Dissertation > Excellent graduate degree dissertation topics show

The Study of both the DNA Addcuts and the Expression of Chk1 and Cdc25A Repair Genes in Rats Poisoned Acutely by Nickel Carbonyl

Author: MaHaiXia
Tutor: ChengNing；WangQiuYing
School: Lanzhou University
Course: Immunology
Keywords: Nickel carbonyl SD rats UV absorption spectrum of mobile DNA adducts Damage repair genes Reverse transcriptase polymerase chain reaction The cell cycle checkpoint kinase 1 (Chk1) Cell division cycle gene protein 25A (Cdc25A) mRNA Linear equation Related
CLC: R114
Type: Master's thesis
Year: 2009
Downloads: 20
Quote: 0
Read: Download Dissertation

Abstract

Purpose. Acute nickel carbonyl on blood, lung tissue, liver tissue and kidney tissue genomic DNA molecules plus cooperation with, and to provide a scientific basis for clinical emergency and protective. 2 repair related gene cell cycle checkpoint kinase 1 (Chk1) and cell division cycle protein 25A (Cdc25A) mRNA expression in rat lung tissue and liver tissue damage. Study acute nickel carbonyl poisoning from the molecular level to its poisoning repair mechanism. Method 1. Using UV absorption spectral shift of four doses of group (A, B, C group, the nickel carbonyl group, D group, the chlorine group) as well as the normal control group (E) SD rats blood, lung tissue, liver tissue and renal tissue, the DNA extracted in the 250nm-275nm wavelength of the determination of the OD value, and obtaining the average value and plotted comparing the highest absorption peak of about displacement concluded. By reverse transcription polymerase chain reaction (RT-PCR) method of the four groups of exposure dose group (A, B, C group as nickel carbonyl group, D group the chlorine group) and normal control group (E group) SD rat lung tissue and the liver tissue specimens of Chk1 and Cdc25A gene expression analysis, a preliminary analysis of nickel carbonyl poisoning molecular repair mechanisms. 1 blood each exposure group exposed 1d, 2d, 3d and 7d after comparison with the normal control group, and has a maximum absorption peak displacement and right offset 1nm. No obvious lung, liver and kidney tissues around displacement. With the upward trend the the maximum absorbance large exposure day increase in the number of lung, liver and kidney tissue were tested first decreased and exposure the 3d after minimum; maximum absorbance of the group D is lower than that of other groups. Intensity of of Chk1 gene mRNA expression in the lung tissue, area, the average density of carbonyl nickel exposure dose was a positive linear correlation. The intensity and dose linear equation Y = 116.189 0.235X (r ~~ 2 = 0.671; F = 20.403, p = 0.001; the X coefficient: t_β = 4.517, p = 0.001), area dose linear equation Y = 1185.788 2.779 X (r-2 = 0.641; F = 17.829, p = 0.002; the X coefficient: t_β = 4.222, p = 0.002), the average density with dose linear equation Y = 115.691 0.204X (r ~~ 2 = 0.866; F = 64.371, p = 0.000; the X coefficient: t_β = 8.023, p = 0.000); average density and exposure dose of the the Chk1 gene mRNA expression linear equation was the best. 4 in lung tissue the Cdc25A gene mRNA expression of strength, area, average density of nickel carbonyl exposure doses showed positive linear correlation. Strength dose linear equation Y = 132.813 0.238X (r ~~ 2 = 0.551; F = 12.274, p = 0.006; the X coefficient: t_β = 3.503, p = 0.006), area dose linear equation Y = 1112.168 3.386 X (r ~~ 2 = 0.765; F = 32.610, p = 0.000; X-coefficient: t_β = 5.710, p = 0.000), average density with dose linear equation was Y = 139.995 0.198X (r ~~ 2 = 0.448; F = 8.100, p = 0.017; the X coefficient: t_β = 2.846, p = 0.017); area of ??the Cdc25A gene mRNA expression with doses of the linear equation was the best. Chk1 and Cdc25A mRNA expression in liver tissue strength, area, average density, the standard amount of nickel carbonyl exposure doses and drawn between the time were not found in the relationship (p> 0.05). Conclusion 1. Nickel carbonyl and plus cooperation with chlorine in the blood and DNA in lung tissue, liver tissue and kidney tissue and increase cooperation in the DNA molecule is very weak. 2. The DNA absorbance lowest acute nickel carbonyl poisoning 3d organization, suggesting that DNA damage, DNA absorbance gradually increased thereafter, suggesting that DNA gradually repair. The maximum absorbance of Group D in the liver tissue was significantly lower than the other groups, differences prompted chlorine and nickel carbonyl poisoning mechanism. Rat lung tissue Chk1 and Cdc25A gene expression levels and nickel carbonyl acute toxic dose significantly related, suggesting that Chk1 and Cdc25A gene in the regulation of nickel carbonyl acute poisoning cells to repair DNA damage and cycle play an important role. Chk1 and Cdc25A gene expression in the liver tissue of rats with acute toxic dose of nickel carbonyl found no significant correlation.

Related Dissertations

CLC: > Medicine, health > Preventive Medicine,Health > Health - basic science > Health Toxicology
© 2012 www.DissertationTopic.Net Mobile