Developmental Effects of Dioxins

Abstract

The potent developmental toxicity of dioxin in multiple species has been known for a number of years. However, recent studies have indicated that dioxin also induces functional developmental defects, many of which are delayed. Subtle structural deficits, not detectable at birth, have also been described in multiple species and in both sexes. Certain defects have been reported not only in animals but also in children prenatally exposed to complex mixtures containing dioxinlike compounds. None of the effects can be attributed to modulation of any one endocrine system. For example, dioxin does not bind to the estrogen receptor, but it can cause effects that are both estrogenic and antiestrogenic. However, viewing dioxin and related compounds as endocrine disruptors that may alter multiple pathways sheds some light on the complexities of this potent class of growth dysregulators. -Environ Health Perspect 1 03(Suppl 7): 89-94 (1995)

spineless provides a little backbone for dendritic morphogenesis: Figure 1.

“…Mr. Yushchenko's face is heavily scarred with chloracne, the characteristic external feature of dioxin poisoning. Both fetal and adult exposure to elevated levels of dioxin leads to multiple organ defects, including cleft palate, gonadal atrophy, and lymphoid tissue degeneration (Birnbaum 1995), and increased dioxin and polychlorinated biphenyl levels positively correlate with a variety of neural and other tissue abnormalities (ten Tusscher and Koppe 2004). It is generally thought that these effects are due to activation of Ahr.…”

Histopathological Findings of Cleft Palate in Rat Embryos Induced by Triamcinolone Acetonide

“…It may result from disturbances at any stage of palatal development: defective palatal shelf growth, delayed or failed shelf elevation, defective shelf fusion, failure of medial edge epithelial cell (MEE cell) death, postfusion rupture and failure of mesenchymal consolidation and differentiation [10]. Numerous reports have described the effects of glucocorticoids [19,21] or 2,3,7,8-tetrachlorodibenzo-pdioxin (TCDD) [6,8] on the developing fetus through administration during mammalian gestation. Both TCDD and glucocorticoids induce cleft palate by acting through aryl hydrocarbon receptor-and glucocorticoid receptormediated mechanisms, respectively [1,4].…”

Expressing urine from a gel disposable diaper for biomonitoring using phthalates as an example

“…The susceptibilities identified in Table 4 are covered in In chapter 3, the structural and functional features that potenanimal species. For example, as documented in chapter 3, some (Bailey et al, 2003) Embryonic age Neural tube defects from retinoic acid, arsenic, and valproic acid (Adams, 1993;Bennett & Finnell, 1998) Decreased fertility in female rats exposed to dioxin (TCDD) (Gray & Ostby, 1995) Hydronephrosis with dioxin exposure during embryonic or fetal periods in rats (Couture-Haws et al, 1991;Birnbaum, 1995) Fetus Decreased intelligence, increased behavioural problems with lead (Bellinger et al, 1994;Rice, 1996) Cerebral palsy, mental retardation with high-dose methylmercury (Harada, 1978); subtle neurobehavioural effects with low doses (Grandjean et al, 1997) Exposure to several phthalates induces reduced AGD and malformations in male rats (Mylchreest et al, 1999;Gray et al, 2000) Delay in pubertal development from exposure to PBBs Vaginal adenocarcinoma in young women due to DES (Herbst et al, 1971) ACE fetopathy with neonatal renal failure from maternal exposure to angiotensin inhibitors (Tabacova et al, 2003) Maternal smoking causes decreased birth weight and increased risk for later diabetes (Montgomery & Ekbom, 2002) and osteoporosis Decreased T3/T4 levels in infant and juvenile rats (Brouwer et al, 1998) exposed to PCBs (Birnbaum, 1995) Maternal grooming affects ability to respond to stress in adulthood in rats (Gilbert, 2005) Child Brain tumours and meningiomas...…”