Disease relevance of Stearix Orange

• The aim of this study was to assess the genotoxic effects of Sudan I and to identifiy and clarify the reaction mechanisms by use of human hepatoma HepG2 cells [1].
• We found that the commerical Brilliant Lake Red R which has been said to be most important causative agent of pigmented contact dermatitis, contained Sudan I as a major impurity [2].
• Allergic contact dermatitis produced by the application of 1-phenylazo-2-naphthol induced hyperpigmentation after an interval of about 14 days in 10 of the 21 allergy-acquiring animals examined [3].
• Pellets containing 1-phenylazo-2-naphthol significantly increased at each time the incidence of bladder carcinomas relative to that observed with paraffin wax [4].
• Electron microscope investigations on leishmaniasis in the Sudan. I. Morphometric studies on Leishmania amastigotes in various forms of human leishmaniasis [5].

Psychiatry related information on Stearix Orange

• Epidemiology of nocturnal enuresis in a part of Khartoum, Sudan. I. The extensive study [6].

High impact information on Stearix Orange

• On the basis of these studies, we attribute most of Sudan I metabolism in human microsomes to CYP1A1, but participation of CYP3A4 cannot be ruled out [7].
• Moreover, using the nuclease P1-enhanced version of the (32)P-postlabeling assay, we found that human microsomes were competent in activating Sudan I to form adducts with DNA [7].
• Sudan I is a potential carcinogen for humans: evidence for its metabolic activation and detoxication by human recombinant cytochrome P450 1A1 and liver microsomes [7].
• Assay of Sudan I contamination of foodstuff by atmospheric pressure chemical ionization tandem mass spectrometry and isotope dilution [8].
• The present paper shows that Solvent Yellow 14 induces micronuclei in the bone marrow of rats after a single oral dose of 250 mg/kg and above [9].

Chemical compound and disease context of Stearix Orange

• Eight patients suffering from pigmented contact dermatitis caused by the commerical Brilliant Lake Red R were patch tested with purified Sudan I and its several chemical analogues [2].

Biological context of Stearix Orange

• Enzymatic hydrolysis of modified tRNA with subsequent separation of nucleosides by HPLC suggests that the covalent modification of tRNA originating from the formation of more than one adduct with the nucleosides in tRNA is the predominant interaction of the activated Sudan I with tRNA [10].
• Sudan I induces genotoxic effects and oxidative DNA damage in HepG2 cells [1].
• The data suggest that Sudan I caused DNA strand breaks and chromosome breaks [1].
• Also, Solvent Yellow 14 was negative in the in vitro assay, but induced an equivocal DNA repair response in the in vivo-in vitro assay system [11].
• Therefore, the effect of different concentrations of oil-soluble dyes (Solvent Blue 35 [C.I. 61554], Sudan Red 7B [C.I. 26050], Sudan Black B [26150], Sudan Orange G [C.I. 11920], and Sudan I 103624 [C.I. 12055]) on development, mortality, and fecundity of S. frugiperda was evaluated [12].

Anatomical context of Stearix Orange

• Horseradish peroxidase in the presence of hydrogen peroxide (HRP/H2O2) oxidizes a carcinogenic non-aminoazo dye, 1-phenylazo-2-hydroxynaphthalene (Sudan I) to the ultimate carcinogen, which binds to calf thymus DNA [13].
• SY7 was preferentially reduced in the skin cytosol of all species, whereas Sudan I was equally reduced in the skin cytosol and microsomal fractions [14].

Associations of Stearix Orange with other chemical compounds

• Activation of carcinogens by peroxidase. Horseradish peroxidase-mediated formation of benzenediazonium ion from a non-aminoazo dye, 1-phenylazo-2-hydroxynaphthalene (Sudan I) and its binding to DNA [13].
• In the hairless guinea pig, 57.6 +/- 5.9% of the applied Sudan I dose and 67.8 +/- 4.6% of the applied SY7 dose were absorbed in 24 hr [14].
• Development and in-house validation of a liquid chromatography-electrospray-tandem mass spectrometry method for the simultaneous determination of Sudan I, Sudan II, Sudan III and Sudan IV in hot chilli products [15].
• Determination of methyl yellow, Sudan I and Sudan II in water by high-performance liquid chromatography [16].
• Two chemicals reported to be mouse micronucleus-negative and rat-positive, azobenzene and Solvent Yellow 14, and one chemical reported to be mouse-positive and rat-negative, 1,2-dimethylhydrazine, gave positive responses in rat bone marrow and peripheral blood [17].

Gene context of Stearix Orange

• METHODS: High performance liquid chromatography (HPLC) with ultraviolet (UV) detection was employed for the separation of Sudan I metabolites formed by human recombinant CYPs and rat CYP1A1 [18].
• Pretreatment of rats with beta-naphthoflavone or Sudan I, inducers of P450 1A1 and 1A2, and P450 1A1 alone, respectively, significantly stimulated the levels of 3-ABA-derived DNA adducts formed by rat liver microsomes [19].
• Even though levels of CYP1A1 expression are low, <0.7% of total hepatic CYP, the CYP1A1 contribution to oxidation of carcinogenic Sudan I in the test set of human liver microsomes ranges from 12 to 30% [20].
• From a small survey of 30 retail samples, 11 samples of crushed chilli, Italian pasta, chilli-snack and vegetable sauce contained levels of Sudan I ranging from 24 to 5591 microg kg(-1) [21].
• Determination of 1-phenylazo-2-naphthol (Sudan I) in chilli powder and in chilli-containing food products by GPC clean-up and HPLC with LC/MS confirmation [21].

Analytical, diagnostic and therapeutic context of Stearix Orange

• The potential of capillary liquid chromatography (microLC)-quadrupole/time-of-flight mass spectrometry (Q-TOF MS) for the confirmation of Sudan I, II, III and IV azo-dyes as contaminants in hot-chilli food products was demonstrated [22].
• To study the genotoxic effects of Sudan I, the comet assay and micronucleus test (MNT) were used [1].

References