• Korean Journal of Food Science and Technology
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• v.31 no.1
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• pp.246-251
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• 1999

This study was designed to evaluate the mutagenicity and the primary mutagenic mechanism of chloropropanols by using various genotypes of E. coli WP2, E. coli TK and E. coli GW series strains. Chloropropanols showed the low mutagenic activities in E. coli WP2s and WP2 establishing the following order; 2,3-DCP> 3-MCPD>1,3-DCP. As compared with E. coli WP2s, the decrease of mutagenic activity and the increase of survival rate in E. coli WP2 $(WP2s\;uvrA^+)$ suggest that DNA lesions produced by chloropropanols could be easily removed by excision-repair system. From the diminution of mutagenic activity and survival rate in E. coli CM611 (WP2s lexA), it was confirmed that the mutagenesis by chloropropanols was dependent on the SOS-repair system. This fact could be also confirmed from the result that both the mutagenic activity and survival rate in E. coli TK610 (umuC) were much lower than those in E. coli TK603 $(umuC^+)$. In the experiment to examine the possibility that chloropropanols might have effects on the LexA of SOS response negative regulator, there was no variation in ${\beta}-galactosidase$ activities of E. coli GW1105 $[lexA3\;(Ind^-)]$ and GW1107 [lexA51 (Def)] by addition of the compounds, indicating that chloropropanols do not have any effects on the LexA, itself.

• Korean Journal of Food Science and Technology
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• v.30 no.6
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• pp.1464-1469
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• 1998

SOS Chromotest and Ames test were carried out to evaluate the mutagenicity of three chloropropanols. In the SOS Chromotest, 3-monochloro-l,2-propanediol (3-MCPD) and 2,3-dichloro-1-propanol (2,3-DCP) except for 1,3-dichloro-2-propanol (1,3-DCP) induced SOS response in Escherichia coli PQ37 with dose-response relationship and 2,3-DCP was far more genotoxic than 3-MCPD. The genotoxic activities of both compounds, however, were very lower in E. coli PQ35 (PQ37 $uvrA^+)$ as compared to them in E. coli PQ37, whereas much higher in E. coli PQ243 (PQ37 tagA alkA). These results indicate that there are at least two types of DNA lesions caused by these compounds; one is a excision-repairable and the other is 3-methyladenine or any similar lesion which is excision-unrepairable and can induce adaptive response. In Salmonella typhimurium TA100, all the compounds showed strong mutagenicities, establishing the following genotoxic order: 2,3-DCP>3-MCPD>1,3-DCP. But the mutagenic activities were very low in S. typhimurium TA98 and TA97a. These results suggest that the mutation by chloropropanols can be induced by the DNA lesions causing base-pair substitutions. From the result that the mutagenicities of 3-MCPD and 2,3-DCP in S. typhimurium TA1535 were very low as compared to those in S. typhimurium TA100, it was appeared that the mutations by both compounds necessitate error-prone SOS repair.

• Analytical Science and Technology
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• v.21 no.6
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• pp.543-552
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• 2008

This paper described the relatively sensitive and simultaneous analytical method for 3-monochloropropane-1,2-diol (3-MCDP, $C_3H_7ClO_2$, MW. 110) as well as 1,3-dichloropropan-2-ol (1,3-DCP, $C_3H_6Cl_2O$, MW. 128) in various foods. Food samples were homogenized in 5M NaCl solution, mixed with aluminum oxide and eluted with dichloromethane. The extracted chloropropanols were concentrated by rotary evaporator and $N_2$ blow serially were derivatized with HFBA (Heptafluorobutyric anhydride, $C_8F_{14}O_3$, MW. 410) and were determined by GC/MS using isotope dilution method. The characteristic molecular ions at m/z 253, 275, 289, 291, and 453 for HFBA derivatives of 3-MCPD (MW. 502) and 110, 275, and 277 for HFBA derivatives of 1,3-DCP (MW. 325) were chosen in selected ion mode. The method validation data showed sufficiently good properties of LOD (0.003 mg/kg), LOQ (0.010 mg/kg), linearity ($R^2{\geq}0.999$ at 0.010~1.000 mg/kg), and recovery rate (${\approx}97%$). The levels of chloropropanols in soy sauce, sauces, processed meat products, fishery products, and seasonings (n=56/157) determined by the presented method were 0.0~0.3 mg/kg.