To clarify the relationship between chemically-induced cell damage and aryl hydrocarbon hydroxylase (AHH) activity, we used five lines from ataxia telangiectasia (AT) homozygotes (n = 5), AT heterozygotes (n = 5), xeroderma pigmentosum (XP) homozygotes (n = 2), XP heterozygotes (n = 2), and healthy subjects (n = 54). The value of relative fluorescein formation (RFF; an index of cell damage) of cell lines from either AT or XP homozygotes was significantly lower (p < 0.01 and p < 0.001, respectively) than that of lines from healthy subjects. The value of neocarzinostatin (NCS)-treated RFF of cell lines from XP homozygotes, which are sensitive to UV or UV-mimetic chemicals, was also significantly lower than that of healthy subjects (p < 0.05) and similar to that of AT heterozygotes. Since both XP and AT patients have increased risks of internal neoplasms, these might be related to exposure to environmental carcinogens. Although high levels of AHH activity may indicate more conversion of carcinogens into highly reactive intermediates, which interact with DNA to cause carcinogenicity, AHH activity showed no significant difference among these five cell lines. The differences in endogenous activation ability may not be a large factor in the hypersensitivity of XP and AT patients to environmental carcinogens.
|ジャーナル||Medical Science Research|
|出版ステータス||出版済み - 10月 30 1997|
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