Organochlorine pesticides in cerumen were used as a biological marker to monitor the exposure of organochlorine pesticides in the human body. The amount of sample used was about 10 mg. The order of magnitude of HCH (hexachlorocyclohexane) isomer content in cerumen was beta greater than alpha greater than gamma greater than delta; for DDT, the order was p,p'-DDE greater than p,p'-DDT. There was little o,p'-DDT and p,p'-DDD. The contents of beta-HCH and p,p'-DDE in cerumen were highly significantly correlated with those in adipose tissue of the same individuals. Approximately 3800 cerumen samples collected from 35- to 54-year-old healthy adults in the general populations of 35 counties were analyzed for HCH and DDT. The accumulation levels of beta-HCH had a geographical character with obvious gradient differences, and the levels were higher in males than in females. The accumulation levels of beta-HCH in the populations studied were highly significantly correlated with the mortality rates from liver cancer, colon/rectum cancer, and lung cancer in males as well as colon/rectum cancer in females (P less than 0.01), suggesting that the effect of HCH on the above cancers should be studied further.
"In China, CRC incidence is significantly related to residual DDT in rice (Chen et al., 2004). However, some reports found no significant correlation between DDT and CRC (Caldwell et al., 1981; Hardell, 1981; Howsam et al., 2004; Purdue et al., 2007; Wang et al., 1988). These contradictory epidemiological results make the contribution of DDT exposure to CRC risk unclear. "
[Show abstract][Hide abstract] ABSTRACT: Dichlorodiphenyltrichloroethane (DDT), an organochlorine pollutant, is associated with several types of cancer. However, the relationship between DDT and colorectal cancer is uncertain. In this study, the impact of p,p'-DDT on colorectal cancer growth was evaluated using both in vitro and in vivo models. Our results indicated that the proliferation of human colorectal adenocarcinoma DLD1 cells was significantly promoted after exposed to low concentrations of p,p'-DDT ranging from 10(-12) to 10(-7)M for 96h. Exposure to p,p'-DDT from 10(-10) to 10(-8)M led to upregulation of phospho-GSK3β (Ser9), β-catenin, c-Myc and cyclin D1 in DLD1 cells. Rna interference of β-catenin inhibited the proliferation of DLD1 cells stimulated by p,p'-DDT. Inhibiting of estrogen receptors (ERs) had no significant effect on the action of p,p'-DDT. Treatment with p,p'-DDT induced production of intracellular reactive oxygen species (ROS) and inhibited superoxide dismutase (SOD) activity in DLD1 cells. Treatment with N-acetyl-L-cysteine (NAC), a ROS inhibitor, suppressed the induction of Wnt/β-catenin signaling and DLD1 cell proliferation by p,p'-DDT. Moreover, in a mouse xenograft model, 5nmol/kg p,p'-DDT resulted in increased tumor size, oxidative stress and Wnt/β-catenin signaling. These results indicated that low concentrations of p,p'-DDT promoted colorectal cancer growth through Wnt/β-catenin signaling, which was mediated by oxidative stress. The finding suggests an association between low concentrations of p,p'-DDT exposure and colorectal cancer progression.
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