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Boric acid: a potential chemoprotective agent against aflatoxin b(1) toxicity in human blood.

Authors
Type
Published Article
Journal
Cytotechnology
0920-9069
Publisher
Springer-Verlag
Publication Date
Volume
62
Issue
2
Pages
157–165
Identifiers
DOI: 10.1007/s10616-010-9272-2
PMID: 20431944
Source
Medline

Abstract

Aflatoxin B(1) is the most potent pulmonary and hepatic carcinogen. Since the eradication of Aflatoxin B(1) contamination in agricultural products has been difficult, the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. Boric acid is the major component of industry and its antioxidant role has recently been reported. The present study assessed, for the first time, the effectiveness of boric acid following exposure to Aflatoxin B(1) on human whole blood cultures. The biochemical characterizations of glutathione and some enzymes have been carried out in erythrocytes. Alterations in malondialdehyde level were determined as an index of oxidative stress. The sister-chromatid exchange and micronucleus tests were performed to assess DNA damages in lymphocytes. Aflatoxin B(1) treatment significantly reduced the activities of antioxidants by increasing malondialdehyde level (30.53 and 51.43%) of blood, whereas, the boric acid led to an increased resistance of DNA to oxidative damage induced by Aflatoxin B(1) in comparison with control values (P < 0.05). In conclusion, the support of boric acid was especially useful in Aflatoxin-toxicated blood. Thus the risk on tissue targeting of Aflatoxin B(1) could be reduced ensuring early recovery from its toxicity.

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