Aflatoxin B1 is a mycotoxin produced by Aspergillus flavus and Aspergillus parasiticum, which may be present as food contaminant. It is known to cause acute toxic effect and act as a carcinogenetic agent. The carcinogenetic action has been related to its ability to form unstable adducts with DNA, which represent possible mutagenic sites. On the other hand the primary cellular target responsible for its toxic action has not yet been clearly identified. Previous data suggested a possible correlation between cell proliferation and responsiveness to aflatoxin toxicity; these observations led us to investigate the effect of the toxin on cell cycle progression of three human cell lines, which display a different response to toxin exposure. We report the results of a cytofluorometric analysis, which in fact shows a significant alterations of cell cycle progression as a result of toxin treatment. Cells exposed to a 24 hr toxin treatment accumulate in S phase and their ability to recover from the block of DNA synthesis, caused by the toxin, varies in the cell lines under study. A ready resumption of DNA synthesis appears to be related to the absence of p53 control of cell cycle progression.
Impairment of cell cycle progression by aflatoxin b1 in human cell lines
2002
Abstract
Aflatoxin B1 is a mycotoxin produced by Aspergillus flavus and Aspergillus parasiticum, which may be present as food contaminant. It is known to cause acute toxic effect and act as a carcinogenetic agent. The carcinogenetic action has been related to its ability to form unstable adducts with DNA, which represent possible mutagenic sites. On the other hand the primary cellular target responsible for its toxic action has not yet been clearly identified. Previous data suggested a possible correlation between cell proliferation and responsiveness to aflatoxin toxicity; these observations led us to investigate the effect of the toxin on cell cycle progression of three human cell lines, which display a different response to toxin exposure. We report the results of a cytofluorometric analysis, which in fact shows a significant alterations of cell cycle progression as a result of toxin treatment. Cells exposed to a 24 hr toxin treatment accumulate in S phase and their ability to recover from the block of DNA synthesis, caused by the toxin, varies in the cell lines under study. A ready resumption of DNA synthesis appears to be related to the absence of p53 control of cell cycle progression.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
