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rat hepatocytes and rat liver in vivo. In human and rat act as genotoxicants through generation of free radicals
[52]
glioblastoma cells and mouse hypothalamic cells, production during metabolism of the toxins through reactions of either
of ROS was increased after exposure to 10-100 μmol/L of FB electrophiles or nucleophiles with DNA. This interaction
1
for 48-144 h. Exposure to 10-100 μmol/L of FB for 72 h creates changes in their sequences that ultimately results in
[53]
1
had no effect on production of ROS in human fibroblasts, or the formation of new priming sites and/or disappearances
in primary cultures of rat astrocytes exposed to the same of existing priming sites for the RAPD primers. Thus, it gives
concentrations of FB for as long as 6 days. [54,55] Exposure different RAPD profiles for cells exposed to toxins. [63]
1
to concentrations as high as 20 μmol/L of FB did not
1
significantly reduce the viability of IPEC-J2 cells. [56] Random amplification of polymorphic DNA-PCR suffers
from inherent limitations such as a lack of reproducibility
In the current study, EC could not be calculated for and occurrence of pseudo-bands which prevent its routine
50
FB because viability of cells exposed to 200 μmol/L was application. However, if conditions of the assays are
[64]
1
reduced only 41.6%, which is consistent with previously properly optimized, these limitations can be resolved. [65,66]
published results. In yet another study, FB was only By optimizing conditions of the analysis, cloning the PCR
[44]
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weakly cytotoxicity. The EC for AFB was 1.87 μmol/L, products and further sequencing the products, RAPD can
[57]
50
1
which is similar to that observed previously by others, [58-60] be useful in analyzing the nature and mode of action of the
who reported EC values ranging from 0.065 μmol/L for genotoxicants. [65,66] While in the present study RAPD could
50
B-CMV1A2 cells to 14 μmol/L in BE12-6 cells. Exposure detect toxin-induced DNA damage, further studies would
of H4IIE-luc cells to greater concentrations of AFB and be needed before it could be used regularly as a tool in
1
FB resulted in lethality that was a concentration- and the detection of alterations in DNA sequence due to the
1
time-dependent. This effect was greater in cells treated genotoxicants.
with AFB or AFB + FB . The interaction of FB and AFB
1
1
1
1
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in the induction of DNA damage and its correlation with Previous studies have demonstrated that certain compounds in
biomarkers of cellular oxidative status has previously been the diet can offer protection against toxicity of mycotoxins.
[67]
reported to occur in vivo. [4,8,22,61] These reports suggested that Natural vitamins, carotenoids, polyphenol and trace elements
genotoxicity and carcinogenicity of AFB were enhanced by are potentially beneficial in protection against mycotoxicosis.
[68]
1
exposure to FB . The in vivo results indicated that these Green leafy vegetables are known to be dietary sources of
[8]
1
effects were due to the production of ROS, which resulted minerals, trace elements and phytochemicals that contribute
in lipid peroxidation. [4,61] to health. Molecular evidence has suggested that trace
[69]
elements and antioxidant molecules in green, leafy vegetables
AFB is a well-known genotoxicant. When the mechanism lessen risks of cancer and cardiovascular diseases through
1
by which the aqueous extract of C. olitorius protected mechanisms that modulate free radical attack on nucleic acids,
H4IIE-luc rat hepatoma cells against genetic damage proteins, and polyunsaturated fatty acids. C. olitorius is an
[70]
caused by AFB and/or FB was investigated by use of RAPD economically important fiber crop, the edible leaves of which
1
1
analysis, there were statistically significant differences in the contain significant quantities of phenolics and flavonoids
profiles of expression of the investigated genes, between which are known antioxidants. [33,71-74] Although in the current
the control and the treated cell lines at all concentrations study the active compound(s) in the aqueous extract of C.
tested. Differences in the profile between the control and olitorius were not isolated or identified, flavonoids are possible
[33]
the treated samples were due to point mutations and/or base candidates among the active compound(s) in C. olitorius. C.
modifications of the genome caused by AFB and/or FB . olitorius contains abundant amounts of a number of flavonoids
[62]
1
1
Changes were observed for all genes for which primers were that could act as antioxidants, including: 5-caffeoylquinic acid,
used. In our study, both qualitative and quantitative analyses 3,5-dicaffeoylquinic acid, quercetin 3-galactoside, quercetin
showed that both mycotoxins increased instability of DNA 3-glucoside, quercetin 3-(6-malonylglucoside), quercetin
templates of cells, in time- and concentration-dependent 3-(malonylgalactoside), ascorbic acid, a-tocopherol, and
manners. This result supports the conclusion that both chlorophyll. Furthermore, C. olitorius contains relatively
[29]
mycotoxins are direct-acting, genotoxicants that have the high levels of quercetin glycosides. Several novel flavonol
potential to attack hotspots present in DNA. The number glycosides named corchorusides A and B, in addition to a major
of stable bands increased as a function of time and dose. component, capsugenin-25, 30-O-β-diglucopyranoside have
Inconsistency in profiles of bands in RAPD analyses might been isolated from C. olitorius. Recently, several flavonoids,
[26]
have been observed because the two mycotoxins are such as rutin, and quercetin and phenolic compounds,
acting directly as genotoxicants. However, they might including gallic acid, chlorogenic acid, p-cumaric acid, ferulic
82 Hepatoma Research | Volume 1 | Issue 2 | July 15, 2015