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References
Category:FoxPro software
Category:2005 softwareDiphenyleneiodonium salts, phenylhydroperoxide-metabolizing enzymes and the induction of liver tumors by aflatoxin B1 in rats.
Diphenyleneiodonium (DPI) derivatives inhibit a liver microsomal Fenton-like reaction, catalyzed by cytochrome P-450 (CYP), but the mechanism of their antitumor activity is unknown. A role for metabolic activation by microsomes, generating a phenoxy radical (PhOX) as a carcinogen intermediate, was investigated. A cDNA encoding a phenylhydroperoxide-metabolizing enzyme (tetramethyl-3-phenyl-2-oxazoline-5-thione oxidase; tm-TPOx) was cloned from liver, and tm-TPOx mRNA was detected in all tissues. tm-TPOx coexpression with CYP increased the sensitivity of rat hepatocytes to the in vitro formation of PhOX from aflatoxin B1 (AFB1) but not from benzo[a]pyrene. In contrast, coexpression of tm-TPOx with CYP was not sufficient to transform hepatocytes to tumorigenicity by AFB1 in vivo. It is unlikely that tm-TPOx-mediated metabolism is a major determinant of the carcinogenicity of AFB1 because (i) it is not expressed in human hepatocytes; (ii) levels of tm-TPOx transcript were reduced in microsomes from rats fed on a diet containing AFB1 (20 ppm) for three weeks; (iii) the tumor incidence for AFB1 was the same in tm-TPOx-deficient and wild-type rats; and (iv) purified tm-TPOx efficiently metabolized phenol to the PhOX, which can be detected in the liver at levels found in vivo. These findings indicate that the carcinogenicity of AFB1 is mediated by a reaction that is not linked to the generation of PhOX.A comparison of the quality of life in patients with chronic plaque-type psoriasis treated with flexibly dosed methotrexate and calcipotriene or calcitriol. be359ba680
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