Long-term Mercury Exposure Accelerates the Development of Hypertension in Prehypertensive Spontaneously Hypertensive Rats Inducing Endothelial Dysfunction: the Role of Oxidative Stress and Cyclooxygenase-2

Simões, Rakel Passos; Fardin, P; Vassallo, Dalton Valentim; Padilha, Alessandra Simão

doi:10.1007/s12011-019-01952-8

Cited by 9 publications

(3 citation statements)

References 45 publications

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“…The organism contains multiple antioxidant defense mechanisms, which keep oxidative stress to the appropriate levels. Regarding superoxide anion, the main enzyme responsible for its physiological metabolism is SOD, the activity and expression of which are reduced in the cardiovascular system in hypertension [86,87]. Regarding several studies, manipulation of gut microbiota with different approaches, including supplementation with synbiotics and probiotics, restored these alterations [88][89][90].…”

Section: Discussionmentioning

confidence: 99%

Supplementation with the Symbiotic Formulation Prodefen® Increases Neuronal Nitric Oxide Synthase and Decreases Oxidative Stress in Superior Mesenteric Artery from Spontaneously Hypertensive Rats

et al. 2022

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In recent years, gut dysbiosis has been related to some peripheral vascular alterations linked to hypertension. In this work, we explore whether gut dysbiosis is related to vascular innervation dysfunction and altered nitric oxide (NO) production in the superior mesenteric artery, one of the main vascular beds involved in peripheral vascular resistance. For this purpose, we used spontaneously hypertensive rats, either treated or not with the commercial synbiotic formulation Prodefen® (108 colony forming units/day, 4 weeks). Prodefen® diminished systolic blood pressure and serum endotoxin, as well as the vasoconstriction elicited by electrical field stimulation (EFS), and enhanced acetic and butyric acid in fecal samples, and the vasodilation induced by the exogenous NO donor DEA-NO. Unspecific nitric oxide synthase (NOS) inhibitor L-NAME increased EFS-induced vasoconstriction more markedly in rats supplemented with Prodefen®. Both neuronal NO release and neuronal NOS activity were enhanced by Prodefen®, through a hyperactivation of protein kinase (PK)A, PKC and phosphatidylinositol 3 kinase-AKT signaling pathways. The superoxide anion scavenger tempol increased both NO release and DEA-NO vasodilation only in control animals. Prodefen® caused an increase in both nuclear erythroid related factor 2 and superoxide dismutase activities, consequently reducing both superoxide anion and peroxynitrite releases. In summary, Prodefen® could be an interesting non-pharmacological approach to ameliorate hypertension.

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Section: Discussionmentioning

confidence: 99%

Supplementation with the Symbiotic Formulation Prodefen® Increases Neuronal Nitric Oxide Synthase and Decreases Oxidative Stress in Superior Mesenteric Artery from Spontaneously Hypertensive Rats

et al. 2022

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“…A study of non-Hispanic Asians using NHANES data found that higher blood Hg levels were associated with hypertension [ 177 ]. Studies using spontaneously hypertensive rats (SHR) found that exposure to Hg accelerated the development of hypertension by increasing the production of nitric oxide and other ROS [ 178 , 179 ]. However, it appears that Hg also induces vasoprotective mechanisms such as increased plasma levels of nitric oxide and hydrogen peroxide to counteract other vasoconstrictive effects [ 179 ].…”

Section: Molecular Effects Of Environmental Toxicants On Ckd Progressionmentioning

confidence: 99%

Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease

Mishra

Nichols

Dave

et al. 2022

IJMS

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Chronic kidney disease (CKD) is a progressive disease that affects millions of adults every year. Major risk factors include diabetes, hypertension, and obesity, which affect millions of adults worldwide. CKD is characterized by cellular injury followed by permanent loss of functional nephrons. As injured cells die and nephrons become sclerotic, remaining healthy nephrons attempt to compensate by undergoing various structural, molecular, and functional changes. While these changes are designed to maintain appropriate renal function, they may lead to additional cellular injury and progression of disease. As CKD progresses and filtration decreases, the ability to eliminate metabolic wastes and environmental toxicants declines. The inability to eliminate environmental toxicants such as arsenic, cadmium, and mercury may contribute to cellular injury and enhance the progression of CKD. The present review describes major molecular alterations that contribute to the pathogenesis of CKD and the effects of arsenic, cadmium, and mercury on the progression of CKD.

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“…11,17,18 Additionally, the toxic effects of mercury chloride exposure on the cardiovascular system are well described in the literature, but mainly in male rats. [19][20][21][22] However, little information is available about the toxicity of this metal in the female cardiovascular system. Because female hormones exhibit vascular protection, we investigated the effects of mercury chloride on the blood pressure and vascular reactivity of the aorta, as well as the role played by the endothelium, nitric oxide and cyclooxygenase-2 (COX-2)-derived prostanoids, to clarify the effects of mercury chloride poisoning in female rats and a putative effect on oestrogen signalling.…”

mentioning

confidence: 99%

Chronic mercury exposure induces oxidative stress in female rats by endothelial nitric oxide synthase uncoupling and cyclooxygenase‐2 activation, without affecting oestrogen receptor function

Schereider

Vassallo

2021

Basic Clin Pharma Tox

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Mercury has been shown to be a significant health risk factor and is positively associated with cardiovascular diseases. Evidence reveals that men are more likely to develop cardiovascular diseases than women during reproductive age.However, the effects of mercury in females remain poorly investigated, despite the finding that female hormones demonstrate a cardioprotective role. In the present study, we evaluated whether chronic mercury chloride exposure could alter blood pressure and vascular function of the female rat aorta.Ten-week-old female Wistar rats were divided into two groups: control (vehicle) and mercury treated (first dose of 4.6 μg/kg, subsequent daily doses of 0.07 μg/kg), im. Mercury treatment did not modify systolic blood pressure (SBP) but increased vascular reactivity due to the reduction of nitric oxide bioavailability associated with the increase in reactive oxygen species from endothelial nitric oxide synthase (eNOS) uncoupling. Furthermore, increased participation of the cyclooxygenase-2 pathway occurred through an imbalance in thromboxane 2 and prostacyclin 2. However, the oestrogen signalling pathway was not altered in either group. These results demonstrated that chronic exposure to mercury in females induced endothelial dysfunction and, consequently, increased aortic vascular reactivity, causing vascular damage to the female rat aorta and representing a risk of cardiovascular diseases.endothelial dysfunction, eNOS uncoupling, female rats, mercury chloride, vascular reactivity | INTRODUCTIONMercury has been recognized by the Agency for Toxic Substances and Disease Registry 1 as ranking third, behind arsenic and lead, on the priority list of substances that pose potential threats to human health due to its high toxicity and ability to biomagnify and bioaccumulate in the food chain. 2 Studies have shown that acute and chronic mercury exposure lead to adverse effects, such as the development of atherosclerosis, coronary artery disease, hypertension, changes in the oestrous cycle and features of polycystic ovary syndrome. [3][4][5][6][7]

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Long-term Mercury Exposure Accelerates the Development of Hypertension in Prehypertensive Spontaneously Hypertensive Rats Inducing Endothelial Dysfunction: the Role of Oxidative Stress and Cyclooxygenase-2

Cited by 9 publications

References 45 publications

Supplementation with the Symbiotic Formulation Prodefen® Increases Neuronal Nitric Oxide Synthase and Decreases Oxidative Stress in Superior Mesenteric Artery from Spontaneously Hypertensive Rats

Supplementation with the Symbiotic Formulation Prodefen® Increases Neuronal Nitric Oxide Synthase and Decreases Oxidative Stress in Superior Mesenteric Artery from Spontaneously Hypertensive Rats

Molecular Mechanisms of Cellular Injury and Role of Toxic Heavy Metals in Chronic Kidney Disease

Chronic mercury exposure induces oxidative stress in female rats by endothelial nitric oxide synthase uncoupling and cyclooxygenase‐2 activation, without affecting oestrogen receptor function

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