Dioxins and cytogenetic status of villagers after 40 years of agent Orange application in Vietnam.

We have examined cytogenetic status of the rural population living on dioxin-contaminated territories (DCT, TCDD in soil 2.6 ng/kg) compared to the villagers of the control area (TCDD in soil 0.18 ng kg(-1)). The examination took place almost 40 years after the war. The consequences of some confounding factors (years of residence in the region, farming, and aging) has been examined. Karyological analysis of buccal and nasal epitheliocytes among healthy adult males living on DCT and control area (26 and 35 persons) was conducted. A wide range of cytogenetic (micronuclei, nuclear protrusions), proliferative (binucleated cells and cells with doubled nucleus) and endpoints of cell death (cells with perinuclear vacuoles, with damaged nucleus membrane, condensed chromatin, pyknosis, karyorrhexis, karyolysis) had been analyzed. The frequent amount of cells with nuclear protrusions in both epithelia was slightly decreased in the DСT group. Biomarkers of early and late stages of nuclear destruction in buccal epithelium (cells with damaged nuclear membrane, karyolysis) were elevated significantly in DCT. Higher level of the same parameters was also identified in nasal epithelium. The cytogenetic status of healthy adult males on DCT had got "normalization" by present moment in comparison with our early data. Nevertheless, in exposed group some alteration of the cytogenetic status was being registered (mostly biomarkers of apoptosis). Years of residence (and exposure to dioxins) affected the cytogenetic status of DCT inhabitants, whereas no influence of farming factors (pesticides, fertilizers, etc.) had been discovered. Some biomarkers of proliferation and cell death were affected by aging.

Investigation of genotoxic and cytotoxic effects of micro- and nanosized titanium dioxide in six organs of mice in vivo.

Titanium dioxide is manufactured worldwide in large quantities for use in a wide range of applications including as food additives, in cosmetics and pigments for coloring ingested and externally applied drugs. Although TiO(2) is chemically inert it can cause negative health effects, such as lung cancer in rats. However, the mechanisms involved in TiO(2)-induced genotoxicity and carcinogenicity have not been clearly defined and are poorly studied in vivo. In the present research genotoxicity and carcinogenicity of titanium dioxide were studied in a mouse model. We treated CBAB6F1 mice by oral gavage with titanium dioxide particles (microsized, TDM, 160nm; nanosized, TDN, 33nm) in doses of 40, 200 and 1000mg/kg bw, daily for seven days. Genotoxic effects were analyzed in the cells of brain, liver and bone marrow by means of the Comet assay and in the cells of bone marrow, forestomach, colon and testis with a poly-organ karyological assay (analysis of micronuclei, nuclear protrusions, atypical nuclei, multinucleated cells, mitotic and/or apoptotic index). TDM induced DNA-damage and micronuclei in bone-marrow cells and TDN induced DNA-damage in the cells of bone marrow and liver. TDM and TDN increased the mitotic index in forestomach and colon epithelia, the frequency of spermatids with two and more nuclei, and apoptosis in forestomach (only TDN) and testis. This is one of the first poly-organ studies of TDM- and TDN-induced genotoxicity in vivo in mice. These effects are caused by a secondary genotoxic mechanism associated with inflammation and/or oxidative stress. Given the increasing use of TiO(2) nanoparticles, these findings indicate a potential health hazard associated with exposure to TiO(2) particles.