Inhibition of 3,3′,4,4′,5-Pentachlorobiphenyl-Induced Chicken Embryotoxicity by 2,2′,4,4′,5,5′-Hexachlorobiphenyl

Teratogenic and biochemical effects of a formulation containing dicofol in the chick embryo

“…Manner et al (2003) observed that only 50% of suramin treated embryos survived until embryonic day 8 when exposed on embryonic day 3 as compared with control embryos. However in contrast to our results, dose-dependent increase in embryolethality was observed by Verrett et al (1969), Korhonen, Hemminki, and Vainio (1983), Kumar and Devi (1992), Zhao et al (1997), Pourmirza (2000), Sahu and Ghatak (2002), Rachid, Houria, and Reda (2008), Wagh, Deshpande, and Salokhe (2011), and Mobarak and Al-Asmari (2011) in chick embryo exposed to various xenobiotics. It is difficult to compare the presently estimated mortality result in chick embryo with that of chronic toxic study conducted by El-Kashoury et al (2009) because they reported only 25% and 30% mortality rate in male rate exposed to 30 ppm and 120 ppm of Kelthane (different commercial formulation of dicofol), respectively.…”

“…Furthermore, Kumar and Devi (1992) reported teratological abnormalities such as short neck, abdominal hernias, and hemorrhagic spots in brain and upper body which were predominant in 20-day-old chick embryos exposed to methyl parathion on embryonic days 4 and 6. The majority of malformations are in agreement with previous studies in developing chick embryos with captan and related compounds (Verrett et al 1969), 2,2 0 ,4,4 0 ,5,5 0 -hexachlorobiphenyl (Zhao et al 1997), dimecron (Sahu and Ghatak 2002), suramin (Manner et al 2003), chlorpyrifos and cypermethrin (Uggini, Patel, and Balakrishnan 2012), hexavalent chromium (Asmatullah and Shakoori 1998), bendiocarb (Petrovova et al 2010), lufenuron (Wagh, Deshpande, and Salokhe 2011), and methylmercury (Heinz et al 2011). Growth retardation effect of pesticide (dicofol) on the developing chick could be due to its inhibitory effect/disturbance on metabolism or after disruption of the retinoid signaling pathway in cells, which play an essential role in the proliferation, development, and differentiation of cells and disruption that can lead to malformation or abnormal development of eye, brain, heart, and limbs during the ''critical'' growing phase (Mobarak and Al-Asmari 2011).…”

Toxic equivalency factors (TEFs) for PCBs, PCDDs, PCDFs for humans and wildlife.

“…Recendy, these nonadditive interactions of PCB on dioxinlike effects have been reviewed (193). In summary, the following antagonistic effects ofnondioxinlike PCBs were described: induction of EROD activity in chick embryo hepatocytes (194), splenic PFC response to sheep erythrocytes in mice (195), splenic PFC response to trinitrophenyl-lipopolysaccharide in mice (196), serum IgM units in mice (91), mouse fetal deft palate (110,195), and chick embryo malformations and edema and liver lesions (197). The apparent antagonism by PCB 153 of the TCDD-induced immunosupression is due to the enhanced immune response induced by PCB 153 (198).…”

Flavonoids as aryl hydrocarbon receptor agonists/antagonists: effects of structure and cell context.

“…However, in mixtures containing PCBs, there is also evidence that for some AhR-mediated responses, nonadditive antagonist interactions can be observed (Safe 1998a(Safe , 1998b. For example, the antagonistic interactions between many environmentally significant PCBs, including 2,2´,4,4´,5,5´-hexachlorobiphenyl (PCB congener 153) interactions with TCDD or 3,3´,4,4´,5-pentachlorobiphenyl (PCB 126), for several AhRmediated responses in several in vivo and in vitro models have been reported (Biegel et al 1989; Safe 1988, 1989;Morrissey et al 1992;Tysklind et al 1995;Zhao et al 1997aZhao et al , 1997b. These results are consistent with a receptor-mediated pathway where both agonist and antagonist ligands are routinely identified.…”