ArticleToxicology and applied pharmacology2015
High level of oxygen treatment causes cardiotoxicity with arrhythmias and redox modulation.
Article in Toxicology and applied pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 36 citations in OpenAlex.
- Supplemental oxygen induced cardiovascular pathophysiology in an end-of-life care model in mice.Physiological reports · 2026Article
- Review
- Influence of age and sex on physical, cardiac electrical and functional alterations in progressive hyperoxia treatment: A time course study in a murine model.Experimental gerontology · 2024Article
- Cardioprotective Effects of Dexmedetomidine in an Oxidative-Stress In Vitro Model of Neonatal Rat Cardiomyocytes.Antioxidants (Basel, Switzerland) · 2023Article
- Article
- Oxygen toxicity: cellular mechanisms in normobaric hyperoxia.Cell biology and toxicology · 2023Review
- Cardioprotective Effects of 1-(3,6-Dibromo-carbazol-9-yl)-3-Phenylamino-Propan-2-Ol in Diabetic Hearts via Nicotinamide Phosphoribosyltransferase Activation.The Journal of pharmacology and experimental therapeutics · 2022Article
- Hyperoxia and Acute Kidney Injury: A Tale of Oxygen and the Kidney.Seminars in nephrology · 2022Review
- Nampt activator P7C3 ameliorates diabetes and improves skeletal muscle function modulating cell metabolism and lipid mediators.Journal of cachexia, sarcopenia and muscle · 2022Article
- BMI1 Silencing Induces Mitochondrial Dysfunction in Lung Epithelial Cells Exposed to Hyperoxia.Frontiers in physiology · 2022Article
- The implications of hyperoxia, type 1 diabetes and sex on cardiovascular physiology in mice.Scientific reports · 2021Article
- The Acute Effect of Hyperoxia on Onset of Blood Lactate Accumulation (OBLA) and Performance in Female Runners during the Maximal Treadmill Test.International journal of environmental research and public health · 2021Article
- Metabolic regulation of Kv channels and cardiac repolarization by Kvβ2 subunits.Journal of molecular and cellular cardiology · 2019Article
- Impact of hyperoxia on cardiac pathophysiology.Journal of cellular physiology · 2019Review
- Cardiovascular Risks Associated with Gender and Aging.Journal of cardiovascular development and disease · 2019Review
- Physiological role of Kvβ2 (AKR6) in murine skeletal muscle growth and regulation.Acta physiologica (Oxford, England) · 2018Article
- Hyperoxia-induced cardiotoxicity and ventricular remodeling in type-II diabetes mice.Heart and vessels · 2018Article
- Diabetes Mellitus and Ischemic Heart Disease: The Role of Ion Channels.International journal of molecular sciences · 2018Review
- Corticosteroids and aldose reductase inhibitor Epalrestat modulates cardiac action potential via Kvβ1.1 (AKR6A8) subunit of voltage-gated potassium channel.Molecular and cellular biochemistry · 2017Article
- Proteomic analysis of mitochondrial proteins in the guinea pig heart following long-term normobaric hyperoxia.Molecular and cellular biochemistry · 2017Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Hyperoxia exposure in mice leads to cardiac hypertrophy and voltage-gated potassium (Kv) channel remodeling. Because redox balance of pyridine nucleotides affects Kv function and hyperoxia alters cellular redox potential, we hypothesized that hyperoxia exposure leads to cardiac ion channel disturbances and redox changes resulting in arrhythmias. In the present study, we investigated the electrical changes and redox abnormalities caused by 72h hyperoxia treatment in mice. Cardiac repolarization changes were assessed by acquiring electrocardiogram (ECG) and cardiac action potentials (AP). Biochemical assays were employed to identify the pyridine nucleotide changes, Kv1.5 expression and myocardial injury. Hyperoxia treatment caused marked bradycardia, arrhythmia and significantly prolonged (ms) the, RR (186.2 ± 10.7 vs. 146.4 ± 6.2), PR (46.8 ± 3.1 vs. 39.3 ± 1.6), QRS (10.8 ± 0.6 vs. 8.5 ± 0.2), QTc (57.1 ± 3.5 vs. 40 ± 1.4) and JT (13.4 ± 2.1 vs. 7.0 ± 0.5) intervals, when compared with normoxia group. Hyperoxia treatment also induced significant increase in cardiac action potential duration (APD) (ex-APD90; 73.8 ± 9.5 vs. 50.9 ± 3.1 ms) and elevated levels of serum markers of myocardial injury; cardiac troponin I (TnI) and lactate dehydrogenase (LDH). Hyperoxia exposure altered cardiac levels of mRNA/protein expression of; Kv1.5, Kvβ subunits and SiRT1, and increased ratios of reduced pyridine nucleotides (NADH/NAD & NADPH/NADP). Inhibition of SiRT1 in H9C2 cells using Splitomicin resulted in decreased SiRT1 and Kv1.5 expression, suggesting that SiRT1 may mediate Kv1.5 downregulation. In conclusion, the cardiotoxic effects of hyperoxia exposure involve ion channel disturbances and redox changes resulting in arrhythmias.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.