Background: Exercise induces a multitude of physiological and biochemical changes in blood that can affect its redox status. Exercise causes an increase in oxygen consumption by the whole body and particularly by the exercising muscle. As a result of this process there is a rise in the production of reactive oxygen species (ROS), which are capable to trigger a chain of damaging biochemical and physiological changes known as lipid peroxidation and oxidative stress. Since the early work of Dillard et al. in 1978, and findings of increased lipid peroxidation following acute aerobic exercise, the topic of exercise-induced oxidative stress has received considerable attention.
Objectives: The aim of this study was to examine how swimming to the point of exhaustion affects oxidative stress generation and nonenzymatic antioxidant activity in an animal model.
Material And Methods: The experiments were conducted on 10 male Dunkin-Hartley guinea pigs, and the swimming program used in the study, described as swimming to exhaustion, was defined by Dawson and Horvath. Peripheral blood samples were taken at rest and immediately after the exercise test, and the following parameters were evaluated: total plasma peroxide concentration (TPPC), total plasma thiols (TPT), plasma xanthine oxidase activity (XOD), plasma antioxidant capacity and total plasma proteins.
Results: No significant difference was found between TPPC measured at rest and immediately after exercise swimming test (p = 0.138). Two other parameters--TPT and XOD activity--showed significant differences before and after the swimming exercise test: After the test the TPT value decreased significantly (p = 0.022), while XOD activity increased significantly (p = 0.039). Comparing antioxidant activity in plasma before and after the exercise test, although the value decreased, the difference was not statistically significant (p = 0.755).
Conclusions: The results of this study show that exercise to exhaustion induces the generation of oxidative stress primarily by oxidative modification of protein molecules. The results also indicated that the prooxidative enzyme xanthine oxidase is an important source of ROS during exercise-induced oxidative injury.
Download full-text PDF |
Source |
---|
Proc Natl Acad Sci U S A
January 2025
Shenzhen Hospital, Southern Medical University, Shenzhen 518000, China.
ADAR is highly expressed and correlated with poor prognosis in hepatocellular carcinoma (HCC), yet the role of its constitutive isoform ADARp110 in tumorigenesis remains elusive. We investigated the role of ADARp110 in HCC and underlying mechanisms using clinical samples, a hepatocyte-specific knock-in mouse model, and engineered cell lines. ADARp110 is overexpressed and associated with poor survival in both human and mouse HCC.
View Article and Find Full Text PDFPLoS One
January 2025
Chemistry and Biochemistry, University of St. Thomas, Houston, TX, United States of America.
Cardiovascular disease (CVD) remains the leading cause of morbidity and mortality globally, with oxidative stress playing a pivotal role in its progression. Free radicals produced via oxidative stress contribute to lipid peroxidation, leading to subsequent inflammatory responses, which then result in atherosclerosis. Antioxidants inhibit these harmful effects through their reducing ability, thereby preventing oxidative damage.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Department of Clinical Veterinary Medicine, College of Veterinary Medicine, Jilin University, Changchun, 130062, China.
Microbial transmission from mother to infant is important for offspring microbiome formation and health. However, it is unclear whether maternal gut inflammation (MGI) during lactation influences mother-to-infant microbial transmission and offspring microbiota and disease susceptibility. In this study, it is found that MGI during lactation altered the gut microbiota of suckling pups by shaping the maternal microbiota in the gut and mammary glands.
View Article and Find Full Text PDFJ Agric Food Chem
January 2025
Department of Chemistry, The Hong Kong University of Science and Technology, Clear Water Bay, Kowloon, Hong Kong.
Inadvertent exposure to aristolochic acids (AAs) is causing chronic renal disease worldwide, with aristolochic acid I (AA-I) identified as the primary toxic agent. This study employed chemical methods to investigate the mechanisms underlying the nephrotoxicity and carcinogenicity of AA-I. Aristolochic acid II (AA-II), which has a structure similar to that of AA-I, was investigated with the same methods for comparison.
View Article and Find Full Text PDFDiabetes
January 2025
Department of Biology & Institute of Biochemistry, Carleton University, Ottawa, ON, Canada.
Cancer survivors have an increased risk of developing Type 2 diabetes compared to the general population. Patients treated with cisplatin, a common chemotherapeutic agent, are more likely to develop metabolic syndrome and Type 2 diabetes than age- and sex-matched controls. Surprisingly, the impact of cisplatin on pancreatic islets has not been reported.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!