Imazethapyr and imazapic, bispyribac-sodium and penoxsulam: zooplankton and dissipation in subtropical rice paddy water.

Herbicides are very effective at eliminating weed and are largely used in rice paddy around the world, playing a fundamental role in maximizing yield. Therefore, considering the flooded environment of rice paddies, it is necessary to understand the side effects on non-target species. Field experiment studies were carried out during two rice growing seasons in order to address how the commonly-used herbicides imazethapyr and imazapic, bispyribac-sodium and penoxsulam, used at recommended dosage, affect water quality and the non-target zooplankton community using outdoor rice field microcosm set-up. The shortest (4.9 days) and longest (12.2 days) herbicide half-life mean, estimated of the dissipation rate (k) is shown for imazethapyr and bispyribac-sodium, respectively. Some water quality parameters (pH, conductivity, hardness, BOD5, boron, potassium, magnesium, phosphorus and chlorides) achieved slightly higher values at the herbicide treatment. Zooplankton community usually quickly recovered from the tested herbicide impact. Generally, herbicides led to an increase of cladocera, copepods and nauplius population, while rotifer population decreased, with recovery at the end of the experiment (88 days after herbicide treatment).

Enzymatic recognition of DNA damage induced by UVB-photosensitized titanium dioxide and biological consequences in Saccharomyces cerevisiae: evidence for oxidatively DNA damage generation.

Although titanium dioxide (TiO(2)) has been considered to be biologically inert, finding use in cosmetics, paints and food colorants, recent reports have demonstrated that when TiO(2) is attained by UVA radiation oxidative genotoxic and cytotoxic effects are observed in living cells. However, data concerning TiO(2)-UVB association is poor, even if UVB radiation represents a major environmental carcinogen. Herein, we investigated DNA damage, repair and mutagenesis induced by TiO(2) associated with UVB irradiation in vitro and in vivo using Saccharomyces cerevisiae model. It was found that TiO(2) plus UVB treatment in plasmid pUC18 generated, in addition to cyclobutane pyrimidine dimers (CPDs), specific damage to guanine residues, such as 8-oxo-7,8-dihydroguanine (8-oxoG) and 2,6-diamino-4-hydroxy-5-formamidopyrimidine (FapyG), which are characteristic oxidatively generated lesions. In vivo experiments showed that, although the presence of TiO(2) protects yeast cells from UVB cytotoxicity, high mutation frequencies are observed in the wild-type (WT) and in an ogg1 strain (deficient in 8-oxoG and FapyG repair). Indeed, after TiO(2) plus UVB treatment, induced mutagenesis was drastically enhanced in ogg1 cells, indicating that mutagenic DNA lesions are repaired by the Ogg1 protein. This effect could be attenuated by the presence of metallic ion chelators: neocuproine or dipyridyl, which partially block oxidatively generated damage occurring via Fenton reactions. Altogether, the results indicate that TiO(2) plus UVB potentates UVB oxidatively generated damage to DNA, possibly via Fenton reactions involving the production of DNA base damage, such as 8-oxo-7,8-dihydroguanine.