Sudan I (Solvent Yellow 14)

CI Solvent Yellow 14 (Sudan I) identified as the allergen in a plastic part of glasses

Repeated-dose liver and gastrointestinal tract micronucleus assays with CI Solvent Yellow 14 (Sudan I) using young adult rats

The in vivo genotoxicity of CI Solvent Yellow 14 (Sudan I) was examined using repeated-dose liver and gastrointestinal tract micronucleus (MN) assays in young adult rats. Sudan I is a mono-azo dye based on aniline and 1-amino-2-hydroxynaphthalene. This dye was demonstrated as a rat liver carcinogen in a National Toxicology Program (NTP) bioassay, and genotoxicity was noted in a rat bone marrow micronucleus (BMMN) assay. In the present study, Sudan I was administered orally to rats for 14-days, and the MN frequency in the liver, stomach, colon, and bone marrow were analyzed. The frequency of micronucleated hepatocytes (MNHEPs) was not significantly increased by the administration of the Sudan I. Gastrointestinal tract MNs were also not induced. However, in the BMMN assay, a significant increase in micronucleated immature erythrocytes (MNIMEs) was observed in a dose-dependent manner. While Sudan I has been reported to lack hepatic genotoxicity, it has also exhibited tumor-promoting activities. These results are consistent with the lack of induction of MN in the hepatocytes. The lack of MN induction in cells of the gastrointestinal tract was also logical because azo-compounds are reported to be unlikely to induce DNA damage in the rat gut. The repeated-dose rat liver and gastrointestinal tract MN assays have the potential to be used in the evaluation of the genotoxicity of a chemical in each organ in accordance with its mode of action.

Carcinogenesis Bioassay of C.I. Solvent Yellow 14 (CAS No. 842-07-9) in F344/N Rats and B6C3F1 Mice (Feed Study)

A carcinogenesis bioassay of C.I. Solvent Yellow 14 (94.1% pure), a widely used monoazo dye, was conducted by feeding diets containing 250 or 500 ppm of C.I. Solvent Yellow 14 to groups of 50 F344 rats of either sex for 103 weeks. Similar groups of 50 B6C3F1 mice received diets containing 500 or 1,000 ppm of C.I. Solvent Yellow 14 for 103 weeks. Groups of 50 untreated rats and mice of either sex served as controls. Throughout the bioassay, mean body weights of dosed rats and mice were slightly lower than those of controls. No compound-related clinical signs or effects on survival were observed. Increases in nonneoplastic lesions included cardiac valve fibrosis for male and female rats, lymphoid hyperplasia of the lung for male rats, and for female rats, bile duct hyperplasia, focal atrophy of the pancreatic acinus, and nephropathy. None of these effects were observed in mice. Neoplastic nodules of the liver occurred in rats of either sex with a dose-related trend that was significant (male, P<0.001; female, P=0.005), and the incidences in the high-dose groups were significantly higher than those in the controls (male: control, 5/50; low-dose, 10/50; high-dose, 30/50, P<0.001 and female: control, 2/50; low-dose, 3/49; high-dose, 10/48, P=0.011). Lymphomas or leukemias occurred in low-dose female mice at an incidence significantly (P<0.05) higher than that in the controls (12/50, 23/50, 17/50). Because of the lack of a dose-related trend and because the incidence in the high-dose group was not significant, the association between the increased incidence of hematopoietic tumors in the low-dose group and the administration of C.I. Solvent Yellow 14 is not clearly established. The incidence of lymphomas or leukemias in male mice was higher (not statistically significant) than that in the corresponding controls (5/49, 10/50, 10/50); in both low-and high-dose rats of either sex the incidence was significantly (P<0.001) lower than that in controls. Under the conditions of this bioassay, C.I. Solvent Yellow 14 was carcinogenic in male and female F344/N rats, as evidenced by increased incidences of neoplastic nodules of the liver. C.I. Solvent Yellow 14 was not carcinogenic for B6C3F1 mice of either sex. Levels of Evidence of Carcinogenicity: Male Rats: Positive Female Rats: Positive Male Mice: Negative Female Mice: Negative Synonym: 1-(phenylazo)-2-naphthol

Detoxication products of the carcinogenic azodye Sudan I (solvent yellow 14) bind to nucleic acids after activation by peroxidase

The C-hydroxyderivatives of the carcinogenic dye Sudan I, 1-phenylazo-2,6-dihydroxynaphthalene and 1-(4-hydroxyphenylazo)-2-hydroxynaphthalene, which are considered to be detoxication products of this dye bind to DNA or tRNA after oxidation into active metabolites by peroxidase and H2O2 in vitro. The 32P-postlabeling analysis of DNA modified by active metabolites of both Sudan I derivatives provides evidence that the covalent binding to DNA is the principal type of DNA modification. Since the urinary bladder is rich in peroxidases, the participation of these enzymes in activation of detoxicating products of Sudan I may be involved in the initiation of Sudan I-carcinogenesis in this organ.

Peroxidase-activated carcinogenic azo dye Sudan I (Solvent Yellow 14) binds to guanosine in transfer ribonucleic acid

Peroxidase in the presence of hydrogen peroxide catalyzes in vitro the activation of the carcinogenic azo dye Sudan I (1-phenylazo-2-hydroxynaphthalen) to tRNA-, homopolyribonucleotide- and 5'-monophosphate nucleoside-bound products. tRNA, poly G and guanosine 5'-monophosphate modified by activated Sudan I become colored and have an absorption maximum of approx. 480 nm. Cochromatographic analysis of adducts obtained by a reaction with tRNA and guanosine 5'-monophosphate on a thin layer of cellulose showed that the major Sudan I-tRNA adduct was formed by a reaction of activated Sudan I with guanosine in tRNA. The radical mechanism of the binding of the Sudan I molecule, containing the whole azo aromatic system, to nucleic acids is discussed.