Comparative toxicity of N-hydroxy-2-acetylaminofluorene in several strains of rats.

نویسنده

  • C C Irving
چکیده

Male Spraque-Dawley rats were 6 or 7 times more susceptible than females to the acute toxic effects of a single i.p. injection of N-hydroxy-2-acetylaminofluorene. The N-hydroxy compound were equally toxic in male and female Fischer rats and about twice as toxic to male as to female Wistar rats. A negative correlation between the 50% lethal dose of N-hydroxy-2-acetylaminofluorene and hepatic N-hydroxy-2-acetylaminofluorene sulfotransferase activity was found. These data substantiate earlier indications that the level of the liver sulfotransferase is an important factor in determining the degree of toxicity of N-hydroxy-2-acetylaminofluorene. It is suggested that the reported sex difference in the hepatocarcinogenicity of N-hydroxy-2-acetylaminofluorene might be peculiar to the Sprague-Dawley rat.

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

منابع مشابه

Effects of neonatal and adult castration on the in vitro metabolism of steroids and xenobiotics in rat liver.

Previous studies in our laboratory have shown that the sex-differentiated metabolism of 4-androstene-3,17-dione and of several other steroid hormones in adult rat liver is "feminized" following neonatal castration of male rats, due to an influence via the hypothalamo-pituitary-liver axis. The metabolism of many xenobiotics is also sex differentiated, and an important question is whether endocri...

متن کامل

Effect of glutathione depletion on the hepatotoxicity and covalent binding rat liver macromolecules of N-hydroxy-2-acetylaminofluorene.

Glutathione plays an important role in the protection of the liver against several hepatotoxins. The hepatocarcinogen N-hydroxy-2-acetylaminofluorene is converted in the rat in vivo to reactive metabolites that bind covalently to cellular macromolecules. These metabolites may also react with glutathione, resulting in the formation of glutathione conjugates and in the detoxification of reactive ...

متن کامل

Repair synthesis of DNA induced by the urinary N-hydroxy metabolites of carcinogenic arylamines in urothelial cells of susceptible species.

Urinary N-hydroxy metabolites of the bladder carcinogens, 2-aminofluorene and 4-aminobiphenyl, were examined for the induction of unscheduled DNA synthesis (UDS) in urothelial cells of several susceptible species. N-Hydroxy-2-aminofluorene, N-hydroxy-2-acetylaminofluorene (N-OH-AAF), N-hydroxy-4-aminobiphenyl, N-hydroxy-4-acetylaminobiphenyl, and the N-glucuronides of these two hydroxylamines i...

متن کامل

Induction of unscheduled DNA synthesis in primary culture of dog, rat, and mouse urothelial cells by arylamine and nitrofuran derivatives.

The induction of unscheduled DNA synthesis in primary cultures of urothelial cells from rats, mice, and dogs by nitrofurans and arylamines and their derivatives was examined. Electron microscopy of the culture from rat cells showed the characteristics of epithelial cells. The cultured cells were exposed to the test chemicals in a serum-free medium containing 10 mM hydroxyurea and [3H]thymidine ...

متن کامل

The Effects of Hepatotoxic Agents and of Liver Growth on the Urinary Excretion of the N-hydroxy Metabolite of 2-acetylaminofluorene by Rats.

Adult rats subjected to a number of treatments which cause liver damage and/or growth (administration of hepatotoxic agents, partial hepatectomy, or protein deple tion-repletion) and young growing rats excreted in the urine a greater percentage of a test dose of 2-acetylaminofluorene (AAF) as the carcinogenic Af-hydroxy metabolite than did normal adult rats. Alterations in the urinary excretion...

متن کامل

ذخیره در منابع من


  با ذخیره ی این منبع در منابع من، دسترسی به آن را برای استفاده های بعدی آسان تر کنید

برای دانلود متن کامل این مقاله و بیش از 32 میلیون مقاله دیگر ابتدا ثبت نام کنید

ثبت نام

اگر عضو سایت هستید لطفا وارد حساب کاربری خود شوید

عنوان ژورنال:
  • Cancer research

دوره 35 11 Pt 1  شماره 

صفحات  -

تاریخ انتشار 1975