AI Article Synopsis
Article Abstract
Aims: Aluminum (Al) is an important environmental contaminant; however, there are not enough evidences of Al-induced cardiovascular dysfunction. We investigated the effects of acute exposure to aluminum chloride (AlCl) on blood pressure, vascular reactivity and oxidative stress.
Methods And Results: Male Wistar rats were divided into two groups: Untreated: vehicle (ultrapure water, ip) and AlCl: single dose of AlCl (100mg/kg,ip). Concentration-response curves to phenylephrine in the absence and presence of endothelium, the nitric oxide synthase inhibitor l-NAME, the potassium channel blocker tetraethylammonium, and the NADPH oxidase inhibitor apocynin were performed in segments from aortic and mesenteric resistance arteries. NO released was assessed in aorta and reactive oxygen species (ROS), malondialdehyde, non-protein thiol levels, antioxidant capacity and enzymatic antioxidant activities were investigated in plasma, aorta and/or mesenteric arteries. After one hour of AlCl exposure serum Al levels attained 147.7±25.0μg/L. Al treatment: 1) did not affect blood pressure, heart rate and vasodilator responses induced by acetylcholine or sodium nitroprusside; 2) decreased phenylephrine-induced vasoconstrictor responses; 3) increased endothelial modulation of contractile responses, NO release and vascular ROS production from NADPH oxidase; 4) increased plasmatic, aortic and mesenteric malondialdehyde and ROS production, and 5) decreased antioxidant capacity and affected the antioxidant biomarkers non-protein thiol levels, glutathione peroxidase, glutathione-S-transferase, superoxide dismutase and catalase enzymatic activities.
Conclusion: AlCl-acute exposure reduces vascular reactivity. This effect is associated with increased NO production, probably acting on K channels, which seems to occur as a compensatory mechanism against Al-induced oxidative stress. Our results suggest that Al exerts toxic effects to the vascular system.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.taap.2016.10.023 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Genome-wide characterization of RsHDAC gene members unravels a positive role of RsHDA9 in thermotolerance in radish (Raphanus sativus L.).
Plant Physiol Biochem
December 2024
Key Laboratory of Horticultural Crop Biology and Genetic Improvement (East China) of MOAR, College of Horticulture, Sanya Institute, Nanjing Agricultural University, Nanjing 210095, PR China. Electronic address:
Radish is an economically important root vegetable crop worldwide. Histone deacetylases (HDACs), one of the most important epigenetic regulators, play prominent roles in plant growth and development as well as abiotic stress responses. Nevertheless, the systematical characterization and critical roles of HDAC gene members in thermogenesis remains elusive in radish.
View Article and Find Full Text PDFHyperbaric Oxygen Therapy Improved Neovascularisation Following Limb Ischaemia-The Role of ROS Mitigation.
J Cell Mol Med
December 2024
Division of Plastic Surgery, Department of Surgery, Chi-Mei Medical Center, Tainan, Taiwan.
Hyperbaric oxygen (HBO) therapy has emerged as a potential treatment, shown to enhance blood flow and angiogenesis. However, specific effects and mechanisms of HBO on limb ischaemia responding to a hypoxic environment remain largely unknown. We aimed to investigate the therapeutic potential of HBO in the treatment of limb ischaemia.
View Article and Find Full Text PDFNuclear respiratory factor-1 (NRF1) induction as a powerful strategy to deter mitochondrial dysfunction and senescence in mesenchymal stem cells.
Aging Cell
December 2024
Department of Nanomedicine, Houston Methodist Research Institute, Houston, Texas, USA.
Mesenchymal stem cells (MSCs) are promising candidates for regenerative therapies due to their self-renewal and differentiation capabilities. Pathological microenvironments expose MSCs to senescence-inducing factors such as reactive oxygen species (ROS), resulting in MSC functional decline and loss of stemness. Oxidative stress leads to mitochondrial dysfunction, a hallmark of senescence, and is prevalent in aging tissues characterized by elevated ROS levels.
View Article and Find Full Text PDFMelatonin attenuates responses to angiotensin II in isolated aortic rings of STZ-induced type 1-like DM rats.
Endocr Res
December 2024
Department of Biology, College of Science, Salahaddin University-Erbil, Erbil, Kurdistan Region, Iraq.
Background: In patients with diabetes mellitus (DM), vascular endothelial dysfunction (VED) is the main reason for impaired life expectancy. Melatonin (MEL) demonstrates wide-ranging effects across various organs and exhibits pleiotropic characteristics. The current study aims to investigate the modulatory roles of MEL vascular response to angiotensin II (Ang II) and its receptors including angiotensin type 1 receptor (AT-1 R) and angiotensin type 2 receptor (AT-2 R) in isolated thoracic aorta of non-diabetes (non-DM) and diabetes (DM) rats.
View Article and Find Full Text PDFSQSTM1 upregulation-induced iron overload triggers endothelial ferroptosis in nicotine-exacerbated atherosclerosis.
Life Sci
December 2024
Department of Anesthesiology, Fujian Provincial Hospital, Shengli Clinical Medical College of Fujian Medical University & Fujian Emergency Medical Center, Fujian Provincial Key Laboratory of Emergency Medicine, Fujian Provincial Key Laboratory of Critical Medicine, Fujian Provincial Co-constructed Laboratory of "Belt and Road", Fuzhou, Fujian 350001, China. Electronic address:
Aims: Nicotine-exacerbated atherosclerosis significantly increases global mortality. Endothelial cells, which line the interior of blood vessels, are crucial for maintaining vascular function. How nicotine is involved in vascular remodeling in atherosclerosis via modulating endothelial dysfunction remains unknown.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!