Aryl-4-hydroxylase and

Brunstrom, B. 1986. Activities in chick embryos of 7-ethoxycoumarin O-deethylase and aryl hydrocarbon (benzo[a]pyrene) hydroxylase and their induction by 3,3, 4,4 -tetrachlorobiphenyl in early embryos. Xenobiotica 16 865-872. 

Janz, D.M. and C.D. Metcalfe. 1991b. Nonadditive interactions of 2,3,7,8-TCDD and 3,3, 4,4 -tctrachIorobi-phenyl on aryl hydrocarbon hydroxylase induction in rainbow trout (Oncorhynchus mykiss). Chemosphere 23 467-472. 

Kiyohara, C., Nakanishi, Y., Inutsuka, S., Takayama, K., Hara, N., Motohiro, A., Tanaka, K., Kono, S. and Hirohata, T. (1998) The relationship between CYP1A1 aryl hydrocarbon hydroxylase activity and lung cancer in a Japanese population. Pharmacogenetics, 8 (4), 315-323. 

Bend, J. R., Hall, P., and Foureman, G. L. Comparison of benzo(a)pyrene hydroxylase (aryl hydrocarbon hydroxylase, AHH) activities in hepatic microsomes from untreated and 1,2,3,4-dibenzanthracene (DBA)-induced little skate (Raja erinacea). Bull. Mt. Desert Island Biol. Lab. (1976) 16. 3-5. 

Robertson LW, Andres JL, Safe SH, et al. 1983a. Toxicity of 3,3, 4,4 - and 2,2, 5,5 -tetrabromobiphenyl correlation of activity with aryl hydrocarbon hydroxylase induction and lack of protection by antioxidants. J Toxicol Environ Health 11 81-91. 

Slaga, T.J., and Bracken, W.M. The Effect of Antioxidants on Skin Tumor Initiation and Aryl Hydrocarbon Hydroxylase. 

Many of the toxic and biological effects induced by polychlorinated dibenzo-p-dioxins and furans (PCDD/Fs) and PCBs such as carcinogenesis, reproductive disturbances and immunotoxic effects are believed to be mediated via the hepatic cytosolic aryl hydrocarbon receptor (Ah receptor) [254,255]. Based on in vitro and in vivo studies, the toxicity of individual organochlorines have been determined relative to 2,3,7,8-tetrachlorodibenzo-p -dioxin (TCDD) and expressed as toxic equivalency factors (TEFs) [254, 256]. In addition to PCDD/F, structurally related PCBs and PCNs bind to the Ah receptor. After binding to the Ah-receptor, the receptor-ligand complex is transferred into the nucleus where it binds to specific DNA sequences and causes transcription of structural genes, which in turn causes synthesis of various cytochrome P4501A1-dependent enzymes such as ethoxyresorufin O-deethylase (EROD) and aryl hydrocarbon hydroxylase (AHH). TEFs for PCNs have been estimated from enzyme-induction assays of EROD and AHH [10, 257] and Luciferase assays in rat cells [12] cf. Table 4. 

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