Prenatal phthalate exposure, infant growth, and global DNA methylation of human placenta

2014 ◽  
Vol 56 (3) ◽  
pp. 286-292 ◽  
Author(s):  
Yan Zhao ◽  
Hui-jing Shi ◽  
Chang-ming Xie ◽  
Jiao Chen ◽  
Hannah Laue ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Human Placenta ◽  
Infant Growth ◽  
Global Dna Methylation ◽  
Phthalate Exposure

scholarly journals In Utero Exposures, Infant Growth, and DNA Methylation of Repetitive Elements and Developmentally Related Genes in Human Placenta

2012 ◽  
Vol 120 (2) ◽  
pp. 296-302 ◽  
Author(s):  
Charlotte S. Wilhelm-Benartzi ◽  
E. Andres Houseman ◽  
Matthew A. Maccani ◽  
Graham M. Poage ◽  
Devin C. Koestler ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Human Placenta ◽  
In Utero ◽  
Infant Growth ◽  
Repetitive Elements ◽  
In Utero Exposures

scholarly journals Third trimester phthalate exposure is associated with DNA methylation of growth-related genes in human placenta

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Yan Zhao ◽  
Jiao Chen ◽  
Xiu Wang ◽  
Qi Song ◽  
Hui-Hui Xu ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Human Placenta ◽  
Third Trimester ◽  
Phthalate Exposure

Global DNA Methylation is influenced by smoking behavior

2007 ◽  
Vol 40 (05) ◽  
Author(s):  
MAN Muschler ◽  
T Hillemacher ◽  
H Frieling ◽  
S Moskau ◽  
A Semmler ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Smoking Behavior ◽  
Global Dna Methylation

DNA Methylation at Birth Is Associated with Adiposity and Infant Growth during the First Six Months of Life in the Healthy Start Study

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 342-OR
Author(s):  
SARAH J. BORENGASSER ◽  
ANNE P. STARLING ◽  
WEIMING ZHANG ◽  
JACOB FRIEDMAN ◽  
RICHARD F. HAMMAN ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Infant Growth ◽  
Healthy Start

scholarly journals Associations among phthalate exposure, DNA methylation of TSLP, and childhood allergy

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Wan-Ru Wang ◽  
Nai-Tzu Chen ◽  
Nai-Yun Hsu ◽  
I-Ying Kuo ◽  
Hsin-Wen Chang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Methylation Level ◽  
Respiratory Symptoms ◽  
Smoking Status ◽  
Phthalate Esters ◽  
Allergic Diseases ◽  
Percentage Increase ◽  
Phthalate Exposure ◽  
Settled Dust ◽  
Butyl Phthalate

Abstract Background Dysregulation of thymic stromal lymphopoietin (TSLP) expressions is linked to asthma and allergic disease. Exposure to phthalate esters, a widely used plasticizer, is associated with respiratory and allergic morbidity. Dibutyl phthalate (DBP) causes TSLP upregulation in the skin. In addition, phthalate exposure is associated with changes in environmentally induced DNA methylation, which might cause phenotypic heterogeneity. This study examined the DNA methylation of the TSLP gene to determine the potential mechanism between phthalate exposure and allergic diseases. Results Among all evaluated, only benzyl butyl phthalate (BBzP) in the settled dusts were negatively correlated with the methylation levels of TSLP and positively associated with children’s respiratory symptoms. The results revealed that every unit increase in BBzP concentration in the settled dust was associated with a 1.75% decrease in the methylation level on upstream 775 bp from the transcription start site (TSS) of TSLP (β =  − 1.75, p = 0.015) after adjustment for child’s sex, age, BMI, parents’ smoking status, allergic history, and education levels, PM2.5, formaldehyde, temperature; and relative humidity. Moreover, every percentage increase in the methylation level was associated with a 20% decrease in the risk of morning respiratory symptoms in the children (OR 0.80, 95% CI 0.65–0.99). Conclusions Exposure to BBzP in settled dust might increase children’s respiratory symptoms in the morning through decreasing TSLP methylation. Therefore, the exposure to BBzP should be reduced especially for the children already having allergic diseases.

scholarly journals Oxidative damage, inflammation, genotoxic effect, and global DNA methylation caused by inhalation of formaldehyde and the purpose of melatonin

2020 ◽  
Vol 9 (6) ◽  
pp. 778-789
Author(s):  
Letícia Bernardini ◽  
Eduardo Barbosa ◽  
Mariele Feiffer Charão ◽  
Gabriela Goethel ◽  
Diana Muller ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Bone Marrow ◽  
Oxidative Damage ◽  
Bronchoalveolar Lavage ◽  
Bone Marrow Cells ◽  
Histological Study ◽  
Global Dna Methylation ◽  
Protective Effects ◽  
Global Methylation ◽  
Protein Thiols

Abstract Formaldehyde (FA) exposure has been proven to increase the risk of asthma and cancer. This study aimed to evaluate for 28 days the FA inhalation effects on oxidative stress, inflammation process, genotoxicity, and global DNA methylation in mice as well as to investigate the potential protective effects of melatonin. For that, analyses were performed on lung, liver and kidney tissues, blood, and bone marrow. Bronchoalveolar lavage was used to measure inflammatory parameters. Lipid peroxidation (TBARS), protein carbonyl (PCO), non-protein thiols (NPSH), catalase activity (CAT), comet assay, micronuclei (MN), and global methylation were determined. The exposure to 5-ppm FA resulted in oxidative damage to the lung, presenting a significant increase in TBARS and NO levels and a decrease in NPSH levels, besides an increase in inflammatory cells recruited for bronchoalveolar lavage. Likewise, in the liver tissue, the exposure to 5-ppm FA increased TBARS and PCO levels and decreased NPSH levels. In addition, FA significantly induced DNA damage, evidenced by the increase of % tail moment and MN frequency. The pretreatment of mice exposed to FA applying melatonin improved inflammatory and oxidative damage in lung and liver tissues and attenuated MN formation in bone marrow cells. The pulmonary histological study reinforced the results observed in biochemical parameters, demonstrating the potential beneficial role of melatonin. Therefore, our results demonstrated that FA exposure with repeated doses might induce oxidative damage, inflammatory, and genotoxic effects, and melatonin minimized the toxic effects caused by FA inhalation in mice.

Decreased expression of DNA methyltransferases in the testes of patients with non-obstructive azoospermia leads to changes in global DNA methylation levels

2019 ◽  
Vol 31 (8) ◽  
pp. 1386 ◽  
Author(s):  
Fatma Uysal ◽  
Gokhan Akkoyunlu ◽  
Saffet Ozturk
Keyword(s):  
Dna Methylation ◽  
Male Infertility ◽  
De Novo ◽  
Biological Effects ◽  
Testicular Biopsy ◽  
Round Spermatid ◽  
Dna Methyltransferases ◽  
Global Dna Methylation ◽  
Obstructive Azoospermia ◽  
Spermatogenic Cells

DNA methylation plays key roles in epigenetic regulation during mammalian spermatogenesis. DNA methyltransferases (DNMTs) function in de novo and maintenance methylation processes by adding a methyl group to the fifth carbon atom of the cytosine residues within cytosine–phosphate–guanine (CpG) and non-CpG dinucleotide sites. Azoospermia is one of the main causes of male infertility, and is classified as obstructive (OA) or non-obstructive (NOA) azoospermia based on histopathological characteristics. The molecular background of NOA is still largely unknown. DNA methylation performed by DNMTs is implicated in the transcriptional regulation of spermatogenesis-related genes. The aim of the present study was to evaluate the cellular localisation and expression levels of the DNMT1, DNMT3A and DNMT3B proteins, as well as global DNA methylation profiles in testicular biopsy samples obtained from men with various types of NOA, including hypospermatogenesis (hyposperm), round spermatid (RS) arrest, spermatocyte (SC) arrest and Sertoli cell-only (SCO) syndrome. In the testicular biopsy samples, DNMT1 expression and global DNA methylation levels decreased gradually from the hyposperm to SCO groups (P<0.05). DNMT3A expression was significantly decreased in the RS arrest, SC arrest and SCO groups compared with the hyposperm group (P<0.05). DNMT3B expression was significantly lower in the RS arrest and SCO groups than in the hyposperm group (P<0.05). Although both DNMT1 and DNMT3A were localised in the cytoplasm and nucleus of the spermatogenic cells, staining for DNMT3B was more intensive in the nucleus of spermatogenic cells. In conclusion, the findings suggest that significant changes in DNMT expression and global DNA methylation levels in spermatogenic cells may contribute to development of male infertility in the NOA groups. Further studies are needed to determine the molecular biological effects of the altered DNMT expression and DNA methylation levels on development of male infertility.

scholarly journals Potential effect of tobacco cigarettes smoking on global DNA methylation status and protamines transcripts in human spermatozoa

2021 ◽  
Vol 26 (1) ◽  
Author(s):  
Mohammed M. Laqqan ◽  
Maged M. Yassin
Keyword(s):  
Dna Methylation ◽  
Cigarette Smoking ◽  
Dna Fragmentation ◽  
Methylation Status ◽  
Human Spermatozoa ◽  
Global Dna Methylation ◽  
Transcription Level ◽  
Heavy Smokers ◽  
Protamine 1 ◽  
Protamine 2

Abstract Background Epigenetics refers to an alteration in gene expression without alteration in the sequence of DNA and this process may be affected by environmental factors and lifestyle like cigarette smoking. This study was designed to evaluate the potential effect of cigarette smoking on the global DNA methylation status and the transcription level of protamine 1 and protamine 2 in human spermatozoa. A total of 188 semen samples were collected from men with a mean age of 34.9 ± 5.8 years old (98 heavy smokers and 90 non-smokers). The DNA and RNA were isolated from purified spermatozoa, then the status of global DNA methylation and the transcription level of protamine 1 and protamine 2 were evaluated using ELISA and qPCR, respectively. The chromatin non-condensation and DNA fragmentation in human spermatozoa were evaluated using chromomycin A3 staining and TUNEL assay, respectively. Results A significant increase has been found in the status of global DNA methylation in spermatozoa of heavy smokers compared to non-smokers (7.69 ± 0.69 ng/μl vs. 4.90 ± 0.40 ng/μl, P < 0.001). Additionally, a significant reduction has been found in transcription level of protamine 1 (25.49 ± 0.31 vs. 23.94 ± 0.40, P < 0.001) and protamine 2 (28.27 ± 0.39 vs. 23.45 ± 0.30, P < 0.001) in heavy smokers. A downregulation has been found in the transcription level of protamine 1 and protamine 2 with a fold change of 0.497 and 0.047, respectively. A significant increase has been shown in the level of DNA fragmentation and chromatin non-condensation in heavy smokers compared to non-smokers (P < 0.001). On the other hand, a significant positive correlation has been found between sperm chromatin non-condensation, sperm DNA fragmentation, transcription level of protamine 1, transcription level of protamine 2, and global DNA methylation status (r = 0.304, P < 0.001; r = 0.399, P < 0.001; r = 0.216, P = 0.003; r = 0.494, P < 0.001, respectively). Conclusion Tobacco cigarette smoking has a potential influence on the global DNA methylation and the transcription level of protamine genes in human spermatozoa, and consequently, affect negatively on the semen parameters.

Global DNA methylation, DNMT1, and MBD2 in patients with systemic lupus erythematosus

Lupus ◽  
2010 ◽  
Vol 20 (2) ◽  
pp. 131-136 ◽  
Author(s):  
CC Liu ◽  
TT Ou ◽  
CC Wu ◽  
RN Li ◽  
YC Lin ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Dna Methylation ◽  
Lupus Erythematosus ◽  
Global Dna Methylation ◽  
Systemic Lupus
Sign in / Sign up

Export Citation Format

Share Document