Low-Dose Oxidant Toxicity and Oxidative Stress in Human Papillary Thyroid Carcinoma Cells K1

Medical gas plasmas are of emerging interest in pre-clinical oncological research. Similar to an array of first-line chemotherapeutics and physics-based therapies already approved for clinical application, plasmas target the tumor redox state by generating a variety of highly reactive species eligible for local tumor treatments. Considering internal tumors with limited accessibility, medical gas plasmas help to enrich liquids with stable, low-dose oxidants ideal for intratumoral injection and lavage. Pre-clinical investigation of such liquids in numerous tumor entities and models in vitro and in vivo provided evidence of their clinical relevance, broadening the range of patients that could benefit from medical gas plasma therapy in the future. Likewise, the application of such liquids might be promising for recurrent BRAF(V600E) papillary thyroid carcinomas, resistant to adjuvant administration of radioiodine. From a redox biology point of view, studying redox-based approaches in thyroid carcinomas is particularly interesting, as they evolve in a highly oxidative environment requiring the capability to cope with large amounts of ROS/RNS. Knowledge on their behavior under different redox conditions is scarce. The present study aimed to clarify resistance, proliferative activity, and the oxidative stress response of human papillary thyroid cancer cells K1 after exposure to plasma-oxidized DMEM (oxDMEM). Cellular responses were also evaluated when treated with different dosages of hydrogen peroxide and the RNS donor sodium nitroprusside (SNP). Our findings outline plasma-oxidized liquids as a promising approach targeting BRAF(V600E) papillary thyroid carcinomas and extend current knowledge on the susceptibility of cells to undergo ROS/RNS-induced cell death

Evaluation of resistance training to improve muscular strength and body composition in cancer patients undergoing neoadjuvant and adjuvant therapy: a meta-analysis

Purpose: Muscle atrophy and strength decline are two of the most prominent characteristics in cancer patients undergoing cancer therapy, leading to decreased functional ability and reduced quality of life. Therefore, the aim is to systematically review research evidence of the effects of resistance exercise (RE) on lower-limb muscular strength, lean body mass (LBM), and body fat (BF) in cancer patients undertaking neoadjuvant or adjuvant therapy. Methods: This research was conducted using the following online database: Clinical Trial Register, Cochrane Trial Register, PubMed, SPORT Discus, and SciELO, from September 2014 until May 2015. We used the following keywords in various combinations with a systematic search: “Cancer therapy,” “Wasting muscle,” “Muscle loss,” “Muscle function,” “Neoadjuvant therapy,” “Adjuvant thera-py,” “Resistance Training,” “Weight training,” and “Exercise.” After selection of 272 full-text articles, 14 publications were included in this meta-analysis. Results: Resistance exercise (RE) during neoadjuvant or adjuvant therapy increased lower-limb muscular strength (mean: 26.22\ua0kg, 95% CI [16.01, 36.43], heterogeneity: P\ua0=\ua

Low-Dose Oxidant Toxicity and Oxidative Stress in Human Papillary Thyroid Carcinoma Cells K1

Medical gas plasmas are of emerging interest in pre-clinical oncological research. Similar to an array of first-line chemotherapeutics and physics-based therapies already approved for clinical application, plasmas target the tumor redox state by generating a variety of highly reactive species eligible for local tumor treatments. Considering internal tumors with limited accessibility, medical gas plasmas help to enrich liquids with stable, low-dose oxidants ideal for intratumoral injection and lavage. Pre-clinical investigation of such liquids in numerous tumor entities and models in vitro and in vivo provided evidence of their clinical relevance, broadening the range of patients that could benefit from medical gas plasma therapy in the future. Likewise, the application of such liquids might be promising for recurrent BRAF(V600E) papillary thyroid carcinomas, resistant to adjuvant administration of radioiodine. From a redox biology point of view, studying redox-based approaches in thyroid carcinomas is particularly interesting, as they evolve in a highly oxidative environment requiring the capability to cope with large amounts of ROS/RNS. Knowledge on their behavior under different redox conditions is scarce. The present study aimed to clarify resistance, proliferative activity, and the oxidative stress response of human papillary thyroid cancer cells K1 after exposure to plasma-oxidized DMEM (oxDMEM). Cellular responses were also evaluated when treated with different dosages of hydrogen peroxide and the RNS donor sodium nitroprusside (SNP). Our findings outline plasma-oxidized liquids as a promising approach targeting BRAF(V600E) papillary thyroid carcinomas and extend current knowledge on the susceptibility of cells to undergo ROS/RNS-induced cell death

Metformin inhibits the inflammatory and oxidative stress response induced by skin UVB-irradiation and provides 4-hydroxy-2-nonenal and nitrotyrosine formation and p53 protein activation

Skin exposure to ultraviolet B (UVB) radiation leads to local oxidative stress, inflammation, systemic immunosuppression and, ultimately, the development of skin cancer. Metformin is the most prescribed drug for type 2 diabetes, and it has been shown that chronic treatments with this drug reduces skin cancer incidence.Objective. Our aim was to analyze the effects of metformin on UVB-induced acute local damage.Methods. C57/BL6 mice were pretreated with 90 mg/kg of metformin for 11 days and exposed to 400 mJ/cm2 of UVB radiation. Twenty-four hours later, we obtained skin samples to determine oxidative stress and the inflammatory response. Results. We observed that metformin did not prevent UVB-induced epidermal damage, Langerhans cells loss or mitochondrial alterations in epidermal cells. However, it improved the reducing state in the skin, increasing antioxidant molecules that led to reduced 4-hidroxynonenal and nitrotyrosine labeling. Local inflammatory mediators increased by UVB radiation, such as IL-6 and IL-1β, were also reduced by metformin.Conclusion. We demonstrated that metformin reduces UVB-induced local and systemic damage, changes that could explain its antitumoral effect. Thus, the use of metformin as a potential agent to maintain skin homeostasis and prevent UVB-induced lesions requires evaluation.Fil: Pinheiro Souza Neto, Fernando. Universidade Estadual de Londrina; BrasilFil: Marinello, Poliana Camila. Universidade Estadual de Londrina; BrasilFil: Melo, Gabriela Pasqual. Universidade Estadual de Londrina; BrasilFil: Zambeli Naira Ramalho, Leandra. Universidade Estadual de Londrina; BrasilFil: Cela, Eliana M.. Universidade de Sao Paulo; BrasilFil: Campo, Valeria Evelyn. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni; ArgentinaFil: Gonzalez Maglio, Daniel Horacio. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni. Universidad de Buenos Aires. Facultad de Farmacia y Bioquímica. Instituto de Estudios de la Inmunidad Humoral Prof. Ricardo A. Margni; ArgentinaFil: Cecchini, Rubens. Universidade Estadual de Londrina; BrasilFil: Lourenço Cecchini, Alessandra. Universidade Estadual de Londrina; Brasi