Intron 4 polymorphism of the endothelial nitric oxide synthase (eNOS) gene is associated with decreased NO production in a mercury-exposed population

Marco, Kátia Cristina de; Antunes, Lusânia Maria Greggi; Tanus‐Santos, José Eduardo; Barbosa, Fernando

doi:10.1016/j.scitotenv.2011.11.010

Cited by 18 publications

(12 citation statements)

References 45 publications

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“…Changes in hemodynamics (22), vascular thrombotic tendency due to hypercoagulability (32), and hypofibrinolysis (9,33,34) have all been suggested to be significant factors in the pathogenesis of LCPD. Intron 4 and G894T polymorphisms of eNOS have been shown to decrease NO levels in human plasma (35,36). As a result, polymorphisms of the eNOS gene and resultant reductions in the quantity of synthesized NO are likely to lead to different types of vascular diseases, as previously mentioned; these diseases may share some common risks through inheritance or exposure.…”

Section: Discussionmentioning

confidence: 96%

Endothelial nitric oxide synthase gene polymorphism is associated with Legg-Calvé-Perthes disease

Zhao

Liao

et al. 2016

Experimental and Therapeutic Medicine

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Abstract. The aim of this study was to assess the association of 27-bp variable number tandem repeat (VNTR) polymorphism in intron 4 and G894T polymorphism in exon 7 of the endothelial nitric oxide synthase (eNOS) gene with Legg-Calvé-Perthes disease (LCPD), and to provide a scientific basis for further research into the pathogenic mechanism. A total of 80 patients with LCPD and 100 healthy subjects were recruited in this case-control study. The 27-bp VNTR and G894T polymorphisms of the eNOS gene were genotyped using polymerase chain reaction (PCR) and PCR-restriction fragment length polymorphism, respectively, followed by agarose gel electrophoresis and DNA sequencing. Allelic and genotypic frequencies were computed in the two groups and subjected to statistical analysis. For the 27-bp VNTR polymorphism, individuals with LCPD showed a higher frequency of the ab genotype [27.5 vs. 14%; odds ratio (OR), 2.33; 95% confidence interval (CI), 1.10-4.92; P=0.024]. For the G894T polymorphism, the LCPD case group showed a higher frequency of the heterozygous genotype GT than the healthy control group (35 vs. 17%; OR, 2.67; 95% CI, 1.33-5.36; P=0.005). The results indicate that these eNOS gene polymorphisms may be a risk factor for LCPD. The 27-bp VNTR polymorphism in intron 4 and G894T polymorphism in exon 7 may be involved in the etiology of LCPD.

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Section: Discussionmentioning

confidence: 96%

Endothelial nitric oxide synthase gene polymorphism is associated with Legg-Calvé-Perthes disease

Zhao

Liao

et al. 2016

Experimental and Therapeutic Medicine

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“…Age, gender, and the presence of the intron 4 polymorphism contributed to nitrite reduction as a result of the blood mercury concentration. Their results suggested that the 27 nt repeat polymorphism of intron 4 in the eNOS gene increases susceptibility to cardiovascular diseases after MeHg exposure by modulating NO levels [31]. …”

Section: Contribution Of Genetics To Methylmercury Toxicitymentioning

confidence: 99%

Recent Advances in Mercury Research

Martinez-Finley

Aschner

2014

Curr Envir Health Rpt

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Mercury (Hg) is a highly toxic, non-essential, naturally occurring metal with a variety of uses. Mercury is not required for any known biological process and its presence in the human body may be detrimental, especially to the nervous system. Both genetic and behavioral studies suggest that mercury levels, age (both of exposure and at testing), and genetic background determine disease processes and outcome. The metal receptors and genes responsible for mercury metabolism also appear to play a pivotal role in the etiology of mercury-induced pathology. This review presents information about the latest advances in mercury research, with particular focus on low-level exposures and the contribution of genetics to toxic outcome. Future studies should address the contribution of genetics and low-level mercury exposure to disease, namely gene x environment interactions, taking into consideration age of exposure as developing animals are exquisitely more sensitive to this metal. In addition to recent advances in understanding the pathology associated with mercury exposure, the review highlights transport mechanisms, cellular distribution and detoxification of mercury species in the body.

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“…Age, gender and the presence of intron 4 polymorphism contributed to nitrite reduction as a result of blood Hg concentration. Their results suggest increased susceptibility to cardiovascular diseases after MeHg exposure in carriers of the 27nt repeat polymorphism of intron 4 in the eNOS gene 85 .…”

Section: Modifiers Of Toxicitymentioning

confidence: 96%

Mechanisms and modifiers of methylmercury-induced neurotoxicity

Fretham

Caito

Martinez-Finley

et al. 2012

Toxicology Research

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The neurotoxic consequences of methylmercury (MeHg) exposure have long been known, however a complete understanding of the mechanisms underlying this toxicity is elusive. Recent epidemiological and experimental studies have provided many mechanistic insights, particularly into the contribution of genetic and environmental factors that interact with MeHg to modify toxicity. This review will outline cellular processes directly and indirectly affected by MeHg, including oxidative stress, cellular signaling and gene expression, and discuss genetic, environmental and nutritional factors capable of modifying MeHg toxicity.

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Intron 4 polymorphism of the endothelial nitric oxide synthase (eNOS) gene is associated with decreased NO production in a mercury-exposed population

Cited by 18 publications

References 45 publications

Endothelial nitric oxide synthase gene polymorphism is associated with Legg-Calvé-Perthes disease

Endothelial nitric oxide synthase gene polymorphism is associated with Legg-Calvé-Perthes disease

Recent Advances in Mercury Research

Mechanisms and modifiers of methylmercury-induced neurotoxicity

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