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Objective: This study aims to investigate the potential effects of carotenoid supplementation on mitigating exercise-induced oxidative stress and to provide guidance for future research.
Methods: We conducted a systematic review and meta-analysis using Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. We searched multiple databases from inception to August 2024 for randomized clinical trials investigating the effects of carotenoid supplementation on biomarkers of oxidative stress, inflammatory markers, antioxidant levels, and metabolic parameters in the context of exercise-induced oxidative stress. The search terms included "carotenoids," "supplementation," "exercise," "oxidative stress," "inflammation," "antioxidants," "metabolic parameters," and their synonyms. Two reviewers independently extracted study data, with disagreements resolved by a third reviewer. Quality was assessed by the Cochrane risk-of-bias method. Random and fixed effects models were used for the analysis of standard mean differences (SMD) or weighted mean differences (MDs) with 95% confidence intervals (CI).
Results: A total of 12 studies were included in the final analysis. Carotenoid supplementation led to significant effects in assessing oxidative stress induced by exercise (overall oxidative stress: SMD = -0.55, 95% CI [-1.04, -0.06]; malondialdehyde: MD = -0.05, 95% CI [-0.09,-0.02]; total antioxidant capacity: MD = 0.03, 95% CI [0.02, 0.03]; 8-isoprostane: MD = -35.70, 95% CI [-59.32, -12.09]; lipid peroxide: SMD = -1.07, 95% CI [-1.94, -0.20]; and nitric oxide: MD = -8.07, 95% CI [-12.54,-3.59]), inflammatory markers (inflammatory levels: SMD = 1.63, 95% CI [0.81, 2.46]; interleukin levels: SMD = 1.54, 95% CI [0.69, 2.40]; and C-reactive protein: MD = 4.56, 95% CI [0.97, 8.14]), antioxidant levels (SMD = 0.84, 95% CI [0.14, 1.53]), and metabolic parameters (energy expenditure: SMD = -0.52, 95% CI [-0.78, -0.26]; p < .05).
Conclusion: Carotenoid supplementation appears to attenuate exercise-induced oxidative stress and the inflammatory response and improve antioxidant levels and metabolic capabilities. However, these results may be influenced by participant variability or methodological differences. Further research with larger sample sizes, longer supplementation periods, higher doses, and carotenoid bioavailability is needed to confirm these findings.
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http://dx.doi.org/10.1123/ijsnem.2024-0256 | DOI Listing |
J Trace Elem Med Biol
September 2025
Department of Neurology, Children's Hospital of Fudan University, National Children's Medical Center, Shanghai, China. Electronic address:
Objective: We previously documented that exposure to a spectrum of elements is associated with autism spectrum disorder (ASD). However, there is a lack of mechanistic understanding as to how elemental mixtures contribute to the ASD development.
Materials And Methods: Serum and urinary concentrations of 26 elements and six biomarkers of ASD-relevant pathophysiologic pathways including serum HIPK 2, serum p53 protein, urine malondialdehyde (MDA), urine 8-OHdG, serum melatonin, and urine carnitine, were measured in 21 ASD cases and 21 age-matched healthy controls of children aged 6-12 years.
Mol Pharm
September 2025
Affiliated Hospital of Shandong Second Medical University, Shandong Second Medical University, Weifang 261053, Shandong, P. R. China.
Myocardial injury constitutes a life-threatening complication of sepsis, driven by synergistic oxidative-inflammatory pathology involving dysregulated production of reactive oxygen species (ROS), reactive nitrogen species (RNS), and proinflammatory cytokines. This pathophysiological cascade remarkably elevates morbidity and mortality rates in septic patients, emerging as a key contributor to poor clinical outcomes. Despite its clinical significance, no clinically validated therapeutics currently exist for managing septic cardiomyopathy.
View Article and Find Full Text PDFPol Merkur Lekarski
September 2025
I. HORBACHEVSKY TERNOPIL NATIONAL MEDICAL UNIVERSITY, TERNOPIL, UKRAINE.
Objective: Aim: To evaluate the state of oxidation processes and morphological changes in the heart of rats with chronic hypodynamia during the development of epinephrine heart damage (EHD)..
Patients And Methods: Materials and Methods: The study was performed on 144 white male Wistar rats.
Exp Physiol
September 2025
Department of Hepatobiliary Surgery, The Affiliated Huaian No.1 People's Hospital of Nanjing Medical University, Huaian, Jiangsu, China.
Hepatic ischaemia-reperfusion (IR) injury is a serious clinical issue, especially in patients with type 2 diabetes mellitus (T2DM). As mitochondria play a critical role in the regulation of IR-induced liver damage, mitochondria-targeted treatment is of the utmost significance for improving outcomes. The present study explored the mitoprotective role of combined ginsenoside-MC1 (GMC1) and irisin administration in diabetic rats with hepatic IR injury.
View Article and Find Full Text PDFPLoS One
September 2025
Department of Cardiac Surgery, Faculty of Medicine and University Hospital Cologne, University of Cologne, Cologne, Germany.
Background: Cardiac ischemia reperfusion (I/R) injury is a serious consequence of reperfusion therapy for myocardial infarction (MI). Peptidylarginine deiminase 4 (PAD4) is a calcium-dependent enzyme that catalyzes the citrullination of proteins. In previous studies, PAD4 inhibition protected distinct organs from I/R injury by preventing the formation of neutrophil extracellular traps (NETs) and attenuating inflammatory responses.
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