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Title:
Mercury and metabolic syndrome: a review of experimental and clinical observations | BioMetals
Description:
A significant interrelation between heavy metal exposure and metabolic syndrome (MetS) development has been demonstrated earlier. Despite the presence of a number of works aimed at the investigation of the role of Hg in MetS development, the existing data remain contradictory. Therefore, the primary objective of the current work is to review the existing data regarding the influence of mercury on universal mechanisms involved in the pathogenesis of the development of MetS and its components. The brief chemical characterization of mercury is provided. The role of mercury in induction of oxidative stress has been discussed. In particular, Hg-induced oxidative stress may occur due to both prooxidant action of the metal and decrease in antioxidant enzymes. Despite the absence of direct indications, it can be proposed that mercury may induce endoplasmic reticulum stress. As it is seen from both in vivo and in vitro studies, mercury is capable of inducing inflammation. The reviewed data demonstrate that mercury affects universal pathogenetic mechanisms of MetS development. Moreover, multiple investigations have indicated the role of mercury in pathogenesis of MetS components: dyslipidemia, hypertension, insulin resistance, and obesity to a lesser extent. The present state of data regarding the interrelation between mercury and MetS denotes the following perspectives: (1) Further clinic-epidemiologic and experimental studies are required to estimate the association between mercury exposure and the development of MetS components, especially obesity; (2) Additional investigations of the possible effect of organismās mercury content modulation on MetS pathogenesis should be undertaken.
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Keywords {š}
pubmed, google, scholar, cas, mercury, stress, central, toxicol, oxidative, res, exposure, health, metabolic, environ, syndrome, biol, methylmercury, cells, blood, chem, med, chloride, role, effects, pharmacol, glutathione, trace, rats, diabetes, rat, sci, mercuric, kim, endoplasmic, reticulum, hypertension, effect, activity, vitro, human, lipid, obesity, disease, elem, int, peroxidation, zhang, insulin, cell, biochem,
Topics {āļø}
n-acetyl-beta-d-hexosaminidase c-jun n-terminal kinase p3b72-pro-inflammatory cytokine patiern mercury-mercury spin-spin coupling month download article/chapter pancreatic beta-cell death phosphoinositide 3-kinase/akt signaling decreases methylmercury-induced cerebral relativistic coupled-cluster method guinea-pig taenia coli long-term past exposure methylmercury-induced mitochondrial depolarization methylmercury-induced hypercholesterolemia play genetically determined low-responders signaling regulator grp78/bip displays long-lasting protection serum antinuclear/antinucleolar antibodies methylmercury-induced cell death mouse kidney mn-sod mercuric chloride-induced apoptosis long-lasting oxidative stress nitric oxide-dependent vasorelaxation gamma-glutamyl transferase activity autism spectrum disorders dahl salt-sensitive rats oxidative stress-induced apoptotic insulin-stimulated glucose uptake urinary 8-hydroxy-2ā²-deoxyguanosine concentrations inorganic mercury-induced injury redox-active complexes formed mercury-accessible-sh groups th2-type cytokine production lead-induced endoplasmic reticulum middle-aged japanese men mercury-induced oxidative stress population-based twin study mercury-induced immune activation mercury-induced h2o2 production free radical formation heavy metal-treated erythrocytes additive pro-oxidative effects hg-induced oxidative stress isolated fat cells mercury activates phospholipase mammalian pancreatic -cells abnormal antioxidant system hemoglobin-catalyzed lipid peroxidation privacy choices/manage cookies local angiotensin production reactive oxygen species
Questions {ā}
- Ceriello A, Motz E (2004) Is oxidative stress the pathogenic mechanism underlying insulin resistance, diabetes, and cardiovascular disease?
- Mackness M, Mackness B (2004) Paraoxonase 1 and atherosclerosis: is the gene or the protein more important?
- Meltzer HM, Mundal HH, Alexander J, Bibow K, Ydersbond TA (1994) Does dietary arsenic and mercury affect cutaneous bleeding time and blood lipids in humans?
- Moreira EL, de Oliveira J, Dutra MF, Santos DB, GonƧalves CA, Goldfeder EM, de Bem AF, Prediger RD, Aschner M, Farina M (2012) Does methylmercury-induced hypercholesterolemia play a causal role in its neurotoxicity and cardiovascular disease?
- Vanni E, Bugianesi E, Kotronen A, De Minicis S, Yki-JƤrvinen H, Svegliati-Baroni G (2010) From the metabolic syndrome to NAFLD or vice versa?
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headline:Mercury and metabolic syndrome: a review of experimental and clinical observations
description:A significant interrelation between heavy metal exposure and metabolic syndrome (MetS) development has been demonstrated earlier. Despite the presence of a number of works aimed at the investigation of the role of Hg in MetS development, the existing data remain contradictory. Therefore, the primary objective of the current work is to review the existing data regarding the influence of mercury on universal mechanisms involved in the pathogenesis of the development of MetS and its components. The brief chemical characterization of mercury is provided. The role of mercury in induction of oxidative stress has been discussed. In particular, Hg-induced oxidative stress may occur due to both prooxidant action of the metal and decrease in antioxidant enzymes. Despite the absence of direct indications, it can be proposed that mercury may induce endoplasmic reticulum stress. As it is seen from both in vivo and in vitro studies, mercury is capable of inducing inflammation. The reviewed data demonstrate that mercury affects universal pathogenetic mechanisms of MetS development. Moreover, multiple investigations have indicated the role of mercury in pathogenesis of MetS components: dyslipidemia, hypertension, insulin resistance, and obesity to a lesser extent. The present state of data regarding the interrelation between mercury and MetS denotes the following perspectives: (1) Further clinic-epidemiologic and experimental studies are required to estimate the association between mercury exposure and the development of MetS components, especially obesity; (2) Additional investigations of the possible effect of organismās mercury content modulation on MetS pathogenesis should be undertaken.
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description:A significant interrelation between heavy metal exposure and metabolic syndrome (MetS) development has been demonstrated earlier. Despite the presence of a number of works aimed at the investigation of the role of Hg in MetS development, the existing data remain contradictory. Therefore, the primary objective of the current work is to review the existing data regarding the influence of mercury on universal mechanisms involved in the pathogenesis of the development of MetS and its components. The brief chemical characterization of mercury is provided. The role of mercury in induction of oxidative stress has been discussed. In particular, Hg-induced oxidative stress may occur due to both prooxidant action of the metal and decrease in antioxidant enzymes. Despite the absence of direct indications, it can be proposed that mercury may induce endoplasmic reticulum stress. As it is seen from both in vivo and in vitro studies, mercury is capable of inducing inflammation. The reviewed data demonstrate that mercury affects universal pathogenetic mechanisms of MetS development. Moreover, multiple investigations have indicated the role of mercury in pathogenesis of MetS components: dyslipidemia, hypertension, insulin resistance, and obesity to a lesser extent. The present state of data regarding the interrelation between mercury and MetS denotes the following perspectives: (1) Further clinic-epidemiologic and experimental studies are required to estimate the association between mercury exposure and the development of MetS components, especially obesity; (2) Additional investigations of the possible effect of organismās mercury content modulation on MetS pathogenesis should be undertaken.
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