Please use this identifier to cite or link to this item: https://doi.org/10.1016/0300-483X(94)03008-P
DC FieldValue
dc.titleInvolvement of reactive oxygen species in aflatoxin B1-induced cell injury in cultured rat hepatocytes
dc.contributor.authorShen, H.-M.
dc.contributor.authorOng, C.-N.
dc.contributor.authorShi, C.-Y.
dc.date.accessioned2012-04-02T06:53:05Z
dc.date.available2012-04-02T06:53:05Z
dc.date.issued1995
dc.identifier.citationShen, H.-M., Ong, C.-N., Shi, C.-Y. (1995). Involvement of reactive oxygen species in aflatoxin B1-induced cell injury in cultured rat hepatocytes. Toxicology 99 (1-2) : 115-123. ScholarBank@NUS Repository. https://doi.org/10.1016/0300-483X(94)03008-P
dc.identifier.issn0300483X
dc.identifier.urihttp://scholarbank.nus.edu.sg/handle/10635/31782
dc.description.abstractThe role of reactive oxygen species (ROS) in AFB1-induced cell injury was investigated using cultured rat hepatocytes. Malonaldehyde (MDA) generation and Tactate dehydrogenase (LDH) release were determined as indices of lipid peroxidation and cell injury, respectively. Exposure to AFB1 for up to 72 h resulted in significantly elevated levels of LDH being released into the medium as well as the MDA generation in cultured hepatocytes. These effects were dose-dependent, indicating that AFB1 was capable of inducing oxidative damages in the cell. Further, MDA generation and LDH release were effectively inhibited by the addition of the following: (1) superoxide dismutase (500 units/ml), (2) catalase (1500 units/ml), (3) 10 mM desferrioxamine (a specific iron chelator), or (4) 260 mM dimethyl sulfoxide (a hydroxyl radical scavenger). These evidences therefore suggest that ROS, such as superoxide radicals, hydroxyl radicals and hydrogen peroxides, are involved in AFB1-induced cell injury in cultured rat hepatocytes.
dc.description.urihttp://libproxy1.nus.edu.sg/login?url=http://dx.doi.org/10.1016/0300-483X(94)03008-P
dc.sourceScopus
dc.subjectAFB1
dc.subjectCell injury
dc.subjectHepatocytes
dc.subjectLipid peroxidation
dc.subjectReactive oxygen species
dc.typeArticle
dc.contributor.departmentCOMMUNITY,OCCUPATIONAL & FAMILY MEDICINE
dc.description.doi10.1016/0300-483X(94)03008-P
dc.description.sourcetitleToxicology
dc.description.volume99
dc.description.issue1-2
dc.description.page115-123
dc.description.codenTXCYA
dc.identifier.isiutA1995RA21500012
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