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Identification of antimutagenic activities in the extract of an edible brown alga, Hijikia fusiforme (Hijiki) by umu gene expression system in Salmonella typhimurium (TA 1535/pSK 1002)
Author(s) -
Okai Yasuji,
HigashiOkai Kiyoka
Publication year - 1994
Publication title -
journal of the science of food and agriculture
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.782
H-Index - 142
eISSN - 1097-0010
pISSN - 0022-5142
DOI - 10.1002/jsfa.2740660115
Subject(s) - antimutagen , salmonella , mutagenesis , sos response , polysaccharide , chemistry , biochemistry , ames test , mutagen , dna , gene , biology , food science , escherichia coli , bacteria , mutation , genetics
A significant antimutagenic activity was found in the hot‐water‐soluble extract of an edible brown alga, Hijikia fusiforme (Hijiki in Japanese) which showed a significant inhibitory effect on the umu gene expression system in SOS response against DNA damage of Salmonella typhimurium induced by typical genotoxic substances such as N ‐methyl‐ N ′‐nitro‐nitrosoguanidine (MNNG), furylfuramide (AF‐2), 2‐acetylaminofluorene(2AAF) and 3‐amino‐1,4‐dimethyl‐5H‐pyrido[4,3‐b]indole (Trp‐P‐1), This activity was divided into polysaccharide and non‐polysaccharide fractions and the former fraction showed a relatively high antimutagenic activity compared with that of the latter fraction. The polysaccharide fraction caused roughly equal inhibitory effects on MNNG‐, AF‐2‐, 2‐AAF‐ or Trp‐P‐1‐induced mutagenesis and the major portion of the antimutagenic activity of this fraction was estimated to have a molecular weight of more than 30 kDa. The non‐polysaccharide fraction also exhibited significant antimutagenic activities against MNNG‐, AF‐2‐, 2‐AAF‐ or Trp‐P‐1‐induced mutagenesis and the major activity or this fraction was associated with low‐molecular‐weight substances with less than 3.5 kDa. We discuss the biological significance of the antimutagenic activities from H fusiforme which were compared with those of Laminaria japonica and Undaria pinnatifida reported previously.

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