Objective. To assess the influence of different physical training status on exercise-induced oxidative stress and changes in cellular redox state. Methods. Thirty male subjects participated in this study and were assigned as well-trained (WT), moderately trained (MT), and untrained (UT) groups. The levels of cortisol, creatine kinase, plasma reduced glutathione to oxidized glutathione (GSH/GSSG), cysteine/cystine (Cys/CySS), and GSH/GSSG ratio in red blood cells (RBCs) were measured immediately and 10 and 30 min after exercise. Results. Following the exercise, plasma GSH/GSSG (p = 0.001) and Cys/CySS (p = 0.005) were significantly reduced in all groups. Reduction in plasma GSH/GSSG ratio in all groups induced a transient shift in redox balance towards a more oxidizing environment without difference between groups (p = 0.860), while RBCs GSH/GSSG showed significant reduction (p = 0.003) and elevation (p = 0.007) in UT and MT groups, respectively. The highest level of RBCs GSH/GSSG ratio was recorded in MT group, and the lowest one was recorded in the WT group. Conclusion. Long term regular exercise training with moderate intensity shifts redox balance towards more reducing environment, versus intensive exercise training leads to more oxidizing environment and consequently development of related diseases.
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http://dx.doi.org/10.1155/2016/3757623 | DOI Listing |
Toxics
November 2024
Laboratory of Metabolic Biochemistry, Institute of Exact and Biological Sciences, UFOP, Ouro Preto 35402-136, MG, Brazil.
Paracetamol (APAP) overdose is the leading cause of drug-induced liver injury, leading to acute liver failure. However, the role of concurrent acute or chronic ethanol ingestion in this context requires further clarification. In this study, we investigated the effects of acute and chronic ethanol ingestion on APAP-induced hepatotoxicity.
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December 2024
Institute of Chemical Biology, National Hellenic Research Foundation, 11635 Athens, Greece.
: DNA damage response (DDR) is a network of molecular pathways associated with the pathogenesis and progression of several diseases, as well as the outcome of chemotherapy. Moreover, the intracellular redox status is essential for maintaining cell viability and controlling cellular signaling. Herein, we analyzed DDR signals and redox status in peripheral blood mononuclear cells (PBMCs) from patients with lung cancer with different response rates to platinum-based chemotherapy.
View Article and Find Full Text PDFAntioxidants (Basel)
November 2024
Laboratory of Biochemistry and Molecular Biology, Department of Movement, Human and Health Sciences, Università degli Studi di Roma "Foro Italico", Piazza Lauro De Bosis 6, 00135 Roma, Italy.
Skeletal muscle tissue can regenerate after damage through the action of satellite cells, which proliferate as myoblasts when activated. Oxidative stress, marked by high rates of reactive oxygen species (e.g.
View Article and Find Full Text PDFMol Carcinog
January 2025
Key Laboratory of Computer-Aided Drug Design of Dongguan City, The First Dongguan Affiliated Hospital, School of Pharmacy, Guangdong Medical University, Dongguan, Guangdong, China.
The progression of tumors has been demonstrated to have a strong correlation with ferroptosis. Bis(4-hydroxy-3,5-dimethylphenyl) sulfone (TMBPS) has been shown to effectively inhibit the proliferation of hepatocellular carcinoma (HCC), but its underlying mechanism is not clear. In this study, ferrostatin-1 (Fer-1) was employed to explore whether the death of HCC cells caused by TMBPS is related to ferroptosis.
View Article and Find Full Text PDFBioorg Chem
December 2024
Institute of Geriatrics, The 2nd Medical Center, China National Clinical Research Center for Geriatric Disease, Chinese People's Liberation Army General Hospital, Beijing, China. Electronic address:
Background: Hederagenin (HG), derived from ivy seeds, is known to offer protection against Alzheimer's disease (AD). However, the specific molecular pathways through which it counters ferroptosis-induced neurotoxicity are not fully elucidated. This investigation seeks to delineate the processes by which HG mitigates neurotoxic effects in HT22 cells subjected to glutamate (Glu)-induced ferroptosis.
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