We used the bone marrow
DNA strand breaks, micronucleus formations, spermatocyte
chromosomal aberrations, and sperm characteristic assays to investigate the
chromosomal instability in somatic and germinal cells of diabetic rats treated with multiple doses of
naringin. The obtained results revealed that
naringin was neither cytotoxic nor genotoxic for the rats at all tested doses. Moreover,
naringin significantly reduced the diabetes-induced
chromosomal instability in somatic and germinal cells in a dose-dependent manner. In addition, diabetes induced marked biochemical alterations characteristic of oxidative stress including enhanced lipid peroxidation, accumulation of
oxidized glutathione, reduction in
reduced glutathione, and accumulation of intracellular
reactive oxygen species. Treatment with
naringin ameliorated these
biochemical markers dose-dependently. In conclusion,
naringin confers an appealing protective effect against diabetes-induced
chromosomal instability towards rat somatic and germinal cells which might be explained partially via diminishing the de novo
free radical generation induced by
hyperglycemia. Thus,
naringin might be a good candidate to reduce genotoxic risk associated with
hyperglycemia and may provide decreases in the development of secondary
malignancy and abnormal reproductive outcomes risks, which seems especially important for diabetic patients.