title: Adaptive response to H(2)O(2) protects against SnCl(2) damage: the OxyR system involvement.
abstract: The stannous ion, mainly the stannous chloride (SnCl(2)) salt form, is widely used as a reducing agent to label radiotracers with technetium-99m ((99m)Tc). These radiotracers can be employed as radiopharmaceuticals in nuclear medicine procedures. In this case, there is no doubt about absorption of this complex, because it is intravenously administered in humans, although biological effects of these agents have not been fully understood. In this work we used a bacterial system to study the cytotoxic potential of stannous chloride. It is known that SnCl(2) induces lesions that could be mediated by reactive oxygen species (ROS). We, thus, investigated the existence of cross-adaptive response between hydrogen peroxide (H(2)O(2)) and SnCl(2) and the role of the OxyR system known to promote cellular protection against oxidative damages. Here we describe the results obtained with prior treatment of different Escherichia coli strains with sub-lethal doses of H(2)O(2), followed by incubation with SnCl(2). Our data show that H(2)O(2) is capable of inducing cross-adaptive response against the lethality promoted by SnCl(2), suggesting the OxyR system participation through catalase, alkyl hydroperoxide reductase and superoxide dismutase enzymes
authors.affiliation: Departamento de Biofísica e Biometria, Instituto de Biologia Roberto Alcantara Gomes, Universidade do Estado do Rio de Janeiro, Av. 28 de Setembro, 87, RJ, 20551-030, Rio de Janeiro, Brazil.
authors.forename: M L B
authors.initials: ML
authors.lastname: Assis
authors.forename: J C P
authors.initials: JC
authors.lastname: De Mattos
authors.forename: M R
authors.initials: MR
authors.lastname: Caceres
authors.forename: F J S
authors.initials: FJ
authors.lastname: Dantas
authors.forename: L M B O
authors.initials: LM
authors.lastname: Asad
authors.forename: N R
authors.initials: NR
authors.lastname: Asad
authors.forename: R J A C
authors.initials: RJ
authors.lastname: Bezerra
authors.forename: A
authors.initials: A
authors.lastname: Caldeira-de-Araújo
authors.forename: M
authors.initials: M
authors.lastname: Bernardo-Filho
mesh_terms: D000220:Adaptation, Biological / Q000502:physiology*; D002452:Cell Count; D004249:DNA Damage; D004268:DNA-Binding Proteins; D004926:Escherichia coli / Q000187:drug effects* / Q000502:physiology; D029968:Escherichia coli Proteins; D005838:Genotype; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D010084:Oxidation-Reduction; D010088:Oxidoreductases / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D012097:Repressor Proteins / Q000378:metabolism*; D013997:Time Factors; D017971:Tin Compounds / Q000633:toxicity*; D014157:Transcription Factors / Q000378:metabolism*
chemical_list: D004268:DNA-Binding Proteins; D029968:Escherichia coli Proteins; D017382:Reactive Oxygen Species; D012097:Repressor Proteins; D017971:Tin Compounds; D014157:Transcription Factors; C499299:oxyR protein, E coli; C023599:stannous chloride; D006861:Hydrogen Peroxide; D010088:Oxidoreductases