Source:http://linkedlifedata.com/resource/pubmed/id/15201437
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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2004-8-12
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pubmed:abstractText |
Kojic acid (KA) has been used as a food additive for preventing enzymatic browning of crustaceans and as a cosmetic agent for skin whitening. In the present experiments, effects of KA on the induction of hepatic pre-neoplastic lesions in N-bis(2-hydroxypropyl)nitrosamine-initiated (experiment 1) and non-initiated (experiment 2) models, and its promoting influence in a medium-term liver bioassay (experiment 3) were investigated at dietary doses of up to 2% in male F344 rats. In experiment 1, 2% KA feeding induced significant increases in numbers (22.3 +/- 13.0 vs 8.5 +/- 3.4 in the 0%) and areas (0.37 +/- 0.29 vs 0.05 +/- 0.03 in the 0%) of glutathione-S-transferase P form (GST-P)-positive foci and toxic changes such as vacuolation of hepatocytes and microgranulomas. The development of GST-P-positive foci was pronounced in the animals with hepatocellular toxic changes. In experiment 2, numbers (0.65 +/- 0.57 vs 0.17 +/- 0.28 in the 0%) and areas (0.005 +/- 0.005 vs 0.0007 +/- 0.0012 in the 0%) of GST-P-positive foci and hepatocellular proliferating cell nuclear antigen (PCNA) expression (3.8 +/- 2.3 vs 2.6 +/- 0.7 in the 0%) were significantly increased by the 2% treatment. The PCNA-positive hepatocytes were abundantly localized around the vacuolated and granulomatous legions in both experiments 1 and 2. In experiment 3, significant increases in numbers (16.9 +/- 3.2 vs 8.4 +/- 2.7 in the 0%) and areas (1.62 +/- 0.39 vs 0.77 +/- 0.34 in the 0%) of GST-P-positive foci were again observed with 2% KA. These results demonstrate tumor-promoting and possible hepatocarcinogenic activity of KA at 2%, but the carcinogenic potential is likely to be weak. This study also indicated that enhanced replication of hepatocytes related to toxic changes might be involved as an underlying mechanism.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/2-hydroxypropyl-n-propylnitrosamine,
http://linkedlifedata.com/resource/pubmed/chemical/Antioxidants,
http://linkedlifedata.com/resource/pubmed/chemical/Carcinogens,
http://linkedlifedata.com/resource/pubmed/chemical/Diethylnitrosamine,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Peroxidase,
http://linkedlifedata.com/resource/pubmed/chemical/Glutathione Transferase,
http://linkedlifedata.com/resource/pubmed/chemical/Nitrosamines,
http://linkedlifedata.com/resource/pubmed/chemical/Pyrones,
http://linkedlifedata.com/resource/pubmed/chemical/kojic acid
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
1096-6080
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
81
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
43-9
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pubmed:dateRevised |
2010-9-17
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pubmed:meshHeading |
pubmed-meshheading:15201437-Animals,
pubmed-meshheading:15201437-Antioxidants,
pubmed-meshheading:15201437-Body Weight,
pubmed-meshheading:15201437-Carcinogens,
pubmed-meshheading:15201437-Diethylnitrosamine,
pubmed-meshheading:15201437-Dose-Response Relationship, Drug,
pubmed-meshheading:15201437-Glutathione Peroxidase,
pubmed-meshheading:15201437-Glutathione Transferase,
pubmed-meshheading:15201437-Liver,
pubmed-meshheading:15201437-Liver Neoplasms, Experimental,
pubmed-meshheading:15201437-Male,
pubmed-meshheading:15201437-Nitrosamines,
pubmed-meshheading:15201437-Organ Size,
pubmed-meshheading:15201437-Pyrones,
pubmed-meshheading:15201437-Rats,
pubmed-meshheading:15201437-Rats, Inbred F344
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pubmed:year |
2004
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pubmed:articleTitle |
Enhancement of hepatocarcinogenesis by kojic acid in rat two-stage models after initiation with N-bis(2-hydroxypropyl)nitrosamine or N-diethylnitrosamine.
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pubmed:affiliation |
Division of Pathology, National Institute of Health Sciences, Tokyo 158-8501, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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