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Fusarium moniliforme metabolites: genotoxicity of culture extracts
1Department of Chemical Etiology and Carcinogenesis, Chinese Academy of Medical Sciences, Beijing, People's Republic of China.
Abstract:
Fusarin C (FC) is a potent mutagen which has been isolated from Fusarium moniliforme culture extracts (FME). We have confirmed that the mutagenicity of these extracts is enhanced by phenobarbital- or Aroclor-induced microsomes and shown that: (i) additional, direct-acting, mutagens are present in crude extracts from F. moniliforme cultures; (ii) Salmonella typhimurium TA 100 exposed to FME in the presence of S9 mixtures shows an increased number of DNA strand breaks as detected by intercalation of ethidium bromide; (iii) exposure of polyoma-transformed rat fibroblast cells to HPLC-purified FC induced asynchronous replication of polyoma DNA sequences, a phenomenon also observed when these cells were exposed to a variety of other carcinogens; (iv) FME can alkylate 4-(p-nitrobenzyl)pyridine in the absence of S9 mix, although less efficiently than styrene oxide; and (v) these additional direct-acting mutagens, present in crude extracts from F. moniliforme cultures, may be responsible for the DNA adducts formed by reaction with calf thymus DNA in the absence of metabolic activation and detected by the 32P-postlabeling assay. All of these observations suggest that significant health effects may be associated with human exposure to F. moniliforme and that further studies on its metabolites are needed.
Insights
Fusarin C (FC) from Fusarium moniliforme is a potent mutagen. This study confirms FC
Area of Science:
- Mycology
- Toxicology
- Molecular Biology
Background:
- Fusarin C (FC) is a mutagen isolated from Fusarium moniliforme culture extracts (FME).
- The mutagenicity of FME is enhanced by induced microsomes, suggesting metabolic activation or additional mutagens.
- Previous studies indicate potential health risks associated with F. moniliforme exposure.
Purpose of the Study:
- To investigate the mutagenic properties of Fusarin C and Fusarium moniliforme extracts.
- To identify and characterize additional mutagens present in FME.
- To assess the genotoxic effects of FC and FME on cellular DNA.
Main Methods:
- Bacterial mutagenicity assays using Salmonella typhimurium TA 100 with S9 mix.
- DNA strand break detection using ethidium bromide intercalation.
- Cellular assays with polyoma-transformed rat fibroblast cells exposed to purified FC.
- Chemical alkylation assays using 4-(p-nitrobenzyl)pyridine.
- 32P-postlabeling assay for DNA adducts with calf thymus DNA.
Main Results:
- FME contains additional direct-acting mutagens besides FC.
- Exposure to FME increased DNA strand breaks in Salmonella typhimurium TA 100.
- Purified FC induced asynchronous replication of polyoma DNA sequences in rat fibroblast cells.
- FME exhibited alkylating activity, though less efficient than styrene oxide.
- Direct-acting mutagens in FME formed DNA adducts without metabolic activation.
Conclusions:
- Fusarin C and other FME components are potent mutagens with genotoxic effects.
- F. moniliforme poses potential health risks due to its mutagenic metabolites.
- Further research into F. moniliforme metabolites is crucial for understanding health impacts.