Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 4 de 4
Filter
1.
Chinese Journal of Preventive Medicine ; (12): 193-195, 2007.
Article in Chinese | WPRIM | ID: wpr-290211

ABSTRACT

<p><b>OBJECTIVE</b>To evaluate the association between metabolism of arsenic and DNA oxidative damage in workers in a arsenic mill.</p><p><b>METHODS</b>Urinary organic arsenic and 8-hydroxydeoxyguanine were detected in 37 workers highly exposed to arsenic and 16 administrative and logistic staff with mild exposure in a arsenic mill in Yunnan province, and also 28 local people who did not have the exposure in the near past time. The correlation between metabolism of arsenic and DNA oxidative damage was evaluated.</p><p><b>RESULTS</b>The urinary organic arsenic concentration was respectively (0.48 +/- 0.37) mg/L and (0.08 +/- 0.05) mg/L for men with high and low exposure, and was respectively 0.11 mg/L and (0.30 +/- 0.24) mg/ L for women with high and low exposure, while it was lower than 0.02 mg/L in the controls. Urinary 8-hydroxydeoxyguanine concentration was (18.07 +/- 11.68) micromol/mol creatinine, (11.79 +/- 8.25) micromol/mol creatinine, (10.07 +/- 3.04) micromol/mol creatinine for the males with high and low exposure and of controls, respectively, (P < 0.05), and it was 84.35 micromol/mol creatinine, (21.27 +/- 5.89) micromol/mol creatinine, (14.43 +/- 2.58) micromol/mol creatinine for females with high and low exposure and of controls, respectively. The female workers exposed to arsenic had higher urinary 8-hydroxydeoxyguanine levels than males did (P < 0.05). The increased tendencies of urinary 8-hydroxydeoxyguanine levels with the organic arsenic concentration were found in workers (r(s) = 0.279, P = 0.019).</p><p><b>CONCLUSION</b>Occupational individuals exposed to arsenic have obvious DNA oxidative damage, which is more severe in females. The difference of metabolism of arsenic may play a key role.</p>


Subject(s)
Adult , Female , Humans , Male , Middle Aged , Arsenicals , Urine , China , Guanine , Urine , Occupational Exposure
2.
China Journal of Chinese Materia Medica ; (24): 332-354, 2007.
Article in Chinese | WPRIM | ID: wpr-245979

ABSTRACT

<p><b>OBJECTIVE</b>To study the effects of lutein on apoptosis and its mechanism.</p><p><b>METHOD</b>The cells of human esophageal carcinoma EC9706 were grown in RPMI medium containing 10% bovine serum and were treated with lutein at 100 microg x mL(-1) concentration. Flow cytometry was employed to investigate the effects of lutein on cell apoptosis of EC9706 cells. Histochemistry was performed to determine apoptosis-related protein expresion.</p><p><b>RESULT</b>Flow cytometry analyses revealed that lutein increased EC9706 cell apoptosis ratio when treated with lutein 100 microg x mL(-1) at 96 h. Lutein decreased the expression of Bcl-2 protein and increased the expression of Bax protein in EC9706 cells.</p><p><b>CONCLUSION</b>Lutein could inhibit mitosis and stimulate apoptosis of EC9706 cells. The apoptotic effect may result from the down-regulation of expression of Bcl-2 and up-regulation expression of Bax.</p>


Subject(s)
Humans , Antineoplastic Agents, Phytogenic , Pharmacology , Apoptosis , Carcinoma, Squamous Cell , Metabolism , Pathology , Cell Line, Tumor , Esophageal Neoplasms , Metabolism , Pathology , Lutein , Pharmacology , Proto-Oncogene Proteins c-bcl-2 , Metabolism , bcl-2-Associated X Protein , Metabolism
3.
Chinese Journal of Medical Genetics ; (6): 277-280, 2005.
Article in English | WPRIM | ID: wpr-321107

ABSTRACT

<p><b>OBJECTIVE</b>To study the clinical features and to identify homeobox D13 (HOXD13) gene mutation of the affected individuals in a Chinese synpolydactyly (SPD) kindred.</p><p><b>METHODS</b>Clinical data and peripheral blood samples of SPD family members were obtained through field investigation. For every member of this pedigreeìthe fragment containing mutational hot spots of HOXD13 was amplified by PCR for mutation screening. To examine whether there is any other mutation within coding sequence of HOXD13, exon 1 and exon 2 of HOXD13 were also amplified by PCR. All the amplified fragments were electrophoresed on 2% agarose gels and then the mutant fragments were electrophoresed on 5% polyacrylamide gels to be separated. Purified PCR products of normal and selected mutant alleles were directly sequenced.</p><p><b>RESULTS</b>Comparing the HOXD13 coding sequence of the affected individuals with HOXD13 sequence in the GenBank and with that of the unaffected, an inserted segment coding 8 alanine residues within HOXD13 was found segregating with the disorder. This mutation is also termed polyalanine expansion. The 8-alanine expansion can be interpreted as a reduplication of normal alanines 5-12.</p><p><b>CONCLUSION</b>The results suggest that synpolydactyly in this kindred may be caused by polyalanine expansion in HOXD13.</p>


Subject(s)
Female , Humans , Infant , Male , Base Sequence , China , DNA Mutational Analysis , Homeodomain Proteins , Genetics , Molecular Sequence Data , Mutation , Pedigree , Polymerase Chain Reaction , Syndactyly , Genetics , Transcription Factors , Genetics
4.
Biomedical and Environmental Sciences ; (12): 203-208, 2002.
Article in English | WPRIM | ID: wpr-264316

ABSTRACT

<p><b>OBJECTIVE</b>To design and develop a novel, sensitive and versatile method for in vivo foot printing and studies of DNA damage, such as DNA adducts and strand breaks.</p><p><b>METHODS</b>Starting with mammalian genomic DNA, single-stranded products were made by repeated primer extension, these products were ligated to a double-stranded linker having a randomized 3' overhang, and used for PCR. DNA breaks in p53 gene produced by restriction endonuclease AfaI were detected by using this new method followed by Southern hybridization with DIG-labeled probe.</p><p><b>RESULTS</b>This randomized terminal linker-dependent PCR (RDPCR) method could generate band signals many-fold stronger than conventional ligation-mediated PCR (LMPCR), and it was more rapid, convenient and accurate than the terminal transferase-dependent PCR (TDPCR).</p><p><b>CONCLUSION</b>DNA strand breakage can be detected sensitively in the gene level by RDPCR. Any lesion that blocks primer extension should be detectable.</p>


Subject(s)
Animals , Humans , DNA Adducts , DNA Damage , DNA Primers , Genes, p53 , Genetics , Mammals , Polymerase Chain Reaction , Methods , Sensitivity and Specificity
SELECTION OF CITATIONS
SEARCH DETAIL