Objective: 

Nuclear medicine, which is an important medical discipline, has been using radiopharmaceuticals for diagnostic and therapeutic purposes for many diseases. Technetium-99m methoxyisobutylisonitrile (Tc-99m sestamibi) is a lyphophylic complex that has a positive loaded isonitril group. Aim of the study is to investigate whether Tc-99m sestamibi, which is one of the mostly used radiopharmaceutical in nuclear medicine field, cause oxidative damage or not in rats' heart after an injection.

Methods: 

Sixteen male Sprague-Dawley rats were randomly divided into two groups: (I) Tc-99m sestamibi group (n:8), Tc-99m sestamibi administered intravenously with the dose of 0,35 mCi/kg comparable with the dose used in patients. (II) Control group (n:8), one dose of isotonic sodium chloride was administered intravenous with the same volume as Tc-99m sestamibi group. The animals were killed by decapitation 30 min after injection. Malondialdehyde was used as markers of oxidative stress-induced heart impairment. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities were studied to evaluate the changes of antioxidant status

Results: 

In the Tc-99m sestamibi group (I), treated Tc-99m sestamibi produced a significant decrease in activities of antioxidant enzymes SOD (P=0,004) and CAT (P=0,001) in myocardial tissue, while MDA (P=0,003) level increased when compared with control group (II). On the other hand, the GSH-Px (P=0,011) activities were significantly increased in the Tc-99m sestamibi treated rats, compared with the untreated rats.

Conclusions: 

These findings demonstrate that in vivo acute administration of Tc-99m sestamibi results in the induction of lipid peroxidation and changes the activities of antioxidant enzymes in rat heart tissue, suggesting that free radicals may be involved in the toxic effects of the radiopharmaceutical compounds.