Dioxins and Dioxin-Like Compounds: Toxicological Impacts on Human Health

A special issue of Toxics (ISSN 2305-6304). This special issue belongs to the section "Human Toxicology and Epidemiology".

Deadline for manuscript submissions: 13 December 2024 | Viewed by 1732

Special Issue Editors


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Guest Editor
Department of Public Health, Kanazawa Medical University, Uchinada 920-0293, Japan
Interests: environmental health; environmental epidemiology; dioxin; cadmium
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Department of Environmental Health, School of Medical Sciences, University of Fukui, Eiheiji, Fukui 910-1193, Japan
Interests: environmental health; neurotoxicology; brain development; behavior; neuron; histology; aryl hydrocarbon receptor; dioxin; microscopy imaging

Special Issue Information

Dear Colleagues,

This Special Issue is the continuation of the previous issue on the same topic, with several articles reporting the effects of recent perinatal dioxin exposure on brain development in children and adults. Moreover, in the previous Special Issue, another article reported the usefulness of a method using biological responses in Danio rerio (zebrafish) to evaluate the toxicity of a mixture of dioxins and polycyclic aromatic hydrocarbons (PAHs) which exert their effects through the aryl hydrocarbon receptor (AHR). Recently, it was reported that AHR activation via endogenous ligands plays central roles in maintaining physiological status such as immunity and circadian clockworks. These results suggest that dioxins and dioxin-like compounds may impact human health by disrupting interactions between the AHR and endogenous ligands in various biological systems. Therefore, we are pleased to invite you to submit a paper aiming to investigate the effects of the exposure of AHR ligands such as dioxins and PAHs on human health using not only epidemiological methods, but also in vivo and in vitro experimental approaches. The toxicity of dioxin and its related compounds on developmental and aging processes and maintaining physiological functions is the main scope of the current Special Issue. The studies focused on these topics and reviews covering these fields are also welcome for submission. We look forward to receiving your contributions to outline future directions for the studies on the health effects of exposure to dioxin and its related compounds.

Prof. Dr. Muneko Nishijo
Dr. Eiki Kimura
Guest Editors

Manuscript Submission Information

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Keywords

  • dioxin
  • dioxin-like compounds
  • aryl hydrocarbon receptor
  • environmental health
  • in vitro study
  • in vivo study
  • development
  • maintenance

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Related Special Issue

Published Papers (2 papers)

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Research

14 pages, 1114 KiB  
Article
Relationships among Dioxin-like Mitochondria Inhibitor Substances (MIS)-Mediated Mitochondria Dysfunction, Obesity, and Lung Function in a Korean Cohort
by Hoonsung Choi, Kyungho Ha, Jin Taek Kim, Min Kyong Moon, Hyojee Joung, Hong Kyu Lee and Youngmi Kim Pak
Toxics 2024, 12(10), 735; https://doi.org/10.3390/toxics12100735 - 11 Oct 2024
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Abstract
Mitochondrial dysfunction is closely linked to obesity and diabetes, with declining lung function in aging increasing diabetes risk, potentially due to elevated serum levels of dioxin-like mitochondria inhibitor substances (MIS) from prolonged exposure to environmental pollutants. However, the mechanisms connecting MIS, mitochondria, lung [...] Read more.
Mitochondrial dysfunction is closely linked to obesity and diabetes, with declining lung function in aging increasing diabetes risk, potentially due to elevated serum levels of dioxin-like mitochondria inhibitor substances (MIS) from prolonged exposure to environmental pollutants. However, the mechanisms connecting MIS, mitochondria, lung function, and metabolic disorder remain unclear. In this study, we analyzed data from 1371 adults aged 40–69 years in the 2008 Korean Genome Epidemiologic Study (KoGES) Ansung cohort. We indirectly estimated dioxin-like MIS levels by measuring intracellular ATP (MISATP) and reactive oxygen species (MISROS) in cultured cells treated with the serum of participants. Using correlation analysis and structural equation modeling (SEM), we explored the relationships among MIS, mitochondrial function, body mass index (BMI), and lung function (FEV1 and FVC). Our findings revealed that MISATP was associated with BMI in females and with FVC in males, while MISROS correlated with both BMI and FVC in males, not in females. Significant associations between BMI and FVC were found in the highest MIS subgroup in both sexes. SEM analyses demonstrated that MIS negatively influenced mitochondrial function, which in turn affected BMI and lung function. Age-related declines in lung function were also linked to mitochondrial dysfunction. This study underscores the potential of MIS assays as alternatives for assessing mitochondrial function and highlights the importance of mitochondrial health in metabolic disorders and lung function. Full article
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12 pages, 687 KiB  
Article
Uptake, Elimination and Metabolism of Brominated Dibenzofurans in Mice
by Nguyen Minh Tue, Eiki Kimura, Fumihiko Maekawa, Akitoshi Goto, Naoto Uramaru, Tatsuya Kunisue and Go Suzuki
Toxics 2024, 12(9), 656; https://doi.org/10.3390/toxics12090656 - 7 Sep 2024
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Abstract
Polybrominated dibenzofurans (PBDFs) are major brominated dioxins in the environment, but information on their bioaccumulation potential and toxicokinetics is limited. This study conducted oral exposure experiments with C57BL/6J mice to investigate the uptake ratios, distribution in the liver, plasma and brain, metabolism, and [...] Read more.
Polybrominated dibenzofurans (PBDFs) are major brominated dioxins in the environment, but information on their bioaccumulation potential and toxicokinetics is limited. This study conducted oral exposure experiments with C57BL/6J mice to investigate the uptake ratios, distribution in the liver, plasma and brain, metabolism, and elimination kinetics of four bromine/chlorine-substituted dibenzofurans (TrBDF: 2,3,8-tribromo, TeBDF: 2,3,7,8-tetrabromo, PeBDF: 1,2,3,7,8-pentabromo, TrBCDF: 2,3,7-tribromo-8-chloro) in comparison with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). The hepatic uptake ratios of 2,3,7,8-substituted dibenzofurans were lower than that of TCDD (up to 84% of the administered doses) and decreased with the number of Br substitutions (42%, 33%, and 29% for TrBCDF, TeBDF, and PeBDF, respectively). The brain uptake ratios of these dibenzofurans were less than 0.05%, and the plasma-to-brain transfer ratio also decreased with the Br number. All 2,3,7,8-substituted compounds were eliminated from the liver following first-order kinetics, with half-times in the order of TrBCDF (5.6 days) < TeBDF (8.8 days) ≈ TCDD (8.7 days) < PeBDF (13 days). The non-2,3,7,8-substituted TrBDF was poorly retained in the liver (<0.01% of the dose at 1 day) and rapidly eliminated following two-phase kinetics. All dibenzofurans were metabolised into monohydroxylated products in the liver, but the contribution of this metabolic pathway to hepatic elimination was only significant for TrBDF. As the toxic effects of dioxin-like compounds are influenced by their biological persistence, the slow elimination of TrBCDF, TeBDF, and PeBDF observed in this study suggests that exposure risk of brominated dibenzofurans may be underestimated using the toxic equivalency factors of the less persistent chlorinated analogues. Full article
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