Reduction in Telomere Length in Individuals Exposed In Utero to Glycol Ether

El‐Zein, Randa; Albrecht, Thomas; Knutson, Eugene; Legator, Marvin S.; Abdel‐Rahman, Sherif Z.

doi:10.3200/aeoh.62.3.161-163

Cited by 7 publications

(3 citation statements)

References 15 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…N-nitrosamines exposure may lead to telomere shortening, but there were no strong associations between other exposures and telomere length. El-Zein et al 34 suggested that exposure to ethylene glycol monomethyl ether (EGME) in utero could result in terminal chromosome rearrangements and shortening of telomere length, leading to observed dysmorphic features and idiopathic mental retardation. However, studies have found that toxicants could extend telomere length.…”

Section: Discussionmentioning

confidence: 99%

Changes in the expression of genes involved in cell cycle regulation and the relative telomere length in the process of canceration induced by omethoate

et al. 2017

View full text Add to dashboard Cite

Organophosphorous pesticides (OPs), with high efficiency, broad-spectrum and low residue, are widely used in China. Omethoate is a broad category of organophosphorous pesticides and is more domestically utilized which has chronic toxic effect on human health caused by long-term, low-dose exposure to Ops, recently its potential genotoxicity has attracted wide attention which can cause chromosomal DNA damage. Thus, the aim of this study is screen susceptible biomarkers and explore the mechanism of canceration induced by omethoate. 180 long-term organophosphorus pesticide-exposed workers and 115 healthy controls were recruited. Quantitative polymerase chain reaction method was applied to determine the relative telomere length in peripheral lymphocyte DNA as well as p53 and p21 gene expression levels. Genetic polymorphisms were determined by the polymerase chain reaction-restriction fragment length polymorphism method. Multiple linear regression was conducted to explore the effects of exposure, expression levels, and polymorphisms in genes on the telomere length. The results showed the relative telomere lengths in the exposure group were significantly longer than that in the control group. The messenger RNA expression levels of p53 and p21 in exposure group were significantly lower than that in the control group; telomere lengths of the CA genotype individuals of p21 rs1801270 polymorphism locus were significantly longer than that of the CC genotype in the control group that were estimated using the Bonferroni method; and bivariate correlation analysis showed that the messenger RNA expression level of gene p53 was negatively correlated with telomere length, and the messenger RNA expression level of gene p21 was positively correlated with telomere length. Multivariate analysis found that p53 messenger RNA and p21 messenger RNA had an impact on telomere length. These results demonstrated that the messenger RNA expression levels of p53 and p21 may have a relationship with the changes in telomere length induced by omethoate and provided strong evidence for the mechanism of canceration induced by poison.

show abstract

Section: Discussionmentioning

confidence: 99%

Changes in the expression of genes involved in cell cycle regulation and the relative telomere length in the process of canceration induced by omethoate

et al. 2017

View full text Add to dashboard Cite

show abstract

“…brain, lungs and immune system), the critical 'windows' of developmental vulnerability may continue beyond the in utero stage through the neonatal period and perhaps even into puberty, thereby extending the period of increased vulnerability to adverse effects from environmental chemical exposures. Exposure to chemicals in utero can have direct effects on the genome integrity (5,(207)(208)(209) though epigenetics, as a modifier of the mechanisms maintaining genome integrity, has become the cornerstone of the 'Developmental Origins of Health and Disease' hypothesis, which points to epigenetic regulation as the likely mechanism behind the environment-driven epidemic of non-communicable disease such as many cancers (210)(211)(212). Epigenetics may thus provide a new tool for understanding mechanisms underlying well-recognized gene-environment interactions and their role in carcinogenesis.…”

Section: In Utero Exposurementioning

confidence: 99%

Causes of genome instability: the effect of low dose chemical exposures in modern society

Langie¹,

Koppen²,

Desaulniers

et al. 2015

CARCIN

176

114

View full text Add to dashboard Cite

Genome instability is a prerequisite for the development of cancer. It occurs when genome maintenance systems fail to safeguard the genome's integrity, whether as a consequence of inherited defects or induced via exposure to environmental agents (chemicals, biological agents and radiation). Thus, genome instability can be defined as an enhanced tendency for the genome to acquire mutations; ranging from changes to the nucleotide sequence to chromosomal gain, rearrangements or loss. This review raises the hypothesis that in addition to known human carcinogens, exposure to low dose of other chemicals present in our modern society could contribute to carcinogenesis by indirectly affecting genome stability. The selected chemicals with their mechanisms of action proposed to indirectly contribute to genome instability are: heavy metals (DNA repair, epigenetic modification, DNA damage signaling, telomere length), acrylamide (DNA repair, chromosome segregation), bisphenol A (epigenetic modification, DNA damage signaling, mitochondrial function, chromosome segregation), benomyl (chromosome segregation), quinones (epigenetic modification) and nano-sized particles (epigenetic pathways, mitochondrial function, chromosome segregation, telomere length). The purpose of this review is to describe the crucial aspects of genome instability, to outline the ways in which environmental chemicals can affect this cancer hallmark and to identify candidate chemicals for further study. The overall aim is to make scientists aware of the increasing need to unravel the underlying mechanisms via which chemicals at low doses can induce genome instability and thus promote carcinogenesis.

show abstract

“…As far as we know, there is only one pilot study on TL and prenatal chemical exposure, showing shorter TL measured by quantitative fluorescence in situ hybridisation (FISH) in individuals with prenatal exposure to glycol ether 59. However, since only six in utero-exposed individuals with dysmorphic features, mental retardation and persistent cytogenetic damage were included, larger studies are needed to confirm this finding.…”

Section: Future Directions In Tl Environmental Exposure Using Surrogamentioning

confidence: 99%

Republished: Environmental and occupational exposure to chemicals and telomere length in human studies

Zhang

Lin

Funk

et al. 2013

Postgraduate Medical Journal

View full text Add to dashboard Cite

Telomeres are complexes of tandem repeats of DNA (5'-TTAGGG-3') and protein that cap eukaryotic chromosomes and play a critical role in chromosome stability. Telomeres shorten with aging and this process can be accelerated by increased oxidative stress and episodes of inflammation. Evidence is rapidly growing that telomere length (TL) may be affected by environmental chemicals that have frequently been associated with chronic diseases. In this article, we review the published data on TL in relation to environmental and occupational exposure to several chemicals based on our own and others' studies. The environmental and occupational exposures associated with shorter TL include traffic-related air pollution (ie, particulate matter (PM), black carbon (BC), and benzene and toluene), polycyclic aromatic hydrocarbons (PAHs), N-nitrosamines, pesticides, lead, exposure in car mechanical workshops, and hazardous waste exposure. Arsenic, persistent organic pollutants (POPs) and short-term exposure to PM are associated with longer TL. We discuss the possible reasons for the differences in results, including time- and dose-related issues, study design, and possible mechanisms involved in telomere regulation. We also discuss the future directions and challenges for TL-related environmental and occupational health research, such as investigation of TL in subpopulations of blood leukocytes, and the study of genetic and epigenetic factors that may regulate telomere integrity using longitudinal designs.

show abstract

Reduction in Telomere Length in Individuals Exposed In Utero to Glycol Ether

Cited by 7 publications

References 15 publications

Changes in the expression of genes involved in cell cycle regulation and the relative telomere length in the process of canceration induced by omethoate

Changes in the expression of genes involved in cell cycle regulation and the relative telomere length in the process of canceration induced by omethoate

Causes of genome instability: the effect of low dose chemical exposures in modern society

Republished: Environmental and occupational exposure to chemicals and telomere length in human studies

Contact Info

Product

Resources

About