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Oxidative stress remains one of the most well studied, albeit somewhat contentious, causes of age-related changes in humans. Consequently, a large number of putative antioxidant compounds are freely available in myriad formulations that are often not tested for their efficacy or regulated for quality control. Following the development of a Drosophila model of oxidative-stress dependent aging (p38 MAP K (p38K) mutants) in our laboratory, we attempted to test the protective effect of some of these commonly available formulations against oxidative stress, in the p38K model. As environmental exposure to oxidizing toxins has been linked to a variety of human diseases, we also tested the efficacy of these supplements on chemically-induced models of oxidative stress (paraquat and hydrogen peroxide exposure). Our results suggest that when added as a dietary supplement, some of these over-the-counter compounds, notably containing açai extracts, confer significant protection for both the p38K-dependent genetic model as well as the toxin-induced model. These products were also remarkably effective at dampening stress-induced expression of the detoxifying enzyme GSTD1 and eliminating paraquat induced circadian rhythm deficits. Overall, our results suggest potential benefits of dietary supplementation with some of these compounds, especially under conditions of elevated oxidative stress. These findings should be assessed in the context of other studies that seek to identify active principles in these extracts, determine their effective dosage for human consumption and evaluate the safety of long-term prophylactic applications.
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http://dx.doi.org/10.1016/j.exger.2012.06.016 | 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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