Polyhalogenated dibenzo-p-dioxins and dibenzofurans and the immune system. 1. Effects on peripheral lymphocyte subpopulations of a non-human primate (Callithrix jacchus) after treatment with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)

Neubert, Reinhard; Jacob-Müller, Ursula; Stahlmann, Ralf; Helge, H; Neubert, Diether

doi:10.1007/bf01973455

Cited by 68 publications

(21 citation statements)

References 32 publications

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“…In other studies, a single injection of TCDD in marmosets (Callithrixjacchus) resulted in a decrease in the percentages of CD20+ B cells and CD4+ T cells and an increase in the percentage of CD8+ T cells in the blood without affecting the total numbers of these cells (71). The CD4+ subset that was most affected was the CDo29+ helper-inducer or memory subset, with significant effects observed after a TCDD dose of 10 ng/kg but not after a dose of 3 ng/kg.…”

Section: Studies In Nonhuman Primatesmentioning

confidence: 86%

Immunological Effects of Chlorinated Dibenzo-p-Dioxins

Kerkvliet¹

1995

Environmental Health Perspectives

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Section: Studies In Nonhuman Primatesmentioning

confidence: 86%

Immunological Effects of Chlorinated Dibenzo-p-Dioxins

Kerkvliet¹

1995

Environmental Health Perspectives

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“…Single doses to mice of as little as 100 ng/kg caused enhanced viral mortality (22). A single exposure of 10 ng TCDD/kg resulted in altered patterns of lymphocyte subsets in the marmoset (109). However, at weekly doses of 0.3 ng/kg, no clear-cut change occurred in the total lymphocyte population (110).…”

Section: Toxiic Equivalencymentioning

confidence: 99%

The mechanism of dioxin toxicity: relationship to risk assessment.

Birnbaum

1994

Environ Health Perspect

297

147

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Risk characterization involves hazard identification, determination of dose-response relationships, and exposure assessment. Improvement of the risk assessment process requires inclusion of the best available science. Recent findings in the area of dioxin toxicity have led to a major effort to reassess its risk. 2,3,7,, commonly referred to as "dioxin," is the most toxic member of a class of related chemicals including the polyhalogenated dibenzo-p-dioxins, dibenzofurans, biphenyls, naphthalenes, azo-and azoxy-benzenes, whose toxicities can be expressed as fractional equivalencies of TCDD. These chemicals exert their effects through interaction with a specific intracellular protein, the Ah receptor. While binding to the receptor is necessary, it is not sufficient to bring about a chain of events leading to various responses including enzyme induction, immunotoxicity, reproductive and endocrine effects, developmental toxicity, chloracne, tumor promotion, etc. Some of these responses appear to be linear at low doses. Immunotoxicity and effects on the reproductive system appear to be among the most sensitive responses. The Ah receptor functions as a transcriptional enhancer, interacting with a number of other regulatory proteins (heat shock proteins, kinases, translocases, DNA binding species). Interaction with specific base sequences in the DNA appear to be modulated by the presence of other growth factors, hormones, and their receptors as well as other regulatory proteins. Thus, dioxin appears to function as a hormone, initiating a cascade of events that is dependent upon the environment of each cell and tissue. While Ah receptor variants exist, all vertebrates examined have demonstrated such a protein with similar numbers of receptors and binding affinity for TCDD. Most species respond similarly to dioxin and related compounds. While a given species may be an outlier for a given response, it will behave like other animals for other responses. For both in vivo and in vitro end points where animal and human data exist, such as enzyme induction, chloracne, immunotoxicity, developmental toxicity, and cancer, the sensitivity of humans appears similar to that of experimental animals. Current levels of environmental exposure to this class of chemicals may be resulting in subtle responses in populations at special risk such as subsistence fisherman and the developing infant, as well as in the general population. Increased understanding of the mechanism of dioxin's effects as well as elucidation of exposure-dose relationships is leading to the development of a biologically based dose-response model in the ongoing process of incorporating the best science into the risk assessment of TCDD and related compounds.-Environ Health Perspect 102(Suppl 9) 157-167(1994)

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“…Environmental Health Perspectives * Volume 103, Number 9, September 1995 (82,83). Enhanced viral susceptibility, as measured by increased mortality, occurs in mice at body burdens of approximately 10 ng TCDD/kg (84), which is equivalent to the body burden seen in unexposed humans and approximately twice the level in untreated mice.…”

mentioning

confidence: 99%