Stimulated Human Phagocytes Produce Cytogenetic Changes in Cultured Mammalian Cells

Weitberg, Alan B.; Weitzman, Sigmund A.; Destrempes, Margaret M.; Latt, Samuel A.; Stossel, Thomas P.

doi:10.1056/nejm198301063080107

Cited by 239 publications

(77 citation statements)

References 25 publications

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“…The results obtained by us indicate a significant increase in the ratios of the SCEs and MNs in lymphocytes, which is in accordance with previous reports (Groopman and Kensler 1999;Geyikoglu and Turkez 2005). The SCEs are formed by toxic oxygen metabolites in cultured human leukocytes and other mammalian cells (Weitberg et al 1983). AFB 1 toxicity is also related to LPO and oxidation of DNA in vivo and in vitro (Shen et al 1996).…”

Section: Discussionsupporting

confidence: 92%

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

Türkez

Geyikoğlu

2010

Cytotechnology

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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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Section: Discussionsupporting

confidence: 92%

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

Türkez

Geyikoğlu

2010

Cytotechnology

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“…The SCEs are formed by toxic oxygen metabolites in cultured human leukocytes and other mammalian cells (Weitberg et al 1983). AFB1 toxicity is also related to LPO and oxidation of DNA in vivo and in vitro (Shen et al 1996).…”

Section: Discussionmentioning

confidence: 99%

In vitro studies on chemoprotective effect of borax against aflatoxin B1-induced genetic damage in human lymphocytes

et al. 2012

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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 aflatoxintoxicated blood tissue. Thus, the risk on target tissues of AFB1 could be reduced and ensured early recovery from its toxicity.

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“…OH-like species) can cause DNA strand breaks, DNA base modi®cations, sister chromatid exchanges, and mutations (Halliwell and Aruoma, 1991;Jackson et al, 1989;Weitberg et al, 1983;Weitzman and Stossel, 1982;Birnboim, 1982;Lewis and Adams, 1985;Schraufstatter et al, 1986a,b;Frenkel et al, 1986;Floyd et al, 1986). However, despite the large body of evidence demonstrating the damaging e ects of .…”

Section: Introductionmentioning

confidence: 99%

Stimulated human leukocytes cause activating mutations in the K-ras proto-oncogene

et al. 1997

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Stimulated Human Phagocytes Produce Cytogenetic Changes in Cultured Mammalian Cells

Cited by 239 publications

References 25 publications

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

Boric acid: a potential chemoprotective agent against aflatoxin b1 toxicity in human blood

In vitro studies on chemoprotective effect of borax against aflatoxin B1-induced genetic damage in human lymphocytes

Stimulated human leukocytes cause activating mutations in the K-ras proto-oncogene

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