
Hemosiderin Deposition ◽  
Secondary Aneurysmal Bone Cyst ◽  
Primary Bone ◽  
Chondroblastic Osteosarcoma

Chondroblastoma is a rare primary bone tumor of young people that typically arises in the ends of the long bones. Radiologic investigations show a small, circumscribed, lytic lesion. The tumor is characterized histologically by the proliferation of chondroblasts along with areas of mature cartilage, giant cells, and occasionally, secondary aneurysmal bone cyst formation. Chondroblastoma, however, may also present with atypical features, such as prominent hemosiderin deposition, numerous giant cells, or the presence of a large aneurysmal bone cyst component. Malignant entities such as clear cell chondrosarcoma and chondroblastic osteosarcoma must also be considered. Recently, immunohistochemical stains such as DOG1 and SOX9 have been described in chondroblastoma, and K36M mutations in either the H3F3A or H3F3B genes have also been identified. While generally regarded as a benign entity, chondroblastoma manifests an intermediate type of behavior, given its ability to recur locally, and rarely, metastasize.

scholarly journals Oxidative stress increases megalin expression in the renal proximal tubules during the normoalbuminuric stage of diabetes mellitus

2018 ◽  
Vol 314 (3) ◽  
pp. F462-F470 ◽  
Author(s):  
Yoshifumi Kurosaki ◽  
Akemi Imoto ◽  
Fumitaka Kawakami ◽  
Masanori Yokoba ◽  
Tsuneo Takenaka ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Diabetes Mellitus ◽  
Hydrogen Peroxide ◽  
High Glucose ◽  
Renal Cortex ◽  
Dependent Manner ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphorylated Akt ◽  
Stress Dependent ◽  
Phosphatidylinositol 3

Megalin, an endocytic receptor expressed in proximal tubule cells, plays a critical role in renal tubular protein reabsorption and is associated with the albuminuria observed in diabetic nephropathy. We have previously reported increased oxidant production in the renal cortex during the normoalbuminuric stage of diabetes mellitus (DM); however, the relationship between oxidative stress and renal megalin expression during the normoalbuminuric stage of DM remains unclear. In the present study, we evaluated whether oxidative stress affects megalin expression in the normoalbuminuric stage of DM in a streptozotocin-induced diabetic rat model and in immortalized human proximal tubular cells (HK-2). We demonstrated that increased expression of renal megalin accompanies oxidative stress during the early stage of DM, before albuminuria development. Telmisartan treatment prevented the diabetes-induced elevation in megalin level, possibly through an oxidative stress-dependent mechanism. In HK-2 cells, hydrogen peroxide significantly increased megalin levels in a dose- and time-dependent manner; however, the elevation in megalin expression was decreased following prolonged exposure to severe oxidative stress induced by 0.4 mmol/l hydrogen peroxide. High-glucose treatment also significantly increased megalin expression in HK-2 cells. Concurrent administration of the antioxidant N-acetyl-cysteine blocked the effects of high glucose on megalin expression. Furthermore, the hydrogen peroxide-induced increase in megalin expression was blocked by treatment with phosphatidylinositol 3-kinase and Akt inhibitors. Increase of phosphorylated Akt expression was also seen in the renal cortex of diabetic rats. Taken together, our results indicate that mild oxidative stress increases renal megalin expression through the phosphatidylinositol 3-kinase-Akt pathway in the normoalbuminuric stage of DM.

scholarly journals Comparison of Effects of Different Statins on Contrast-Induced Acute Kidney Injury in Rats: Histopathological and Biochemical Findings

2017 ◽  
Vol 2017 ◽  
pp. 1-10 ◽  
Author(s):  
Xiao-lei Wang ◽  
Tuo Zhang ◽  
Liu-hua Hu ◽  
Shi-qun Sun ◽  
Wei-feng Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Acute Kidney Injury ◽  
Kidney Injury ◽  
Lipid Lowering ◽  
Control Group ◽  
Sprague Dawley ◽  
Atorvastatin Group ◽  
New Strategy ◽  
Ameliorative Effect ◽  
Markers Of Oxidative Stress

Statins are a promising new strategy to prevent contrast-induced acute kidney injury (CI-AKI). In this study we compared the ameliorative effect of different statins in a rat model of CI-AKI. Sprague-Dawley rats were divided into five groups: control group; CI-AKI group; CI-AKI + rosuvastatin group (10 mg/kg/day); CI-AKI + simvastatin group (80 mg/kg/day); and CI-AKI + atorvastatin group (20 mg/kg/day). CI-AKI was induced by dehydration for 72 hours, followed by furosemide intramuscular injection 20 minutes before low-osmolar contrast media (CM) intravenous injection. Statins were administered by oral gavage once daily for 3 consecutive days before CM injection and once 4 hours after CM injection. Rats were sacrificed 24 hours after CM injection, and renal function, kidney histopathology, nitric oxide (NO) metabolites, and markers of oxidative stress, inflammation, and apoptosis were evaluated. The results showed that atorvastatin and rosuvastatin but not simvastatin ameliorated CM-induced serum creatinine elevation and histopathological alterations. Atorvastatin and rosuvastatin showed similar effectiveness against CM-induced oxidative stress, but simvastatin was less effective. Atorvastatin was most effective against NO system dysfunction and cell apoptosis, whereas rosuvastatin was most effective against inflammation. Our findings indicate that statins exhibit differential effects in preventing CI-AKI when given at equivalent lipid-lowering doses.

scholarly journals Isoniazid and Rifampicin Produce Hepatic Fibrosis through an Oxidative Stress-Dependent Mechanism

2020 ◽  
Vol 2020 ◽  
pp. 1-12 ◽  
Author(s):  
Ayan Biswas ◽  
Suman Santra ◽  
Debasree Bishnu ◽  
Gopal Krishna Dhali ◽  
Abhijit Chowdhury ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Liver Injury ◽  
Hepatic Fibrosis ◽  
Stellate Cell ◽  
Progressive Increase ◽  
Drug Induced ◽  
Drug Induced Liver Injury ◽  
Stress Dependent ◽  
Liver Collagen

Background & Aims. Chronic hepatitis (CH) has emerged as a distinct outcome of drug-induced liver injury (DILI). Combination therapy of Isoniazid (INH) and Rifampicin (RMP) which is widely used for prolonged periods can cause acute hepatotoxicity and has been also incriminated in chronic DILI. We sought evidence of the production of hepatic fibrosis on long-term INH-RMP treatment through experiments in BALB/c mice exposed to INH-RMP. Methods. A combined dose of INH (50 mg) and RMP (100 mg) per kg body weight per day was administered to mice by oral gavage, 6 days a week, for 4 to 24 weeks for the assessment of liver injury, oxidative stress, and development of hepatic fibrosis, including demonstration of changes in key fibrogenesis linked pathways and mediators. Results. Progressive increase in markers of hepatic stellate cell (HSC) activation associated with changes in matrix turnover was observed between 12 and 24 weeks of INH-RMP treatment along with the elevation of liver collagen content and significant periportal fibrosis. These were associated with concurrent apoptosis of the hepatocytes, increase in hepatic cytochrome P450 2E1 (CYP2E1), NADPH oxidase (NOX) activity, and development of hepatic oxidative stress. Conclusions. INH-RMP can activate HSC through generation of NOX-mediated oxidative stress, leading to the development of liver fibrosis.

Sign in / Sign up

Export Citation Format

Share Document