Congcong Zhao1, Yuanchen Xie1, Xiaoshan Zhou2, Qiao Zhang1, Na Wang1. 1. College of Public Health, Zhengzhou University, No. 100 Science Avenue, High-tech Zone, Henan 450001, China. 2. Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institute, Karolinska University Hospital, Huddinge, Stockholm 141 86, Sweden.
Abstract
OBJECTIVE: To explore the genetic damage caused by different tar levels in the human body. METHODS: The subjects were divided into high, medium and low (12 mg, 8 mg, 5 mg) tar groups according to the tar levels. Nonsmoking populations served as a control group. 2 ml of peripheral blood was collected on the 10th day after morning fasting. Oxidative and genetic toxicological damage indicators were analysed with enzyme-linked immunosorbent assay, cytokinesis-block micronucleus assay in human lymphocyte and single cell gel electrophoresis. RESULTS: The distribution of hOGG1 concentration was significantly different within all groups, P < 0.01. The concentrations of cotinine, 8-OHdG and Rap-2b were significantly differences between control and medium tar group, control and high tar group, low and medium tar group and low and high tar group, respectively, P < 0.05. The level of PAH-DNA adducts was not significantly changed in the middle tar group and high tar group, P > 0.05. The level of CRP was significantly changed between control and high tar group, low and high tar group and medium and high tar group, respectively, P < 0.0001. The rate of comet tailing was significantly different between all groups. The rate of micronucleus cells was not significantly different between all groups. CONCLUSIONS: The increase of tar content could increase the DNA damage to a certain extent, so the intake of tar content should be monitored.
OBJECTIVE: To explore the genetic damage caused by different tar levels in the human body. METHODS: The subjects were divided into high, medium and low (12 mg, 8 mg, 5 mg) tar groups according to the tar levels. Nonsmoking populations served as a control group. 2 ml of peripheral blood was collected on the 10th day after morning fasting. Oxidative and genetic toxicological damage indicators were analysed with enzyme-linked immunosorbent assay, cytokinesis-block micronucleus assay in human lymphocyte and single cell gel electrophoresis. RESULTS: The distribution of hOGG1 concentration was significantly different within all groups, P < 0.01. The concentrations of cotinine, 8-OHdG and Rap-2b were significantly differences between control and medium tar group, control and high tar group, low and medium tar group and low and high tar group, respectively, P < 0.05. The level of PAH-DNA adducts was not significantly changed in the middle tar group and high tar group, P > 0.05. The level of CRP was significantly changed between control and high tar group, low and high tar group and medium and high tar group, respectively, P < 0.0001. The rate of comet tailing was significantly different between all groups. The rate of micronucleus cells was not significantly different between all groups. CONCLUSIONS: The increase of tar content could increase the DNA damage to a certain extent, so the intake of tar content should be monitored.
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