Article
Environmental Sciences
Jon A. Doering, Markus Brinkmann, Maria Lucio, Serena Stoeck, Alex Vien, Stephanie Petersen, Turk Rhen, Paul D. Jones, Markus Hecker, Anthony Schroeder
Summary: The common snapping turtle, as a model reptile, exhibits higher sensitivity to DLCs in early life compared to other studied vertebrate species, highlighting the importance of assessing ecological risk.
ENVIRONMENTAL TOXICOLOGY AND CHEMISTRY
(2022)
Article
Pharmacology & Pharmacy
Samantha L. VanEtten, Matthew R. Bonner, Xuefeng Ren, Linda S. Birnbaum, Paul J. Kostyniak, Jie Wang, James R. Olson
Summary: Mitochondria are organelles responsible for cellular oxidation and energy production, and their damage can lead to changes in mtDNA copy number. Exposure to TCDD and a mixture of PCB 126 and PCB 153 increased mtDNA copy number in the liver and lung of rats, while exposure to non-DL PCB 153 resulted in decreased or unchanged mtDNA copy number. This suggests that mtDNA copy number could serve as a sensitive biomarker of mitochondrial injury and oxidative stress caused by dioxin-like compounds.
Review
Endocrinology & Metabolism
Tongtong Zhang, Xiang Zhou, Xiaohan Ren, Xu Zhang, Jiajin Wu, Shangqian Wang, Zengjun Wang
Summary: TCDD has negative effects on the male reproductive system of rodents, including reducing testis weight, sperm count, and blood testosterone concentration. The research suggests that TCDD may cause damage to the male reproductive system through direct or indirect exposure. Further research on human-related effects of TCDD is needed.
FRONTIERS IN ENDOCRINOLOGY
(2021)
Article
Environmental Sciences
Michela Novelli, Pascale Beffy, Matilde Masini, Chiara Vantaggiato, Luisa Martino, Lorella Marselli, Piero Marchetti, Vincenzo De Tata
Summary: Exposure to environmental pollutant TCDD affects pancreatic islets, especially beta cells, leading to cell death, ultrastructural alterations, decreased insulin secretion, and changes in gene expression. TCDD exposure significantly reduces cell survival and insulin secretion, causes ultrastructural changes in beta cells, and alters gene expression profiles in isolated islets.
Article
Environmental Sciences
Jae Gon Park, Hisato Iwata, Nguyen Minh Tue, Tatsuya Kunisue, Eun-Young Kim
Summary: Researchers have discovered a naturally occurring dioxin called 1,3,7-tribromodibenzo-p-dioxin (1,3,7-TriBDD) in the marine environment, synthesized by red algae. They investigated the effects of this compound on bird embryos and found that 1,3,7-TriBDD exposure may lead to health issues such as diabetes and cancer. Compared to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), 1,3,7-TriBDD had different impacts on the phenotype and transcriptome of chicken embryos, potentially resulting in different severity of effects.
ECOTOXICOLOGY AND ENVIRONMENTAL SAFETY
(2022)
Article
Marine & Freshwater Biology
Monica S. Yue, Shannon E. Martin, Nathan R. Martin, Michael R. Taylor, Jessica S. Plavicki
Summary: Exposure to TCDD in zebrafish disrupts the development of the subintestinal venous plexus (SIVP) which vascularizes the liver, kidney, gut, and pancreas, as well as the superficial annular vessel (SAV) crucial for retinal vasculature. TCDD exposure also increases the expression of bmp4, a key molecular mediator of SIVP morphogenesis.
AQUATIC TOXICOLOGY
(2021)
Article
Nutrition & Dietetics
Wurood Hantoosh Neamah, Alex Rutkovsky, Osama Abdullah, Kiesha Wilson, Ryan Bloomquist, Prakash Nagarkatti, Mitzi Nagarkatti
Summary: This study demonstrates that Resveratrol (RSV), an AhR antagonist, reduces the induction and function of murine myeloid-derived suppressor cells (MDSCs) induced by 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD). RSV reverses the effects of TCDD on macrophages and dendritic cells, as well as the upregulation of critical molecules involved in TCDD-mediated induction and immunosuppressive functions of MDSCs. RSV treatment decreases the energetic demands induced by TCDD. These findings suggest the potential use of RSV to attenuate the immunosuppressive properties of MDSCs.
Article
Environmental Sciences
Matthew Lee, Gan Liang, Sophie Holland, Casey O'Farrell, Keith Osborne, Michael J. Manefield
Summary: Polychlorinated dibenzo-p-dioxins and furans (PCDD/F) are highly toxic compounds that are difficult to degrade in the environment. This study focuses on the PCDD/F contamination in Sydney Harbour Estuary, with the contamination source area in Homebush Bay being one of the most heavily polluted sites in the world. The researchers found evidence of attenuation of the most toxic congener, 2,3,7,8-TCDD, at the source area. They also discovered a significant population of Dehalococcoidia and Dehalobium, which played a role in the microbial dechlorination of PCDD/F.
MARINE POLLUTION BULLETIN
(2022)
Article
Biochemistry & Molecular Biology
Nicholas Dopkins, Wurood Hantoosh Neameh, Alina Hall, Yunjia Lai, Alex Rutkovsky, Alexa Orr Gandy, Kun Lu, Prakash S. Nagarkatti, Mitzi Nagarkatti
Summary: The study found that acute exposure to TCDD results in immediate dysregulation in the circulating and intestinal metabolome of mice, which affects host immunity and broad-scale metabolic processes. These metabolic changes can serve as biomarkers for TCDD toxicity and early detection of individual exposure.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)
Article
Environmental Sciences
Michelle E. Kossack, Katherine E. Manz, Nathan R. Martin, Kurt D. Pennell, Jessica Plavicki
Summary: Dioxin and dioxin-like compounds are environmental contaminants that induce toxicity by binding to the aryl hydrocarbon receptor (AHR). The zebrafish model has been used to study developmental toxicity caused by exposure to AHR ligands such as dioxin. In this study, targeted gas chromatography (GC) and non-targeted liquid chromatography (LC) were used to quantify TCDD uptake, model its elimination dynamics, and determine its impact on the zebrafish metabolome. The results showed that environmentally relevant body burdens of TCDD were produced in zebrafish through different waterborne exposures, and TCDD exposure affected metabolic pathways associated with AHR signaling and brain development.
Article
Immunology
R. L. Lowery, S. E. Latchney, R. P. Peer, C. E. Lamantia, K. A. Lordy, L. A. Opanashuk, M. McCall, A. K. Majewska
Summary: Recent studies have shown that exposure to AhR ligands during gestational and lactational periods can lead to subtle but durable changes in the transcription of microglial cells in the brain, resulting in a heightened response towards tissue injury. However, this effect can be rectified through depletion and repopulation of microglia cells.
BRAIN BEHAVIOR AND IMMUNITY
(2022)
Article
Multidisciplinary Sciences
Giovan N. Cholico, Karina Orlowska, Russell R. Fling, Warren J. Sink, Nicholas A. Zacharewski, Kelly A. Fader, Rance Nault, Tim Zacharewski
Summary: 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is an environmental contaminant that induces liver damage and changes in hepatic metabolism. In this study, the effects of TCDD on hepatic acetyl-CoA and beta-hydroxybutyrate levels, as well as protein acetylation and beta-hydroxybutyrylation, were examined. The results showed that TCDD reduced hepatic acetyl-CoA and beta-hydroxybutyrate levels and decreased protein acetylation and beta-hydroxybutyrylation. These findings suggest that TCDD induces starvation-like conditions in the liver.
SCIENTIFIC REPORTS
(2023)
Article
Environmental Sciences
Anh T. N. Dao, Sander J. Loenen, Kees Swart, Ha T. C. Dang, Abraham Brouwer, Tjalf E. de Boer
Summary: The ligninolytic fungus Rigidoporus sp. FMD21 produces extracellular enzymes, mainly laccases, that can degrade the highly recalcitrant and toxic pollutant 2,3,7,8-TCDD into 3,4-dichlorophenol. Laccase-mediators such as 1-hydroxybenzotriazole (HBT), syringaldehyde (Syr) and violuric acid (Vio) have an equipotent added effect on the degradation of 2,3,7,8-TCDD by the extracellular enzyme extract.
Article
Environmental Sciences
Jyoti Bhuju, Kristin M. Olesen, Clarisse S. Muenyi, Tejesh S. Patel, Robert W. Read, Lauren Thompson, Omar Skalli, Qi Zheng, Elizabeth A. Grice, Carrie Hayes Sutter, Thomas R. Sutter
Summary: Exposure to TCDD during pregnancy and lactation in mice resulted in skin effects such as acanthosis and chloracne-like sebaceous gland hypoplasia, which were reversible and did not cause long-term immunosuppression. Additionally, increased expression of CYP1A1 and CYP1B1 in the skin of exposed mice was observed, with co-localization with progenitor cells and stem cell niches.
Article
Biochemistry & Molecular Biology
Hye Ran Kim, Jin Cheol Kim, Seok Young Kang, Hye One Kim, Chun Wook Park, Bo Young Chung
Summary: Through mouse model experiments, we found that TCDD aggravated skin inflammation in IMQ-induced psoriatic mice, increasing the expression of AHR, CYP1A1, inflammatory cytokines, and oxidative stress markers while decreasing autophagy-related factors and antioxidant markers. Rapamycin, on the other hand, alleviated TCDD-induced skin inflammation and restored autophagy inhibition, AHR expression, oxidative stress, and inflammatory response in the psoriatic mouse model.
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
(2021)