Advances in Clinical Toxicology (ACT)

ISSN: 2577-4328

Research Article

Re-Evaluation of the Genotoxicity of Currently Used Food Dyes in Mouse Multiple Organs Via Continuous Administration by Drinking Using the Comet Assay

Authors: Yu F Sasaki , Yokohama N , Zenke A , Kawaguchi S , Nakamura T , Ymamoto A , Saito T and Kadoma Y

DOI: 10.23880/act-16000330

Abstract

Among currently used food dyes, we have reported that four azo dye and three xanthene dyes that were given to mice by single
gavage at a low dose (10 or 100 mg/kg) induced DNA damage in mouse gastrointestinal tract (GI-tract). When the susception
of carcinogenicity by genotoxic mechanism cannot be excluded, ADI cannot be set for food additives, pesticides, and veterinary
drugs. Therefore, it is serious issues whether observed their genotoxicity in mouse GI-tract lead to their carcinogenicity.
Although carcinogenicity is examined by long-term administration in feed or drinking water, in vivo genotoxicity tests have
been traditionally performed by single intraperitoneal or gavage administration at MTD. Here, we examined the genotoxicity
of food dyes given continuously by drinking, to re-evaluate DNA damage induced by food dyes given by gavage in mouse GItract.
Although single gavage of food dyes at 2000 mg/kg induced DNA damage in GI-tract, their administration by continuous
drinking at daily intake higher than 2000 mg/kg did not induce DNA damage in GI-tract. Based on our previous discussion that
the results from continuous administration by drinking or feeding are likely to reflect carcinogenicity by genotoxic mechanisms
better than the results from single gavage administration, in spite of the presence of positive responses in mouse GI-tract by
single gavage of food dyes, the absence of positive response in mouse GI-tract by continuous drinking administration of food
dyes could be considered to show the absence of carcinogenicity by genotoxic mechanisms.

Keywords: Food Dyes; Mouse; GI-Tract; Gavage; Drinking; Comet Assay; Carcinogenicity by Genotoxic Mechanism

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