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Aflatoxin-induced structural chromosomal changes and mitotic disruption in mouse bone marrow
Mutation Research
|September 1, 1991
Summary
Ascorbic acid (vitamin C) supplementation reduced chromosomal abnormalities caused by aflatoxin B1 in mice. This protective effect was observed with combined 6-week and 12-week treatments, highlighting vitamin C
Area of Science:
- Toxicology
- Nutritional Science
- Genetics
Background:
- Aflatoxin B1 is a potent mycotoxin known to induce genotoxicity and chromosomal damage.
- Ascorbic acid (vitamin C) possesses antioxidant properties that may counteract toxic effects.
- Understanding the protective role of vitamin C against mycotoxin-induced DNA damage is crucial for public health.
Purpose of the Study:
- To investigate the protective effects of ascorbic acid against aflatoxin B1-induced chromosomal abnormalities in mice.
- To evaluate the impact of different treatment durations (6 and 12 weeks) on the efficacy of ascorbic acid.
Main Methods:
- Swiss albino mice were administered a dietary concentration of aflatoxin B1.
- Ascorbic acid was administered at a dose proportional to the human therapeutic dose (500 mg/day).
- Chromosomal abnormalities in bone marrow cells were analyzed after 6 and 12 weeks of treatment.
Main Results:
- Ascorbic acid significantly decreased the incidence of aflatoxin B1-induced chromosomal abnormalities.
- Aflatoxin B1 alone did not cause significant differences in clastogenicity over 6 or 12 weeks.
- The 6-week vitamin C treatment primarily nullified structural chromosomal changes over mitotic disruptions; the 12-week treatment showed more structural and fewer disruption-type abnormalities.
Conclusions:
- Ascorbic acid demonstrates a protective effect against aflatoxin B1-induced genotoxicity in mice.
- The duration of ascorbic acid administration influences the types of chromosomal abnormalities mitigated.
- Vitamin C supplementation may be a viable strategy to reduce the risk of mycotoxin-induced DNA damage.