摘要
The mutngenicity of urine from individua1s exposed to the combustion products of liquefied petroleum gas (LPG) was detected with Salmonella typhimurium TA98 and its newly developed derivatives YG1021 (nitroreductase overproducing) and YG1024 (O-acetyltransferase overproducing). The detection showed significantly increased mutagenicity for the two YG strains and increased positive rates for all three stralns in the presence of both rat liver S9 and β-glucuronidase. Further analysis demonstrated that urine samples taken from smoking and non-smoking exposed individuals exhibited significantly higher mutagenic potency (revertants/10 μl urine concentrate) than their corresponding controls. These results indicate that the increased urine mutagenicity is caused by the exposure to LPG combustion products or smoking. The mutagenic potency of urine samples of all exposed individuals tested with YG1024 was found to be about 7 times higher than with TA98. The difference in mutagenic potency was smaller for the sarne samples when comparison was made between YG1021 and TA98. This suggests that the mutagenic compounds present in the urine samples contaln mainly arotnatic compounds as glucuronide conugates. our results demonstrate that YG1024 is more sensitive than TA98 in detecting the mutagenicity of these samples. In addition, no significant difference in the mutagenic poency between the' pure' exposed (non-srnokers') and the ' pure' smokers' (unexpeed) samples was found in all three tester strains. This might mean that the exopure extent Of mutagens/carcinogens in LPG combustion products for exmped individuals roughly corresponds to the smoking level of smokers who smoke 20-40 cigarettes per day. Furthermore, the results also suggest that sguergism might exist in the mutagenic effects of exposure to LPG combustion products and cigarette smoking.
The mutngenicity of urine from individua1s exposed to the combustion products of liquefied petroleum gas (LPG) was detected with Salmonella typhimurium TA98 and its newly developed derivatives YG1021 (nitroreductase overproducing) and YG1024 (O-acetyltransferase overproducing). The detection showed significantly increased mutagenicity for the two YG strains and increased positive rates for all three stralns in the presence of both rat liver S9 and β-glucuronidase. Further analysis demonstrated that urine samples taken from smoking and non-smoking exposed individuals exhibited significantly higher mutagenic potency (revertants/10 μl urine concentrate) than their corresponding controls. These results indicate that the increased urine mutagenicity is caused by the exposure to LPG combustion products or smoking. The mutagenic potency of urine samples of all exposed individuals tested with YG1024 was found to be about 7 times higher than with TA98. The difference in mutagenic potency was smaller for the sarne samples when comparison was made between YG1021 and TA98. This suggests that the mutagenic compounds present in the urine samples contaln mainly arotnatic compounds as glucuronide conugates. our results demonstrate that YG1024 is more sensitive than TA98 in detecting the mutagenicity of these samples. In addition, no significant difference in the mutagenic poency between the' pure' exposed (non-srnokers') and the ' pure' smokers' (unexpeed) samples was found in all three tester strains. This might mean that the exopure extent Of mutagens/carcinogens in LPG combustion products for exmped individuals roughly corresponds to the smoking level of smokers who smoke 20-40 cigarettes per day. Furthermore, the results also suggest that sguergism might exist in the mutagenic effects of exposure to LPG combustion products and cigarette smoking.
