In this review, we have examined the biochemical and toxic responses produced by halogenated aromatic hydrocarbons and have tried to develop a model for their mechanism of action. These compounds bind to a cellular receptor and evoke a sustained pleiotropic response. In many tissues this response consists of the expression of a battery of enzymes which are, for the most part, involved in drug metabolism, but in other tissues, those which develop toxicity, an additional set of genes is expressed which effects cellular involution, division, and/or differentiation. The toxicity of these compounds appears to be due to the sustained expression of a normal cellular regulatory system, of which we were previously unaware. In future investigations it is hoped that we will learn the nature and physiologic role of this regulatory system. Only then can we hope to understand the mechanism of toxicity of these compounds.

2,3,7,8-Tetrachlorodibenzo-p-Dioxin and Related Halogenated Aromatic Hydrocarbons: Examination of the Mechanism of Toxicity

The present invention relates to an electronic device comprising anode, cathode and at least one organic layer which comprises a compound of the formula (I) to (IV). The invention furthermore encompasses the use of compounds of the formula (I) to (IV) in an electronic device and to a compound of the formula (Ic) to (IVc).

Materials for electronic devices

The comparative toxicity of chlorinated dibenzo-p-dioxins in mice and guinea pigs.

Aberrant or defective immune responses are known to be the result of primary immunodeficiency diseases, e.g., in the DiGeorge syndrome (thymic hypoplasia) in man, or in homozygous mice with the mut...

https://www.tandfonline.com/doi/pdf/10.1080/15476910701508262

Immune suppression as related to toxicology.

The chemi- and bioluminescence of firefly luciferin: An efficient chemical production of electronically excited states

Organs as targets of "dioxin" (2,3,7,8-tetrachlorodibenzo-p-dioxin) intoxication

Enzymatic functions as targets of the toxicity of "Dioxin" (2,3,7,8-tetrachlorodibenzo-p-dioxin).

Temperaturen; das Enzym erwies sich bis zu etwa 70 ~ stabil. Das pH-Optimum des Enzyms liegt bet 5,7 ~_ 0,3. Unterhalb pH 4,5 und oberhalb pH 6,5 tr i t t irreversible Inaktivierung ein, die in erster Linie auf eine Denaturierung des Enzymproteins und nicht auf eine ~-nderung des Ionisationsgrades funktionell wichtiger Gruppen zuri~ckzufi~hren ist. Das Enzym zeigt keine Produkthemmung dutch 7-Aminobutters~ure, wird aber kompetitiv durch r bet einer Konzentration yon 5 • 10 .3 m zu 50% gehemmt. Ein noch wirksamerer kompetitiver Inhibitor ist Cbo-L-glutamins~ure.

N. P. Buu-Hoï

Papers

Organs as targets of "dioxin" (2,3,7,8-tetrachlorodibenzo-p-dioxin) intoxication

Enzymatic functions as targets of the toxicity of "Dioxin" (2,3,7,8-tetrachlorodibenzo-p-dioxin).

Carcinogenicity of a non-benzenoid hydrocarbon, azuleno[5,6,7-c,d]phenalene, and derivatives.

A non-radiative photochemical model for polycyclic aromatic hydrocarbon-induced carcinogenesis.

ENHANCEMENT OF THE CARCINOGENICITY OF 7,12-DIMETHYLBENZ[a]ANTHRACENE THROUGH REPLACEMENT OF HYDROGEN BY DEUTERIUM: A NEW BIOLOGICAL ISOTOPE EFFECT.