Emodin, an anthraquinone derivative, protects against gamma radiation-induced toxicity by inhibiting DNA damage and oxidative stress.

PURPOSE

In the present study, we explored the modulatory effect of emodin (1,3,8-trihydroxy-6-methylanthraquinone, C(15)H(10)O(5)) against gamma radiation-induced DNA damage and oxidative stress in acellular and cellular systems, respectively.

MATERIALS AND METHODS

For cellular systems, concanavalin A (ConA)-stimulated murine splenocytes were used. Cytotoxic effect of emodin (0-400 μM), radiation (3-12 Gy) and emodin + radiation was measured by MTT [3-(4,5-dimethylthiazol-2-yl) 2,5-diphenyltetrazolium bromide] assay. Gamma radiation (3-12 Gy)-induced production of reactive oxygen species (ROS), an increase in nitric oxide (NO) level and its inhibition by emodin were estimated by DCFDA (2',7'-dichlorofluorescein diacetate) and Griess regent, respectively. Analysis of radiation-induced apoptosis was performed using flow cytometery and acridine orange/ethidium bromide staining. DNA damage was evaluated in acellular system using pBR322 plasmid relaxation assay.

RESULTS

Emodin was able to effectively scavenge radiation- induced free radicals (ROS and NO) in murine splenocytes. Radiation-induced apoptosis and cell death was also inhibited by emodin pre-treatment. It could significantly prevent radiation-induced DNA damage.

CONCLUSIONS

Protection against gamma radiation-induced cell death and DNA damage by emodin could be attributed to its free radical scavenging activity. The present study is the first report of the radioprotective role of emodin in mammalian cells.