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EC number: 233-566-4
CAS number: 10236-47-2
Table 1. DNA strand breaks in bone marrow of nondiabetic
and diabetic rats 24 hours after the last treatment with the indicated
doses of naringin (4 weeks exposures, spaced 24 hours apart) (mean ± SD).
Olive tail moment
14.0 ± 4.8
5.98 ± 1.15
1.96 ± 0.61
4.78 ± 1.23
+ naringin (25)
12.6 ± 4.77
5.76 ± 1.52
2.12 ± 0.43
4.14 ± 0.56
+ naringin (50)
11.8 ± 4.71
4.82 ± 1.76
1.98 ± 0.23
3.20 ± 0.73
27.2 ± 4.91∗
18.6 ± 4.33 ª
8.08 ± 1.54b
2.98 ± 0.85a
5.82 ± 1.27b
15.8 ± 3.96b
6.97 ± 1.53b
2.24 ± 0.7b
4.32 ± 1.18b
< 0.05 and∗∗P
< 0.01 versus nondiabetic control (Kruskal-Wallis test followed by
Dunn’s multiple comparisons test).
aP < 0.05 andbP
< 0.01 versus diabetes alone (Mann-Whitney U test).
An in vivo alkaline comet assay was conducted to determine the
mutagenic potential of the test item in male Wistar rats, by a method
similar to OECD 489, and also its protective effects against DNA damage
caused by Diabetes mellitus. 5 diabetic and 5 non-diabetic male
rats per group were treated with the test item at concentrations of 25
or 50 mg/kg, daily for 4 weeks. Negative/solvent controls were run in
parallel. At the end of the treatment, animals were killed by
cervical dislocation under light anesthesia and bone marrow cells
from one femur were collected in tubes with ice-cold PBS and DNA
strand breaks were studied by alkaline single cell gel electrophoresis.
Naringin treatment did not exhibit any significant difference in the
level of tail length, tail DNA, tail moment, and olive tail moment
compared to the solvent control at either dose tested. Furthermore, when
both doses of naringin were given to diabetic animals for 4 weeks,
decreased rates of DNA strand breaks were significantly observed and the
higher dose of naringin gave the more effective reduction in all
measured parameters. The test item demonstrated no genotoxicity or
citotoxicity at all tested doses, and is therefore considered to
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