Abstract Title:

Cytotoxic and genotoxic effects induced by stannous chloride associated to nuclear medicine kits.

Abstract Source:

Nucl Med Biol. 2006 Oct;33(7):915-21. PMID: 17045172

Abstract Author(s):

Anderson P Guedes, Valbert N Cardoso, Jose C P De Mattos, Flavio J S Dantas, Vanessa C Matos, Josiane C F Silva, Roberto J A C Bezerra, Adriano Caldeira-de-Araujo

Article Affiliation:

Departamento de Biofísica e Biometria, Universidade do Estado do Rio de Janeiro, Instituto de Biologia Roberto Alcantara Gomes, Rio de Janeiro 20551-030, Brazil. anderson-guedes@ig.com.br

Abstract:

At present, more than 75% of routine nuclear medicine diagnostic procedures use technetium-99m (99mTc). The binding between 99mTc and the drug to obtain the radiopharmaceutical needs a reducing agent, with stannous chloride (SnCl2) being one of the most used. There are controversies about the cytotoxic, genotoxic and mutagenic effects of SnCl2 in the literature. Thus, the approaches below were used to better understand the biological effects of this salt and its association in nuclear medicine kits [methylenediphosphonate (MDP) bone scintigraphy and diethylenetriaminepentaacetic acid (DTPA) kidney and brain scintigraphy]: (i) bacterial inactivation experiments; (ii) agarose gel electrophoresis of supercoiled and linear plasmid DNA and (iii) bacterial transformation assay. The Escherichia coli strains used here were AB1157 (wild type) and BW9091 (xthA mutant). Data obtained showed that both MDP and SnCl2 presented a high toxicity, but this was not observed when they were assayed together in the kit, thereby displaying a mutual protect effect. DTPA salt showed a moderate toxicity, and once more, the DTPA kit provided protection, compared to the SnCl2 effect alone. The results suggest a possible complex formation, either MDP-SnCl2 or DTPA-SnCl2, originating an atoxic compound. On the other hand, SnCl2-induced cell inactivation and the decrease in bacterial transformation generated by DTPA found in XthA mutant strain suggest that the lack of this enzyme could be responsible for the effects observed, being necessary to induce DNA damage repair.

Study Type : In Vitro Study
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