Oxidative and cellular stress as bioindicators for metal contamination in freshwater mollusk Lamellidens marginalis
In: Environmental science and pollution research: ESPR, Band 24, Heft 19, S. 16137-16147
ISSN: 1614-7499
27 Ergebnisse
Sortierung:
In: Environmental science and pollution research: ESPR, Band 24, Heft 19, S. 16137-16147
ISSN: 1614-7499
In: Defence science journal: DSJ, Band 60, Heft 2, S. 219-225
ISSN: 0011-748X
In: International journal of critical infrastructures: IJCIS, Band 20, Heft 5, S. 1
ISSN: 1741-8038
In: International journal of critical infrastructures: IJCIS, Band 20, Heft 5, S. 435-446
ISSN: 1741-8038
In: Defence science journal: a journal devotet to science & technology in defence, Band 60, Heft 2, S. 219-226
ISSN: 0011-748X
In: Environmental science and pollution research: ESPR, Band 25, Heft 15, S. 14813-14826
ISSN: 1614-7499
In: PNAS nexus, Band 2, Heft 1
ISSN: 2752-6542
Abstract
2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD), a potent AhR ligand, is an environmental contaminant that is known for mediating toxicity across generations. However, whether TCDD can induce multigenerational changes in the expression of microRNAs (miRs) has not been previously studied. In the current study, we investigated the effect of administration of TCDD in pregnant mice (F0) on gestational day 14, on the expression of miRs in the thymus of F0 and subsequent generations (F1 and F2). Of the 3200 miRs screened, 160 miRs were dysregulated similarly in F0, F1, and F2 generations, while 46 miRs were differentially altered in F0 to F2 generations. Pathway analysis revealed that the changes in miR signature profile mediated by TCDD affected the genes that regulate cell signaling, apoptosis, thymic atrophy, cancer, immunosuppression, and other physiological pathways. A significant number of miRs that showed altered expression exhibited dioxin response elements (DRE) on their promoters. Focusing on one such miR, namely miR-203 that expressed DREs and was induced across F0 to F2 by TCDD, promoter analysis showed that one of the DREs expressed by miR-203 was functional to TCDD-mediated upregulation. Also, the histone methylation status of H3K4me3 in the miR-203 promoter was significantly increased near the transcriptional start site in TCDD-treated thymocytes across F0 to F2 generations. Genome-wide chromatin immunoprecipitation sequencing study suggested that TCDD may cause alterations in histone methylation in certain genes across the three generations. Together, the current study demonstrates that gestational exposure to TCDD can alter the expression of miRs in F0 through direct activation of DREs as well as across F0, F1, and F2 generations through epigenetic pathways.
In: Air quality, atmosphere and health: an international journal, Band 17, Heft 1, S. 51-70
ISSN: 1873-9326
In: Environmental science and pollution research: ESPR, Band 26, Heft 19, S. 19155-19170
ISSN: 1614-7499