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The processes presented in the study enables the separation and disposal of the chloroorganic compounds as by-products from the vinyl chloride plant by using the dichlorethane method and also from the production of propylene oxide by the chlorohydrine method. The integrated purification method of steam stripping and adsorption onto activated carbon allows a complete removal and recovery of the chloroorganic compounds from waste water. Waste distillation fraction is formed during the production of vinyl chloride. 1,1,2-trichloroethane separated from the above fraction, can be processed to vinylidene chloride and further to 1,1,1-trichloroethane. 2,3-Dichloropropene, 2-chloroallyl alcohol, 2-chloroallylamine, 2-chlorothioallyl alcohol or bis(2-chloroallylamine) can be obtained from 1,2,3-trichloropropane. In the propylene oxide plant the waste 1,2-dichloropropane is formed, which can be ammonolysed to 1,2-diaminopropane or used for the production of β-methyltaurine. Other chloroorganic compounds are subjected to chlorinolysis which results in the following compounds: perchloroethylene, tetrachloromethane, hexachloroethane, haxachlorobutadiene and hexachlorobenzene. The substitution of the milk of lime by the soda lye solution during the saponification of chlorohydrine eliminates the formation of the CaCl2 waste.
EN
Oxidative stress and certain environmental carcinogens, e.g. vinyl chloride and its metabolite chloroacetaldehyde (CAA), introduce promutagenic exocyclic adducts into DNA, among them 1,N6-ethenoadenine (εA), 3,N4-ethenocytosine (εC) and N2,3-ethenoguanine (εG). We studied sequence-specific interaction of the vinyl-chloride metabolite CAA with human p53 gene exons 5-8, using DNA Polymerase Fingerprint Analysis (DPFA), and identified sites of the highest sensitivity. CAA-induced DNA damage was more extensive in p53 regions which revealed secondary structure perturbations, and were localized in regions of mutation hot-spots. These perturbations inhibited DNA synthesis on undamaged template. We also studied the repair kinetics of CAA-induced DNA lesions in E. coli at nucleotide resolution level. A plasmid bearing full length cDNA of human p53 gene was modified in vitro with 360 mM CAA and transformed into E. coli DH5α strain, in which the adaptive response system had been induced by MMS treatment before the cells were made competent. Following transformation, plasmids were re-isolated from transformed cultures 35, 40, 50 min and 1-24 h after transformation, and further subjected to LM-PCR, using ANPG, MUG and Fpg glycosylases to identify the sites of DNA damage. In adaptive response-induced E. coli cells the majority of DNA lesions recognized by ANPG glycosylase were removed from plasmid DNA within 35 min, while MUG glycosylase excised base modifications only within 50 min, both in a sequence-dependent manner. In non-adapted cells resolution of plasmid topological forms was perturbed, suggesting inhibition of one or more bacterial topoisomerases by unrepaired ε-adducts. We also observed delayed consequences of DNA modification with CAA, manifesting as secondary DNA breaks, which appeared 3 h after transformation of damaged DNA into E. coli, and were repaired after 24 h.
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