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Studies of tumor because of TBHQ in rats
 2.2.4.1 Rats code         the metabolism of rats like human. The promoting activity of TBHQ in urinary bladder carcinogenesis initiated by N-butyl-N-(4-hydroxybutyl)nitrosamine (BBN) in male F344/Dulrj rats was examined and compared with the effect of   alpha-tocopherol (TP) or propyl gallate (PG). Rats (6-week old) were treated with 0.05% BBN in drinking-water for 4 weeks. Groups of 20 rats received thereafter control diet or diet containing 2.0% TBHQ, 1.0% PG, or 0.4, 0.75, or 1.5% TP. After 36 weeks, the urinary bladders of all animals were examined histologically. The incidence of   papillary or nodular hyperplasia was significantly higher in BBN +TBHQ-treated rats as compared to rats initiated with BBN but receiving control diet. However, there was no significant differences for papillomas or cancer. This indicated a weak promoting activity of   TBHQ in BBN-initiated urinary bladder carcinogenesis. TP and PG were inactive in this respect (Tamano

////et al.,//// 1987).        The effects of TBHQ and 7 other antioxidants on    7,12-dimethylbenz[a]anthracene (DMBA)-initiated mammary gland,    ear duct, and forestomach carcinogenesis were examined in female    Sprague-Dawley rats. Groups of 20 rats were given a single dose of    25 mg/kg bw of DMBA in 0.5 ml of sesame oil by stomach tubing at 50    days of age. Starting one week later, rats were given a basal diet    containing 0.8% of TBHQ or one of the other antioxidants for 51 weeks.    Controls received basal diet only. Groups of 15 rats served as    carcinogen-free controls and received the different diets without    prior treatment with DMBA. Groups receiving antioxidants had reduced    body weights at the end of the experiment. Histological examinations    revealed a reduced rate of mammary tumour development in TBHQ-treated,    and in DMBA-initiated rats as compared to DMBA-treated controls. The incidence of ear duct and forestomach tumours was not affected by TBHQ treatment (Hirose

////et al.,//// 1988).        The modifying activities of BHA, BHT, and TBHQ and of paired    combinations of these phenolic antioxidants on urinary bladder    carcinogenesis in male F344 rats pretreated with BBN were    investigated. Groups of 20 animals (6-weeks old) were given 0.05% BBN    in their drinking-water for 4 weeks, followed by BHA, BHT, or TBHQ    alone (0.8% each) or in pairs (0.4% each) in their diet for 32 weeks.    Controls received no further treatment after BBN administration. A    decrease in body-weight gain was observed in all antioxidant-treated    groups. The incidence of preneoplastic papillary or nodular    hyperplasia (PN hyperplasia) was slightly but significantly higher in    the group treated with BHA+TBHQ after BBN than in controls receiving    BBN only. The densities of PN hyperplasia were also significantly    increased in all treated groups. However, no synergistic enhancing effects were observed. No differences were seen with respect to the incidence and densities of papillomas or carcinomas. Thus BHA, BHT, and TBHQ all exerted enhancing effects in BBN-induced urinary bladder carcinogenesis in rats, but no synergism regarding this promotion occurred (Hagiwara

////et al.,//// 1989).        The effects of TBHQ on urine composition, bladder epithelial    morphology, and DNA synthesis was studied in comparison with other    antioxidants and bladder tumour promoters. Groups of 10 male Fischer    344 rats, 5-week old, were given powdered basal diet containing 2%    TBHQ or one of 11 other compounds, or basal diet only (controls); two    further groups received two other tumour promoters in their    drinking-water. Five rats in each group were killed after 4 weeks for    estimation of DNA synthesis levels and histopathological examination    by light microscopy. The remaining rats were killed at week 8 for    light and scanning electron microscopic examination of the urinary    bladder. During week 4, fresh urine specimens were obtained from rats    in each group and analyzed for pH as well as electrolyte content. TBHQ    brought about an elevation of DNA synthesis in the urothelium and produced morphological surface alterations such as the formation of   pleomorphic or short, uniform microvilli and ropey or leafy microridges. The ability to induce proliferation and cell surface alterations was common to all bladder tumour promoters investigated. TBHQ also caused an increase in urinary pH, and a decrease in   potassium and phosphate contents as well as in osmolality

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