Dioxin antagonist effect

Aroclor 1254 as a 2, 3, 7, 8-tetrachlorod ibenzo-p-dioxin antagonist effects on enzyme induction and immunotoxicity,... 

Fig. (4). Differences between the required pattern of substitution for antagonist effect of dioxin (A) and the naturally occurring pattern (B).

Data are available suggesting that DEHP might act as an antagonist for the hepatic damage caused by other chemicals. DEHP was combined with 2,3,7,8-tetrachlorodibenzo-/ -dioxin (TCDD) to determine if the hypolipidemic effects of DEHP could counteract the hyperlipidemic effects of the TCDD (Tomaszewski et al. 1988). Pretreatment with DEHP mitigated many of the toxic effects of TCDD. 

Although drugs such as acetaminophen bind to AhR, the majority of AhR agonists or antagonists are environmental chemicals. Polychlorinated diben-zodioxins such as 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), dibenzofu-rans, biphenyls, and a number of other chemicals are widespread pollutants in aquatic ecosystems. These compounds cause a high reproductive and developmental toxicity, which is mediated via binding to the AhR. Thus they pose a serious threat to many populations of mammals, birds, and fish. Various adverse effects—including structural malformations, reduced fertility, tumor promotion, immunotoxicity, and skin disorders like chloracne—have been observed [139]. 

However, complex and anomalous findings have caused uncertainty about the biochemical and functional thyroid status of dioxin treated animals (4). This could be related to a complex Interplay of the potential thyroid hormone agonists and antagonists properties of these toxic compounds. Further studies are needed to investigate a possible link between TCDD (and related compounds)-medlated effects and some aspects of thyroid hormone endocrinology. 

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