Effect of resveratrol on chromosomal aberrations induced by doxorubicin in rat bone marrow cells

• Published in: Mutation research. Genetic toxicology and environmental mutagenesis Vol. 766; pp. 1 - 4
• Main Authors: Bingöl, Günsel, Gülkaç, Mehmet Doğan, Dillioğlugil, Meltem Özlen, Polat, Fikriye, Kanli, Aylin Özön
• Format: Journal Article
• Language: English
• Published: Netherlands Elsevier B.V 15.05.2014; Elsevier BV
• Subjects: Animals; Antibiotics, Antineoplastic - adverse effects; Antibiotics, Antineoplastic - pharmacology; Anticlastogenesis; Antimutagenic Agents - pharmacology; Antioxidants; Bone marrow; Bone Marrow Cells - metabolism; Bone Marrow Cells - pathology; Chemotherapy; Chromosome aberration; Chromosome Aberrations - chemically induced; Chromosomes; Doxorubicin; Doxorubicin - adverse effects; Doxorubicin - pharmacology; Male; Metaphase - drug effects; Oncology; Polyphenols; Rat; Rats; Rats, Wistar; Resveratrol; Rodents; Stilbenes - pharmacokinetics; Anticlastogenesis; Rat; Chromosome aberration; Doxorubicin; Resveratrol
• ISSN: 1383-5718; 1879-3592
• DOI: 10.1016/j.mrgentox.2014.03.008

•RES has anticlastogenic effect in bone marrow cells induced by DXR.•Repeated doses of RES at 25mg/kgbw has protection on DXR-induced chromosomal aberration.•Repeated doses of RES at 12.5 and 25mg/kgbw alone do not cause any clastogenicity in bone marrow cells. This study investigated the effects of resveratrol (RES) on doxorubicin (DXR) induced rat bone marrow cell chromosome aberrations. RES, a polyphenolic compound, has attracted considerable attention because of its antioxidant and antimutagenic effects. DXR, a chemotherapeutic agent, is known to cause chromosomal aberrations in healthy cells in cancer patients. In this study, Wistar albino male rats were divided into 6 groups with 6 animals each. The control group received distilled water i.p. and the DXR group received an i.p. injection of doxorubicin (90mg/kgbw). For the 2 RES dose groups (12.5 and 25mg/kgbw, respectively), RES was injected i.p. 5 times during the 24h study period to coincide with the schedule for the DXR+RES groups. The DXR-RES groups received DXR (90mg/kgbw) and RES at either 12.5 or 25mg/kgbw, i.p. 30min before, concurrently, and then every 6h after DXR administration. Bone marrow collection was timed to coincide with 24h after DXR administration in all groups. RES administration alone did not induce any significant increase in frequency of chromosome aberrations or abnormal metaphases compared with controls (p>0.05) while DXR alone did (p<0.05). In the DXR-RES 12.5mg/kgbw group, frequency of chromosome aberrations and abnormal metaphases were slightly reduced compared to DXR alone, but this was not statistically significant. However, in the DXR-RES 25mg/kgbw group, RES resulted in a statistically significant reduction in the frequency of chromosome aberrations and abnormal metaphases compared to those induced by DXR alone (p<0.05). These results indicate that RES (25mg/kgbw) significantly reduces frequency of DXR induced chromosome damage in bone marrow cells.