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Additional resources for Reviews of Environmental Contamination and Toxicology Volume 212
Leibold E, Schwarz L (1993) Inhibition of intercellular communication in rat hepatocytes by phenobarbital, 1,1,1-trichloro-2,2-bis(p-chlorophenyl)ethane (DDT) and g-hexachlorocyclohexane (lindane): Modification by antioxidants and inhibitors of cyclo-oxygenase. Carcinogenesis 14: 2377–2382. Leng JH, Kayama F, Wang PY, Nakamura M, Nakata T, Wang Y (2009) Levels of persistent organic pollutants in human milk in two Chinese coastal cities, Tianjin and Yantai: Influence of fish consumption. Chemosphere 75: 634–639.
Olivero J, Bezdecny SA, Ganey PE (2002) Molecular motif required for the activation of rat neutrophil phospholipase A(2) by organochlorine compounds. Chem Res Toxicol 15: 153–159. Oskarsson A, Ulleras E, Plant KE, Hinson JP, Goldfarb PS (2006) Steroidogenic gene expression in H295R cells and the human adrenal gland: adrenotoxic effects of lindane in vitro. J Appl Toxicol 26: 484–492. , Goudey-Perriere F (2002) Reproductive toxicity of lindane. J Soc Biol 196: 325–338. Pajuelo L, Sanchez J, Del Hoyo N, Pulido J, Perez M (1997) Non-muscarinic and non-adrenergicmediated effects of lindane on phosphoinositide hydrolysis in rat brain cortex slices.
These responses were equal in magnitude to the maximal effect of estradiol, and they were inhibited by inclusion of the antiestrogen ICI164384. However, when tested in a competitive binding assay, b-HCH did not displace 17-beta-[3H]estradiol from the ER even at a concentration that was 40,000-fold higher than the tracer steroid (Steinmetz et al. 1996). These authors suggested that b-HCH stimulation of cell proliferation and gene expression is ER dependent, but its action is not through the classic pathway of binding and activating the ER.