title: Possible repair action of Vitamin C on DNA damage induced by methyl methanesulfonate, cyclophosphamide, FeSO4 and CuSO4 in mouse blood cells in vivo.
abstract: Interaction between Vitamin C (VitC) and transition metals can induce the formation of reactive oxygen species (ROS). VitC may also act as an ROS scavenger and as a metal chelant. To examine these possibilities, we tested in vivo the effect of two doses of VitC (1 and 30 mg/kg of mouse body weight) on the genotoxicity of known mutagens and transition metals. We used the alkaline version of the comet assay to assess DNA damage in peripheral white blood cells of mice. Animals were orally given either water (control), cyclophosphamide (CP), methyl methanesulfonate (MMS), cupric sulfate or ferrous sulfate. A single treatment with each VitC dose was administered after treatment with the mutagens or the metal sulfates. Both doses of VitC enhanced DNA damage caused by the metal sulfates. DNA damage caused by MMS was significantly reduced by the lower dose, but not by the higher dose of VitC. For CP, neither post-treatment dose of VitC affected the DNA damage level. These results indicate a modulatory role of Vitamin C in the genotoxicity/repair effect of these compounds. Single treatment with either dose of VitC showed genotoxic effects after 24 h but not after 48 h, indicating repair. Double treatment with VitC (at 0 and 24 h) induced a cumulative genotoxic response at 48 h, more intense for the higher dose. The results suggest that VitC can be either genotoxic or a repair stimulant, since the alkaline version of the comet assay does not differentiate "effective" strand breaks from those generated as an intermediate step in excision repair (incomplete excision repair sites). Further data is needed to shed light upon the beneficial/noxious effects of VitC.
authors.affiliation: Curso de Nutrição, Departamento de Educação Física e Saúde, Universidade de Santa Cruz do Sul, UNISC, Santa Cruz do Sul, RS, Brazil.
authors.forename: Silvia Isabel Rech
authors.initials: SI
authors.lastname: Franke
authors.forename: Daniel
authors.initials: D
authors.lastname: Prá
authors.forename: Juliana
authors.initials: J
authors.lastname: da Silva
authors.forename: Bernardo
authors.initials: B
authors.lastname: Erdtmann
authors.forename: João Antonio Pêgas
authors.initials: JA
authors.lastname: Henriques
mesh_terms: D000818:Animals; D018906:Antineoplastic Agents, Alkylating / Q000633:toxicity*; D000975:Antioxidants / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D020552:Comet Assay; D019327:Copper Sulfate / Q000633:toxicity*; D003520:Cyclophosphamide / Q000633:toxicity*; D004249:DNA Damage; D004260:DNA Repair; D004639:Emetics / Q000633:toxicity*; D005290:Ferric Compounds / Q000633:toxicity*; D016166:Free Radical Scavengers; D007962:Leukocytes; D008297:Male; D008741:Methyl Methanesulfonate / Q000633:toxicity*; D051379:Mice; D017382:Reactive Oxygen Species
chemical_list: D018906:Antineoplastic Agents, Alkylating; D000975:Antioxidants; D004639:Emetics; D005290:Ferric Compounds; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; C024823:ferric sulfate; D003520:Cyclophosphamide; D008741:Methyl Methanesulfonate; D019327:Copper Sulfate; D001205:Ascorbic Acid