Erythrosine B and quinoline yellow dyes regulate DNA repair gene expression in human HepG2 cells

• Published in: Toxicology and industrial health Vol. 33; no. 10; pp. 765 - 774
• Main Authors: Chequer, Farah MD, Venancio, Vinicius P, Almeida, Mara R, Aissa, Alexandre F, Bianchi, Maria Lourdes P, Antunes, Lusânia MG
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01-10-2017; Sage Publications Ltd
• Subjects: Apoptosis; Base excision repair; Cell cycle; Coloring Agents - toxicity; Cosmetics; Data processing; Deoxyribonucleic acid; DNA; DNA damage; DNA repair; DNA Repair - drug effects; Drugs; Dyes; ERCC1 protein; Erythrosine - toxicity; FEN1 protein; Food; Food dyes; Gadd45A protein; Gene expression; Gene Expression - drug effects; Gene Expression Profiling; Genes; Genotoxicity; Hep G2 Cells; Humans; Lymphocytes B; Mismatch repair; MLH1 protein; Nucleotide excision repair; Nutrigenomics; Polymerase chain reaction; Quinoline; Quinolines - toxicity; Rad1 protein; Repair; Signaling; Skin; erythrosine B; quinoline yellow; Nutrigenomics; synthetic dyes; gene expression
• ISSN: 0748-2337; 1477-0393
• DOI: 10.1177/0748233717715186

Erythrosine B (ErB) is a cherry pink food colorant and is widely used in foods, drugs, and cosmetics. Quinoline yellow (QY) is a chinophthalon derivative used in cosmetic compositions for application to the skin, lips, and/or body surface. Previously, ErB and QY synthetic dyes were found to induce DNA damage in HepG2 cells. The aim of this study was to investigate the molecular basis underlying the genotoxicity attributed to ErB and QY using the RT2 Profiler polymerase chain reaction array and by analyzing the expression profile of 84 genes involved in cell cycle arrest, apoptosis, and DNA repair in HepG2 cells. ErB (70 mg/L) significantly decreased the expression of two genes (FEN1 and REV1) related to DNA base repair. One gene (LIG1) was downregulated and 20 genes related to ATR/ATM signaling (ATR, RBBP8, RAD1, CHEK1, CHEK2, TOPB1), nucleotide excision repair (ERCC1, XPA), base excision repair (FEN1, MBD4), mismatch repair (MLH1, MSH3, TP73), double strand break repair (BLM), other DNA repair genes (BRIP1, FANCA, GADD45A, REV1), and apoptosis (BAX, PPP1R15A) were significantly increased after treatment with QY (20 mg/L). In conclusion, our data suggest that the genotoxic mechanism of ErB and QY dyes involves the modulation of genes related to the DNA repair system and cell cycle.