Lack of Mutagenecity of Green Pigments in Salmonella typhimurium

A greening phenomenon has been observed in some plant foods such as chestnut, sweet potato, burdock, and others during processing. The formation of the pigments was postulated as reactions of primary amino compounds with chlorogenic acid or caffeic acid ester, yielding acridine derivatives. Acridine derivatives have been regarded as mutagenetic agents. For the reason, the bacterial reverse mutation test was carried out to evaluate the genotoxicity of green pigment using Salmonella typhimurium TA98 and TA100. Alanine, arginine, aspartic acid, gly- cine, lysine, and phenylalanine were reacted repectively with chlorogenic acid to synthesize model compound. Green pigment was extracted from sweet potato. Maximum concentration of 2 and 50 mg/plate was tested for the synthetic green pigments and extracted green pigment respectively, taking bacterial survival, solubility, and color intensity into consideration. There was no signigicant increase in the reverse mutation either with or without S9 activation system by any test material. Though further studies with other genotoxicity test system are necessary, both synthetic and sweet potato green pigments seemed not to cause mutation despite the acridine moiety in their structures.

[1]  M. Namiki,et al.  Structure of Green Pigment Formed by the Reaction of Caffeic Acid Esters (or Chlorogenic acid) with a Primary Amino Compound , 2001, Bioscience, biotechnology, and biochemistry.

[2]  W. Denny,et al.  The genetic toxicology of acridines. , 1991, Mutation research.

[3]  G. Holder,et al.  The mutagenicity of dibenz[a,j]acridine, some metabolites and other derivatives in bacteria and mammalian cells. , 1989, Carcinogenesis.

[4]  L. Ferguson,et al.  Comparison of the mutagenic and clastogenic activity of amsacrine and other DNA-intercalating drugs in cultured V79 Chinese hamster cells. , 1984, Cancer research.

[5]  M. Hasegawa,et al.  Comparison of 6-thioguanine-resistant mutation and sister chromatid exchanges in Chinese hamster V79 cells with forty chemical and physical agents. , 1984, Cancer research.

[6]  K. Back,et al.  Comparative mutagenicity of 4 DNA-intercalating agents in L5178Y mouse lymphoma cells. , 1982, Mutation research.

[7]  H. Rosenkranz,et al.  Frameshift mutations: relative roles of simple intercalation and of adduct formation. , 1981, Mutation research.

[8]  R. Fahrig Acridine-induced mitotic gene conversion (paramutation) in Saccharomyces cerevisiae. The effect of two different modes of binding to DNA. , 1970, Mutation research.

[9]  M. Inouye,et al.  Change of a sequence of amino acids in phage T4 lysozyme by acridine-induced mutations. , 1966, Proceedings of the National Academy of Sciences of the United States of America.

[10]  S. Brenner,et al.  Mutagenesis of bacteriophage T4 by acridines. , 1961, Journal of molecular biology.

[11]  T. Skopek,et al.  Frameshift mutagenesis of lambda prophage by 9-aminoacridine, proflavin and ICR-191 , 2004, Molecular and General Genetics MGG.

[12]  P. Müller,et al.  On the glucose effect in acridine-induced frameshift mutagenesis in Escherichia coli. , 1989, Mutation research.

[13]  J. Moutschen Introduction to Genetic Toxicology , 1985 .

[14]  T. Matsui Greening pigments produced reaction of ethyl caffeate with methylamine. , 1981, Journal of nutritional science and vitaminology.

[15]  T. Skopek,et al.  9-Aminoacridine-A frameshift mutagen for Salmonella typhimurium TA 1537 inactive at the hgprt locus in human lymphoblasts. , 1977, Mutation research.