Yusho and its latest findings—A review in studies conducted by the Yusho Group

Mitoma, Chikage; Uchi, Hiroshi; Tsukimori, Kiyomi; Yamada, Hideyuki; Akahane, Manabu; Imamura, Tomoaki; Furue, Masutaka

doi:10.1016/j.envint.2015.05.004

Cited by 48 publications

(30 citation statements)

References 88 publications

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“…As dioxins (TCDD and many other various forms in this class) are retained in hosts for a long time, there is a great chance of impact on human health, to some extent, for a long period of time following single/multiple exposures to this toxicant (Warner et al 2013;Wesselink et al 2014;Mitoma et al 2015;Landgren et al 2015). Here, it was documented that RA was among the various pathologies whose incidence was elevated in the evaluated Vietnamese subjects.…”

Section: Diseasesmentioning

confidence: 91%

Expression of aryl hydrocarbon receptor, inflammatory cytokines, and incidence of rheumatoid arthritis in Vietnamese dioxin-exposed people

Nguyen

Nakahama

Dang

et al. 2017

Journal of Immunotoxicology

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Many Vietnamese citizens have been and continue to be inadvertently exposed to dioxins and dioxin-like compounds deposited in the country during the Vietnam War. Dioxins may be involved in the pathogenesis of inflammatory diseases in part via by affecting expression of aryl hydrocarbon receptor (Ahr) and inflammatory cytokines in animal models. As the role of the Ahr in dioxin-exposed people is not well defined, a study was conducted to examine gene expression levels of Ahr, inflammatory cytokines, and the incidence of diseases in dioxin-exposed citizens who had/still resided near a heavily dioxin-contaminated area in Vietnam. Whole blood from citizens at/around Da Nang airbase and control individuals living in unsprayed areas was collected. Serum levels of dioxins were analyzed by using a dioxins-responsive chemical-activated luciferase gene expression bioassay. Gene expression of Ahr, interleukin (IL)-1β, TNFα, IL-6, and IL-22 in whole blood was examined by quantitative real-time PCR. The results showed levels of dioxins and expression of Ahr, IL-1β, TNFα, and IL-6 were up-regulated while IL-22 expression was down-regulated in dioxin-exposed people. Various disease incidences in the study subjects was also examined. Interestingly, the incidence of rheumatoid arthritis (RA) in these individuals was increased compared to the estimated prevalence of this disease in the general Vietnamese population. Analyses also showed that expression levels of Ahr correlated to those of IL-6 and IL-22 in the dioxin-exposed people. Taken together, dioxins might be involved in an up-regulated expression of Ahr that might possibly relate to changes in level of inflammatory cytokines and, ultimately, in the incidence of select diseases in residents of Vietnam who had/continue to live near a dioxins-contaminated site.

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Section: Diseasesmentioning

confidence: 91%

Expression of aryl hydrocarbon receptor, inflammatory cytokines, and incidence of rheumatoid arthritis in Vietnamese dioxin-exposed people

Nguyen

Nakahama

Dang

et al. 2017

Journal of Immunotoxicology

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“…in blood of these mothers (74)(75)(76). An interesting review of studies conducted by the Yusho Group was recently published (77).…”

Section: Koreamentioning

confidence: 99%

Concentrations of PCDD/Fs in Human Blood: A Review of Data from the Current Decade

Marquès

Domingo

2019

Preprint

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Polychlorinated dibenzo-p-dioxins and polychlorinated dibenzo-p-furans (PCDD/Fs) are environmental pollutants with a great persistence, capacity of bioaccumulation, and well known important toxic effects in humans and animals.Incinerators of hazardous, municipal and medical waste, chlorine bleaching of paper pulp, cement plants, and the traffic of motor vehicles are the most frequent emission sources of these compounds. The diet, followed at a great distance by inhalation, is generally the main way of human exposure to PCDD/Fs. Human biomonitoring is of a great importance to prevent potential adverse effects derived from exposure to chemicals such as PCDD/Fs. In relation to this, blood is among the most used biological monitors. In the current review, we have summarized the recent information (2000)(2001)(2002)(2003)(2004)(2005)(2006)(2007)(2008)(2009) published in the scientific literature (databases: Scopus and PubMed) on the concentrations of PCDD/Fs in blood samples of non-occupationally exposed populations, as well as in some groups of occupationally exposed individuals. We have revised a number of studies conducted in various African American, Asian and European countries, and Australia. Unfortunately, the information is quite limited. No data are available for most countries over the world. Based on the results here reviewed -where available-the current health risks for the general populations do not seem to be of concern. Moreover, taking into account the important reductions observed in the levels of PCDD/Fs in foodstuffs, new decreases in the concentrations of PCDD/Fs in blood -and other biological tissues-are very probable in the immediate years.

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“…Persistent overactivation of AHR by TCDD and other dioxin-related compounds induces prolonged oxidative stress and may cause chloracne (51,68,69). The generation of ROS is also involved in the pathogenesis of contact dermatitis, AD and psoriasis (70)(71)(72).…”

Section: Regulatory Role Of Aryl Hydrocarbon Receptor In Oxidative Stmentioning

confidence: 99%

Antioxidative Phytochemicals Accelerate Epidermal Terminal Differentiation via the AHR-OVOL1 Pathway: Implications for Atopic Dermatitis

Furue¹,

Hashimoto-Hachiya²,

Tsuji³

2018

Acta Derm Venerol

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Aryl hydrocarbon receptor (AHR) is a chemical sensor that is expressed abundantly in epidermal keratinocytes. Oxidative AHR ligands induce the production of reactive oxygen species. However, antioxidant AHR ligands inhibit reactive oxygen species generation via activation of nuclear factor-erythroid 2-related factor-2, which is a master switch for antioxidative signalling. In addition, AHR signalling accelerates epidermal terminal differentiation, but excessive acceleration by oxidative ligands, such as dioxins, may induce chloracne and inflammation. However, antioxidative phytochemical ligands induce the beneficial acceleration of epidermal differentiation that repairs skin barrier disruption. The upregulated expression of differentiation molecules, such as filaggrin, is mediated via the AHR-OVOL1 axis. This AHR-OVOL1 system is capable of counteracting skin barrier dysfunction in T-helper type 2-shifted inflammation. This article reviews the dynamic and multifaceted role of AHR in epidermal biology and discusses the potential use of antioxidative phytochemical ligands for AHR in inflammatory skin diseases, such as atopic dermatitis.

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Yusho and its latest findings—A review in studies conducted by the Yusho Group

Cited by 48 publications

References 88 publications

Expression of aryl hydrocarbon receptor, inflammatory cytokines, and incidence of rheumatoid arthritis in Vietnamese dioxin-exposed people

Expression of aryl hydrocarbon receptor, inflammatory cytokines, and incidence of rheumatoid arthritis in Vietnamese dioxin-exposed people

Concentrations of PCDD/Fs in Human Blood: A Review of Data from the Current Decade

Antioxidative Phytochemicals Accelerate Epidermal Terminal Differentiation via the AHR-OVOL1 Pathway: Implications for Atopic Dermatitis

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