In Vitro Studies on Chemoprotective Effect of Borax Against Aflatoxin B1-Induced Genetic Damage in Human Lymphocytes
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Date
2012
Journal Title
Journal ISSN
Volume Title
Publisher
Springer
Open Access Color
BRONZE
Green Open Access
Yes
OpenAIRE Downloads
OpenAIRE Views
Publicly Funded
No
Abstract
A common dietary contaminant, aflatoxin B1 (AFB1), has been shown to be a potent mutagen and carcinogen in humans and many animal species. Since the eradication of AFB1 contamination in agricultural products has been rare, the use of natural or synthetic free radical scavengers could be a potential chemopreventive strategy. Boron compounds like borax (BX) and boric acid are the major components of industry and their antioxidant role has recently been reported. In the present report, we evaluated the capability of BX to inhibit the rate of micronucleus (MN) and sister chromatid exchange (SCE) formations induced by AFB1. There were significant increases (P < 0.05) in both SCE and MN frequencies of cultures treated with AFB1 (3.12 ppm) as compared to controls. However, co-application of BX (1, 2 and 5 ppm) and AFB1 resulted in decreases of SCE and MN rates as compared to the group treated with AFB1 alone. Borax gave 30-50 % protection against AFB1 induced SCEs and MNs. In conclusion, the support of borax was especially useful in aflatoxin-toxicated blood tissue. Thus, the risk on target tissues of AFB1 could be reduced and ensured early recovery from its toxicity.
Description
Dirican, Ebubekir/0000-0001-9260-5223; Dirican, Ebubekir/0000-0003-2220-4306
Keywords
Aflatoxin B1, Borax, Chemoprevention, Genotoxicity, Human Blood Cultures
Fields of Science
0301 basic medicine, 0303 health sciences, 03 medical and health sciences
Citation
WoS Q
Q4
Scopus Q
Q4

OpenCitations Citation Count
35
Source
Cytotechnology
Volume
64
Issue
6
Start Page
607
End Page
612
PlumX Metrics
Citations
CrossRef : 26
Scopus : 30
PubMed : 11
Captures
Mendeley Readers : 25
SCOPUS™ Citations
30
checked on Apr 12, 2026
Web of Science™ Citations
30
checked on Apr 12, 2026
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