Arsenic exacerbates atherosclerotic lesion formation and inflammation in ApoE-/- mice

Srivastava, Sanjay; Vladykovskaya, Elena; Haberzettl, Petra; Sithu, Srinivas D; D’Souza, Stanley E.; States, J. Christopher

doi:10.1016/j.taap.2009.08.004

Cited by 97 publications

(82 citation statements)

References 45 publications

(58 reference statements)

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“…Consistent with the association with risk factors and CV disease, an association has also been found between As exposure and atherosclerosis (Wang et al 2002;Wang et al 2010;Hsieh et al 2011), and confirmed in experimental animal studies (Bunderson et al 2004;Srivastava et al 2009;Lemaire et al 2011). …”

Section: As In the CV Continuumsupporting

confidence: 62%

Cardiovascular effects of arsenic: clinical and epidemiological findings

Stea

Bianchi

Cori

et al. 2013

Environ Sci Pollut Res

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Section: As In the CV Continuumsupporting

confidence: 62%

Cardiovascular effects of arsenic: clinical and epidemiological findings

Stea

Bianchi

Cori

et al. 2013

Environ Sci Pollut Res

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“…39 IL-6 also increases the formation of ROS. 40 These observations suggest that oxidative stress induced by these inflammatory cytokines may have a role in cardiac remodeling and diastolic dysfunction in DS/obese rats.…”

Section: Discussionmentioning

confidence: 93%

Cardiac remodeling and diastolic dysfunction in DahlS.Z-Leprfa/Leprfa rats: a new animal model of metabolic syndrome

et al. 2011

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We recently characterized male DahlS.Z-Lepr fa /Lepr fa (Dahl salt-sensitive (DS)/obese) rats, which were established from a cross between Dahl salt-sensitive and Zucker rats, as a new animal model of metabolic syndrome (MetS). We have now investigated cardiac pathophysiology and metabolic changes in female DS/obese rats in comparison with homozygous lean female littermates (DahlS.Z-Lepr + /Lepr + , or DS/lean, rats). Animals were maintained on a normal diet and were subjected to echocardiography followed by various pathological analyses at 15 weeks of age. Systolic blood pressure was significantly higher in female DS/obese rats than in DS/lean females at 12 weeks of age and thereafter. The survival rate of DS/obese rats was significantly lower than that of DS/lean rats at 15 weeks. Body weight, as well as visceral and subcutaneous fat mass were significantly increased in DS/obese rats, which also manifested left ventricular (LV) diastolic dysfunction and marked LV hypertrophy and fibrosis. In addition, myocardial oxidative stress and inflammation were increased in DS/obese rats compared with DS/lean rats. Serum insulin and triglyceride levels as well as the ratio of low-density lipoprotein-to high-density lipoprotein-cholesterol levels were markedly elevated in DS/obese rats, whereas fasting serum glucose concentrations were similar in the two rat strains. The phenotype of female DS/obese rats is similar to that of MetS in humans. These animals also develop salt-sensitive hypertension and LV diastolic dysfunction as well as LV hypertrophy and fibrosis, and these changes are associated with increased cardiac oxidative stress and inflammation. Keywords: cardiac hypertrophy; diastolic dysfunction; metabolic syndrome; myocardial fibrosis; salt-sensitive hypertension INTRODUCTION Metabolic syndrome (MetS), a complex of highly debilitating disorders including hypertension, diabetes mellitus and dyslipidemia, is associated with the development of visceral obesity. 1 Adipocytes in visceral fat of obese humans secrete a variety of biological agents that are known as adipocytokines and include proinflammatory cytokines such as tumor necrosis factor (TNF)-a and interleukin (IL)-6 as well as angiotensinogen and leptin. 2 Recent studies have revealed intricate interactions among adipocytes, the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) that contribute to the disturbed metabolic state associated with obesity. 3 Indeed, adipose tissue is thought to have an important role in the development of both hypertension and other complications related to insulin resistance. Activation of the RAAS and associated oxidative stress can result in mitochondrial abnormalities, altered bioenergetics and the accumulation of lipids in the heart, and thereby increase susceptibility to metabolic cardiomyopathy. 4

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“…Many studies show that oxidative stress plays an important role in several clinical conditions such as atherosclerosis 19 , liver and kidney injuries 20 .It was reported that oxidative stress was elevated in arsenic-exposed mice 21 .…”

Section: Discussionmentioning

confidence: 99%

Spirulina platensis, reduced liver and kidney injuries induced by Sodium arsenite

2017

IJPTR

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: Spirulina platensis, a blue-green alga, has vastly therapeutic properties and it is used as food supplement. This study aims to evaluate the protective effect of Spirulina platensis against arsenic hepatorenal toxicity based on its antioxidantproperties,free-radical scavenger and immunological properties. Oral administration of sodium arsenite (6.3mg/Kg, p.o BW) to rats for eight weeks led to a significant increase in serum monocyte chemoattractant protein-1 (MCP-1), tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), cholesterol, triglycerides, liver (AST,ALT, and ALP), and kidney function parameters (urea, uric acid, and creatinine) except serum protein level which was significantly reduced. In addition, arsenic-induced oxidative stress and lipid peroxidation process as evidenced by elevation of malondialdehyde (MDA) and declinein the activities of hepatic and renal catalase (CAT),superoxide dismutase(SOD) enzymes, and glutathione (GSH) levels in which reflected on the final body and liver weights.Hepatorenal pathological changes were observed in the arsenic group.Treatment of rats with spirulina platensis(300mg/kg, p.o BW) mitigates indices of atherosclerosis, hepato-renal oxidative stress and pathological changes of liver and kidney induced by arsenic. These results support the spirulina protective effect of by which it lessens several factors involved in the progression of atherosclerosis and liver and kidney toxicity.

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Arsenic exacerbates atherosclerotic lesion formation and inflammation in ApoE-/- mice

Cited by 97 publications

References 45 publications

Cardiovascular effects of arsenic: clinical and epidemiological findings

Cardiovascular effects of arsenic: clinical and epidemiological findings

Cardiac remodeling and diastolic dysfunction in DahlS.Z-Leprfa/Leprfa rats: a new animal model of metabolic syndrome

Spirulina platensis, reduced liver and kidney injuries induced by Sodium arsenite

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