For Publishers
DiscoveryMetadataPeer reviewHostingPublishing
For Researchers
JoinPublishReviewCollect
Register
Blog
About
Search
Advanced search
My ScienceOpen
Search
For Publishers
For Researchers
Blog
About
7
views
40
references
 Top references
cited by
3
    
0 reviews
 Review
0
comments
 Comment
0
recommends
+1 Recommend
0 collections
    0
    shares
      196
      similar
       All similar
      • Record: found
      • Abstract: found
      • Article: not found

      STAT3 methylation in white blood cells as a novel sensitive biomarker for the toxic effect of low-dose benzene exposure

      Read this article at

      ScienceOpenPublisherPMC
      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          A cross-sectional study was conducted in a sample of 571 workers to explore the toxic effect and early sensitive biomarker of the health effects of low-dose benzene exposure (LDBE), as well as the correlation between DNA methylation and the toxic effect of LDBE.

          Abstract

          Alterations in DNA methylation patterns play an essential role in disease process and are associated with cancer risk. To explore the toxic effect and early sensitive biomarker of the health effects of low-dose benzene exposure (LDBE), and investigate the correlation between DNA methylation and the toxic effect of LDBE, a cross-sectional study was conducted in a sample of 571 workers; 312 workers who were exposed to a 1.82 ± 1.16 mg m −3 air benzene concentration were assigned to the LDBE group, while 259 non-known benzene exposure (NBE) workers were assigned to the control group, with an air benzene concentration of 0.06 ± 0.01 mg m −3. Routine blood indexes, alanine transaminase (ALT), oxidative stress parameters and signal transducer and activator of transcription 3 (STAT3) methylation were detected. Compared with the NBE population, the STAT3 methylation level ( P = 0.001), Platelets (PLTs) ( P = 0.002) and 8-isoprostane-PGFs (8-iso-PGF2a) ( P = 0.001) manifested a significant reduction, while ALT ( P = 0.002) and 8-hydroxy-2 deoxyguanosine (8-OHdG) ( P = 0.002) showed a significant rise in the LDBE population. In addition, a significant correlation was observed between STAT3 methylation and oxidative stress, namely 8-OhdG and 8-iso-PGF2a. Furthermore, a multivariate analysis showed that the STAT3 methylation (structure loadings = 0.909) was the most strongly correlated with the other set of variables, especially with white blood cells (WBCs) (structure loadings = 0.675). Taken together, STAT3 methylation may be the underlying mechanism involved in the early toxic effect of LDBE, therefore, STAT3 methylation can be a novel sensitive biomarker for the toxic effect of low-dose benzene exposure.

          Related collections

          Most cited references40

          • Record: found
          • Abstract: found
          • Article: found
          Is Open Access

          Leukemia and Benzene

          Robert Snyder (2012)
          Excessive exposure to benzene has been known for more than a century to damage the bone marrow resulting in decreases in the numbers of circulating blood cells, and ultimately, aplastic anemia. Of more recent vintage has been the appreciation that an alternative outcome of benzene exposure has been the development of one or more types of leukemia. While many investigators agree that the array of toxic metabolites, generated in the liver or in the bone marrow, can lead to traumatic bone marrow injury, the more subtle mechanisms leading to leukemia have yet to be critically dissected. This problem appears to have more general interest because of the recognition that so-called “second cancer” that results from prior treatment with alkylating agents to yield tumor remissions, often results in a type of leukemia reminiscent of benzene-induced leukemia. Furthermore, there is a growing literature attempting to characterize the fine structure of the marrow and the identification of so called “niches” that house a variety of stem cells and other types of cells. Some of these “niches” may harbor cells capable of initiating leukemias. The control of stem cell differentiation and proliferation via both inter- and intra-cellular signaling will ultimately determine the fate of these transformed stem cells. The ability of these cells to avoid checkpoints that would prevent them from contributing to the leukemogenic response is an additional area for study. Much of the study of benzene-induced bone marrow damage has concentrated on determining which of the benzene metabolites lead to leukemogenesis. The emphasis now should be directed to understanding how benzene metabolites alter bone marrow cell biology.
          Article 0 comments Cited 48 times – based on 0 reviews     Review now
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Obesity and hypercholesterolemia are associated with NOX2 generated oxidative stress and arterial dysfunction.

            Lorenzo Loffredo, Francesco Martino, Roberto Carnevale … (2012)
            To analyze the interplay among oxidative stress, NOX2, the catalytic core of nicotinamide-adenine dinucleotide phosphate oxidase, and endothelial dysfunction in children with obesity and/or hypercholesterolemia. We performed a cross-sectional study comparing flow-mediated arterial dilation (FMD), oxidized low-density lipoprotein, and urinary excretion of isoprostanes (8-iso-PGF2α), as markers of oxidative stress, and NOX2 activity, as assessed by blood levels of soluble NOX2-dp (sNOX2-dp), in a population of 100 children, matched for age and sex, including 40 healthy subjects (HS), 20 children with hypercholesterolemia (HC), 20 obese children (OC), and 20 children with coexistence of hypercholesterolemia and obesity (HOC). HOC had higher sNOX2-dp and oxidized low-density lipoprotein levels compared with HS, HC, and OC. HC, OC, and HOC had lower FMD values compared with HS. Urinary 8-iso-PGF2α excretion was higher in HOC compared with HS. FMD was inversely correlated with sNOX2-dp levels (r = -0.483; P < .001) and with the number of cardiovascular risk factors (r = -0.617; P < .001). Multiple linear regression analysis showed that the number of cardiovascular risk factors was the only independent predictive variable associated with FMD (β: -0.585; P < .001; R(2) = 35%) and sNOX2-dp (β: 0.587; P < .001; R(2) = 34%). The study suggests that NOX2-generating oxidative stress may have a pathogenic role in the functional changes of the arterial wall occurring in HOC. Copyright © 2012 Mosby, Inc. All rights reserved.
            Article 0 comments Cited 27 times – based on 0 reviews     Review now
              Bookmark
              • Record: found
              • Abstract: found
              • Article: not found

              Epigenetics in the development, modification, and prevention of cardiovascular disease.

              Thomas Whayne, Jr (2015)
              Epigenetics has major relevance to all disease processes; cardiovascular (CV) disease and its related conditions are no exception. Epigenetics is defined as the study of heritable alterations in gene expression, or cellular phenotype, and goes far beyond a pure genetic approach. A more precise definition is that epigenetics represents all the meiotically and mitotically inherited changes in gene expression that are not encoded on the deoxyribonucleic acid (DNA) sequence itself. Major epigenetic mechanisms are modifications of histone proteins in chromatin and DNA methylation (which does not alter the DNA sequence). There is increasing evidence for the involvement of epigenetics in human disease such as cancer, inflammatory disease and CV disease. Other chronic diseases are also susceptible to epigenetic modification such as metabolic diseases including obesity, metabolic syndrome, and diabetes mellitus. There is much evidence for the modification of epigenetics by nutrition and exercise. Through these modifications, there is infinite potential for benefit for the fetus, the newborn, and the individual as well as population effects. Association with CV disease, including coronary heart disease and peripheral vascular disease, is evident through epigenetic relationships and modification by major CV risk factors such as tobacco abuse. Aging itself may be altered by epigenetic modification. Knowledge of epigenetics and its relevance to the development, modification, and prevention of CV disease is in a very preliminary stage but has an infinite future.
              Article 0 comments Cited 25 times – based on 0 reviews     Review now
                Bookmark
                All references

                Author and article information

                Journal
                Journal ID (publisher-id): TROEE8
                Title: Toxicology Research
                Abbreviated Title: Toxicol. Res.
                Publisher: Royal Society of Chemistry (RSC)
                ISSN (Print): 2045-452X
                ISSN (Electronic): 2045-4538
                Publication date Created: 2016
                Publication date (Electronic): 2016
                Volume: 5
                Issue: 3
                Pages: 800-807
                Affiliations
                [1 ]Department of Occupational Health and Environmental Health
                [2 ]School of Public Health
                [3 ]Capital Medical University
                [4 ]Beijing 100069
                [5 ]China
                Article
                DOI: 10.1039/C5TX00445D
                PMC ID: 6061912
                PubMed ID: 30090390
                SO-VID: d9836c5c-64a1-46d1-adf7-7138c7433bc0
                Copyright © © 2016
                History

                Data availability:

                Comments

                Comment on this article

                scite_

                Similar content196

                See all similar

                Cited by3

                See all cited by

                Most referenced authors451

                See all reference authors