Please use this identifier to cite or link to this item: https://doi.org/10.1006/taap.1994.1148
DC FieldValue
dc.titleAflatoxin B1-induced lipid peroxidation in rat liver
dc.contributor.authorShen, H.-M.
dc.contributor.authorShi, C.-Y.
dc.contributor.authorLee, H.-P.
dc.contributor.authorOng, C.-N.
dc.date.accessioned2014-12-01T06:53:30Z
dc.date.available2014-12-01T06:53:30Z
dc.date.issued1994
dc.identifier.citationShen, H.-M., Shi, C.-Y., Lee, H.-P., Ong, C.-N. (1994). Aflatoxin B1-induced lipid peroxidation in rat liver. Toxicology and Applied Pharmacology 127 (1) : 145-150. ScholarBank@NUS Repository. https://doi.org/10.1006/taap.1994.1148
dc.identifier.issn0041008X
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/113350
dc.description.abstractAflatoxin B1 (AFB1) is a potent hepatotoxic and hepatocarcinogenic mycotoxin. The mechanism of cellular damages caused by AFB1 has not been fully elucidated. Lipid peroxidation is one of the main manifestations of oxidative damage and has been found to play an important role in the toxicity and carcinogenesis of many carcinogens. In this study, we investigated the induction of lipid peroxidation by AFB1 in the liver of Fischer 344 rats. Malonaldehyde (MDA) and conjugated dienes, both products of lipid peroxidation, were determined in liver homogenate and subcellular fractions. An increase of MDA and conjugated dienes in liver homogenate was detected 1 day after AFB1 administration. It reached the peak level 3 days after dosing and remained at an elevated level up to 14 days. The induction of MDA by AFB1 was also found to be dose-dependent. Measurements of lipid peroxidation in the subcellular fractions revealed that microsomes had the highest concentration of MDA, followed by those of the nuclear fraction and mitochondria. MDA concentration was not detectable in the cytosolic fraction. Further, it was found that pretreatment with selenium and vitamin E, both antioxidants, and deferoxamine, a specific iron chelator, significantly inhibited lipid peroxidation as well as liver cell damage. These results provide in vivo evidence that AFB1 can cause lipid peroxidation in rat liver. Oxidative damages caused by AFB1 may be one of the underlining mechanisms for AFB1-induced cell injury and DNA damage, which eventually lead to tumorigenesis.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1006/taap.1994.1148
dc.sourceScopus
dc.typeArticle
dc.contributor.departmentCOMMUNITY,OCCUPATIONAL & FAMILY MEDICINE
dc.description.doi10.1006/taap.1994.1148
dc.description.sourcetitleToxicology and Applied Pharmacology
dc.description.volume127
dc.description.issue1
dc.description.page145-150
dc.description.codenTXAPA
dc.identifier.isiutA1994NX87900017
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