DDE-induced apoptosis in children exposed to the DDT metabolite [An article from: Science of the Total Environment, The]
Book Details
PublisherElsevier
ISBN / ASINB000PAUN5M
ISBN-13978B000PAUN57
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Description
This digital document is a journal article from Science of the Total Environment, The, published by Elsevier in 2006. The article is delivered in HTML format and is available in your Amazon.com Media Library immediately after purchase. You can view it with any web browser.
Description:
In a preliminary study in children we found a weak positive association between the frequency of apoptosis and the exposure to DDT and DDE (a DDT metabolite). In order to verify this information, more studies were needed with an increased number of children. Thus, the aim of the present work was to see if DDT and its metabolites were able to induce apoptosis of PBMC in exposed children. We performed a study in children living in three communities located in southern Mexico. During the year 2003, we studied a total of 61 healthy children; and during the year 2004, 57 children from the same communities were assessed. Apoptosis frequencies in PBMC in these children ranged from 0.10% to 8.30% during 2003 and from 0.12% to 16.20% during 2004, and although we detected exposure to DDT, DDD and DDE, significant association with apoptosis frequencies was found only with DDE blood levels (p=0.010 and 0.040 for 2003 and 2004 respectively). DNA damage and oxidative DNA damage were also studied in 2004 using the comet assay. The association between exposure to DDT or DDE and DNA damage was significant (p=0.004 and p=0.005 respectively), but the association between DDT or DDE and oxidative DNA damage and that of oxidative damage and apoptosis were not significant. Taking into account that DDE is the most persistent metabolite, it would be important to assess the effects of this DDE-induced apoptosis of PBCM in children living in areas where DDT was sprayed.
Description:
In a preliminary study in children we found a weak positive association between the frequency of apoptosis and the exposure to DDT and DDE (a DDT metabolite). In order to verify this information, more studies were needed with an increased number of children. Thus, the aim of the present work was to see if DDT and its metabolites were able to induce apoptosis of PBMC in exposed children. We performed a study in children living in three communities located in southern Mexico. During the year 2003, we studied a total of 61 healthy children; and during the year 2004, 57 children from the same communities were assessed. Apoptosis frequencies in PBMC in these children ranged from 0.10% to 8.30% during 2003 and from 0.12% to 16.20% during 2004, and although we detected exposure to DDT, DDD and DDE, significant association with apoptosis frequencies was found only with DDE blood levels (p=0.010 and 0.040 for 2003 and 2004 respectively). DNA damage and oxidative DNA damage were also studied in 2004 using the comet assay. The association between exposure to DDT or DDE and DNA damage was significant (p=0.004 and p=0.005 respectively), but the association between DDT or DDE and oxidative DNA damage and that of oxidative damage and apoptosis were not significant. Taking into account that DDE is the most persistent metabolite, it would be important to assess the effects of this DDE-induced apoptosis of PBCM in children living in areas where DDT was sprayed.
