Hepatoprotective Effect of Dexmedetomidine Against Radioiodine Toxicity in Rats: Evaluation of Oxidative Status and Histopathologic Changes

Abstract

Based on the anti-inflammatory, antioxidant, and anti-apoptotic properties of Dexmedetomidine (DEX), the present study was conducted to investigate the possible radioprotective effects of DEX against hepatic radioiodine (I-131) toxicity. Thirty-six rats were randomly divided into 3 groups as untreated control (Group 1); oral radioiodine (RAI, 111 MBq) administrated rats (Group 2), and DEX group (oral radioiodine and daily intraperitoneal 25 μg/kg DEX administrated rats, Group 3). In the third group, DEX administration was started 2 days before and continued for 5 days after RAI administration. Twenty-four hours after the administration of the last dose of DEX, liver samples were taken for evaluation of oxidative stress parameters and histopathologic changes. The tissue malondialdehyde and advanced oxidation protein product levels in DEX group were significantly lower than RAI group. The total tissue sulphydryl and catalase levels of DEX group were higher than RAI group and the difference was statistically significant. The histopathologic damage in the DEX-treated group was significantly less than the damage in the RAI group (P < 0.05 for all pathologic parameters). Treatment with DEX decreased the histopathologic abnormalities when compared with the RAI group. It was presented that DEX had radioprotective effect on the liver after I-131 therapy and anti-inflammatory and antioxidant activities are likely to be involved in the mechanism underlying the radioprotective effects of DEX. After further studies, DEX might be used as a hepatoprotective treatment regimen before administering radioactive iodine therapy particularly in patients with hepatic disease.