Detection of elevated reactive oxygen species level in cultured rat hepatocytes treated with aflatoxin B1

Shen, Han‐Ming; Shi, Chenyang; Shen, Yi; Ong, Choon‐Nam

doi:10.1016/0891-5849(96)00019-6

Cited by 291 publications

(190 citation statements)

References 33 publications

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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). So this xenobiotic could contribute to the modification of the genome leading to carcinogenesis (Amici et al 2007).…”

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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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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“…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). Thus, the genome formation leading to carcinogenesis could be occured by this xenobiotic (Amici et al 2007).…”

Section: Discussionmentioning

confidence: 99%

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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“…To this end, we examined the ability of OHT to generate ROS in either SkBr3 or LNCaP cells by DCFH fluorescence (Shen et al, 1996). As show in c-Jun mediates 4-hydroxytamoxifen-induced apoptosis A Madeo et al type of stimulus as well as on the heterodimeric partner forming the AP-1 transcription factor (Hess et al, 2004;Raivich and Behrens, 2006).…”

Section: Abrogation Of Either C-jun Phosphorylation or Ap-1 Transactimentioning

confidence: 99%

“…It has been shown that tamoxifen-dependent elevation of intracellular Ca 2 þ triggers apoptosis of human hepatoblastoma HepG2 cancer cells through the accumulation of reactive oxygen species (ROS) obtained by not-phagocytic activation of NADPH oxidase (Lee et al, 2000). ROS-induced apoptosis requires the participation of further cell death signaling pathways, including the c-Jun N-terminal kinase (JNK) family of stress-responsive MAPKs (Shen et al, 1996). In particular, it has been shown that prevention of ROS accumulation by antioxidants inhibits both JNK activation and apoptosis in tamoxifen-treated cancer cells (Mandlekar et al, 2000;Mabuchi et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

c-Jun activation is required for 4-hydroxytamoxifen-induced cell death in breast cancer cells

et al. 2009

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Detection of elevated reactive oxygen species level in cultured rat hepatocytes treated with aflatoxin B1

Cited by 291 publications

References 33 publications

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

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

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

c-Jun activation is required for 4-hydroxytamoxifen-induced cell death in breast cancer cells

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