Induction of tumours of the urinary bladder in F344 rats by dietary administration of o-phenylphenol

o‐Phenylphenol and sodium o‐phenylphenol [MAK Value Documentation, 1991]

“…In contrast to the results obtained by Reitz [11] after administration of OPP or OPP-Na for 3 months (see Table 1), Hiraga and Fujii, after administration of OPP [34] and of OPP-Na [36] in the diet of F344/DuCrj rats for a period of 13 weeks, described proliferative lesions of the bladder epithelium (transitional cell papillomas, transitional cell hyperplasia) and bladder tumours (transitional cell carcinomas). In both studies the lesions were observed only in the animals of the highest dose groups when the dose taken in per day and kg body weight exceeded 350-400 mg OPP or OPP-Na.…”

o‐Phenylphenol and sodium o‐phenylphenol [MAK Value Documentation, 1991]

“…In contrast to the results obtained by Reitz [11] after administration of OPP or OPP-Na for 3 months (see Table 1), Hiraga and Fujii, after administration of OPP [34] and of OPP-Na [36] in the diet of F344/DuCrj rats for a period of 13 weeks, described proliferative lesions of the bladder epithelium (transitional cell papillomas, transitional cell hyperplasia) and bladder tumours (transitional cell carcinomas). In both studies the lesions were observed only in the animals of the highest dose groups when the dose taken in per day and kg body weight exceeded 350-400 mg OPP or OPP-Na.…”

Effects of pH on Nonenzymatic Oxidation of Phenylhydroquinone: Potential Role in Urinary Bladder Carcinogenesis Induced by o-Phenylphenol in Fischer 344 Rats

“…Hence, the tumor incidence in OPP-treated rats may be attributed to diet-related factors causing variations in urine pH. This would influence the formation of reactive metabolites via the pH-dependent PHQ autoxidation pathway and may provide an explanation for the consistently higher tumorigenic potency of SOPP than OPP reported in the literature as well as the highly variable results frequently seen in the tumorigenicity studies of OPP (see, for example, refs and ).…”

Induction of mitosis delay, apoptosis and aneuploidy in human cells by phenyl hydroquinone, an Ames test-negative carcinogen

“…OPP and its hepatic metabolite PHQ can produce urinary bladder hyperplasia and tumors (Hiraga and Fujii, 1984) but do not cause DNA damage or gene mutations and are therefore typical of non-genotoxic carcinogens (Brusick, 2005). Many chemicals considered carcinogenic are categorized as non-genotoxic carcinogens (Duesberg and Rasnick, 2000).…”

o‐Phenylphenol and sodium o‐phenylphenol [MAK Value Documentation, 1991]

“…In contrast to the results obtained by Reitz [11] after administration of OPP or OPP-Na for 3 months (see Table 1), Hiraga and Fujii, after administration of OPP [34] and of OPP-Na [36] in the diet of F344/DuCrj rats for a period of 13 weeks, described proliferative lesions of the bladder epithelium (transitional cell papillomas, transitional cell hyperplasia) and bladder tumours (transitional cell carcinomas). In both studies the lesions were observed only in the animals of the highest dose groups when the dose taken in per day and kg body weight exceeded 350-400 mg OPP or OPP-Na.…”

Effects of pH on Nonenzymatic Oxidation of Phenylhydroquinone: Potential Role in Urinary Bladder Carcinogenesis Induced by o-Phenylphenol in Fischer 344 Rats

“…Hence, the tumor incidence in OPP-treated rats may be attributed to diet-related factors causing variations in urine pH. This would influence the formation of reactive metabolites via the pH-dependent PHQ autoxidation pathway and may provide an explanation for the consistently higher tumorigenic potency of SOPP than OPP reported in the literature as well as the highly variable results frequently seen in the tumorigenicity studies of OPP (see, for example, refs and ).…”

Induction of mitosis delay, apoptosis and aneuploidy in human cells by phenyl hydroquinone, an Ames test-negative carcinogen

“…OPP and its hepatic metabolite PHQ can produce urinary bladder hyperplasia and tumors (Hiraga and Fujii, 1984) but do not cause DNA damage or gene mutations and are therefore typical of non-genotoxic carcinogens (Brusick, 2005). Many chemicals considered carcinogenic are categorized as non-genotoxic carcinogens (Duesberg and Rasnick, 2000).…”

o‐Phenylphenol and sodium o‐phenylphenol [MAK Value Documentation, 1991]

“…In contrast to the results obtained by Reitz [11] after administration of OPP or OPP-Na for 3 months (see Table 1), Hiraga and Fujii, after administration of OPP [34] and of OPP-Na [36] in the diet of F344/DuCrj rats for a period of 13 weeks, described proliferative lesions of the bladder epithelium (transitional cell papillomas, transitional cell hyperplasia) and bladder tumours (transitional cell carcinomas). In both studies the lesions were observed only in the animals of the highest dose groups when the dose taken in per day and kg body weight exceeded 350-400 mg OPP or OPP-Na.…”

Effects of pH on Nonenzymatic Oxidation of Phenylhydroquinone: Potential Role in Urinary Bladder Carcinogenesis Induced by o-Phenylphenol in Fischer 344 Rats

“…Hence, the tumor incidence in OPP-treated rats may be attributed to diet-related factors causing variations in urine pH. This would influence the formation of reactive metabolites via the pH-dependent PHQ autoxidation pathway and may provide an explanation for the consistently higher tumorigenic potency of SOPP than OPP reported in the literature as well as the highly variable results frequently seen in the tumorigenicity studies of OPP (see, for example, refs and ).…”

Induction of mitosis delay, apoptosis and aneuploidy in human cells by phenyl hydroquinone, an Ames test-negative carcinogen

“…OPP and its hepatic metabolite PHQ can produce urinary bladder hyperplasia and tumors (Hiraga and Fujii, 1984) but do not cause DNA damage or gene mutations and are therefore typical of non-genotoxic carcinogens (Brusick, 2005). Many chemicals considered carcinogenic are categorized as non-genotoxic carcinogens (Duesberg and Rasnick, 2000).…”