Abstract
This study aimed to determine whether low dietary Se content affects the function and mechanisms mediating the vascular relaxation of rat aortas, and to test the role of oxidative stress in observed differences. Male Sprague Dawley (SD) rats were maintained for 10 weeks on low Se (low-Se group; N = 20) or normal Se content (norm-Se group; N = 20) rat chow. Dose responses to acetylcholine (ACh; 10−9–10−5M) and the response to reduced pO2 were tested in noradrenaline-precontracted aortic rings in the absence/presence of the nitric oxide synthase (NOS) inhibitor nitro-l-arginine methyl ester (l-NAME), the cyclooxygenase 1 and 2 (COX-1, 2) inhibitor Indomethacin, and the antioxidative agent Tempol in tissue bath. mRNA expression of glutathione peroxidase 1 (GPx1), catalase (CAT), and Cu/Zn superoxide dismutase (SOD) was measured in rat aortas. Oxidative stress (Thiobarbituric Acid Reactive Substances; TBARS), antioxidative plasma capacity (ferric reducing ability of plasma assay; FRAP), and protein levels of GPx1 were measured in plasma and serum samples, respectively. Reduced ACh-induced relaxation (AChIR) (dominantly mediated by NO) in the low-Se group compared to the norm-Se group was restored by Tempol administration. Hypoxia-induced relaxation (HIR) (dominantly mediated by COX-1, 2), TBARS, and FRAP as well as GPx1 serum concentrations were similar between the groups. mRNA GPx1 expression in rat aortas was significantly decreased in the low-Se compared to the norm-Se group. These data suggest that low dietary Se content increases the local oxidative stress level, which subsequently affects the NO-mediated vascular response.
Highlights
It is well accepted that an increased oxidative stress level, which represents an imbalance between prooxidants and antioxidants in favor of prooxidants, is one of the main contributors to the development and progression of various pathological conditions linked to cardiovascular diseases (CVDs), including atherosclerosis, hypertension, diabetes mellitus, hypercholesterolemia, obesity, etc. [1,2]
Analysis of isolated rat aortic ring sensitivity to ACh demonstrated that the low-Se rats exhibited reduced sensitivity of isolated aortic rings to ACh compared to isolated aortic rings of the norm-Se rats
In the norm-Se group, the presence of L-NAME and Indomethacin significantly reduced the ACh-induced relaxation (AChIR) of isolated rat aortic rings, which means that AChIR in norm-Se rats was mediated mainly by NO, with a significant contribution of COX-1, -2 vasodilator metabolites as well (Figure 3A)
Summary
It is well accepted that an increased oxidative stress level, which represents an imbalance between prooxidants and antioxidants in favor of prooxidants, is one of the main contributors to the development and progression of various pathological conditions linked to cardiovascular diseases (CVDs), including atherosclerosis, hypertension, diabetes mellitus, hypercholesterolemia, obesity, etc. [1,2]. It is well accepted that an increased oxidative stress level, which represents an imbalance between prooxidants and antioxidants in favor of prooxidants, is one of the main contributors to the development and progression of various pathological conditions linked to cardiovascular diseases (CVDs), including atherosclerosis, hypertension, diabetes mellitus, hypercholesterolemia, obesity, etc. Endothelial dysfunction is considered to be a key early event in the development of CVDs [3,4]. Endothelial cells are susceptible to oxidative stress, through reactive oxygen species (ROS)-mediated cell death, and because of the compromised. Res. Public Health 2017, 14, 591; doi:10.3390/ijerph14060591 www.mdpi.com/journal/ijerph
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