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DNA Oxidative Damage (dna + oxidative_damage)

Distribution by Scientific Domains
Medical Sciences50%

Selected Abstracts

Effects of the Interaction Between , -Carboline-3-carboxylic acid N -Methylamide and Polynucleotides on Singlet Oxygen Quantum Yield and DNA Oxidative Damage

PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 6 2007
Iñigo X. García-Zubiri
The complexation of , -carboline-3-carboxylic acid N -methylamide (,CMAM) with the sodium salts of the nucleotides polyadenylic (Poly A), polycytidylic (Poly C), polyguanylic (Poly G), polythymidylic (Poly T) and polyuridylic (Poly U) acids, and with double stranded (dsDNA) and single stranded deoxyribonucleic acids (ssDNA) was studied at pH 4, 6 and 9. Predominant 1:1 complex formation is indicated from Job plots. Association constants were determined using the Benesi,Hildebrand equation. ,CMAM-sensitized singlet oxygen quantum yields were determined at pH 4, 6 and 9, and the effects on this of adding oligonucleotides, dsDNA and ssDNA were studied at the three pH values. With dsDNA, the effect on ,CMAM triplet state formation was also determined through triplet,triplet transient absorption spectra. To evaluate possible oxidative damage of DNA following singlet oxygen ,CMAM photosensitization, we used thiobarbituric acid-reactivity assays and electrophoretic separation of DNA assays. The results showed no oxidative damage at the level of DNA degradation or strand break. [source]

Electrochemical Characterization of (ZnO/dsDNA)n Layer-by-layer Films and Detection of Natural DNA Oxidative Damage

CHINESE JOURNAL OF CHEMISTRY, Issue 10 2009
Meng Du
Abstract The positively charged nano-ZnO and negatively charged natural DNA were alternately adsorbed on the surface of a gold electrode, forming (ZnO/dsDNA)nlayer-by-layer films. Valuable dynamic information for controlling the formation and growth of the films was obtained by cyclic voltammetry and electrochemical impedance spectroscopy. Differential pulse voltammetric (DPV) measurements showed that the electroactive probe methylene blue (MB) could be loaded in the (ZnO/dsDNA)nfilms from its solution, and then released from the films into Britton-Robinson (B-R) buffer. The complete reloading of MB in the films could be realized by immersing the films in MB solution again. However, after incubation in the solution of carcinogenic metal nickel, the damaged (ZnO/dsDNA)n films could not return to their original and fully-loaded state, and showed smaller DPV peak currents. The results demonstrated that the DNA damage induced by the hydroxyl radical could be achieved by electrochemistry. [source]

Dysfunctional very-low-density lipoprotein synthesis and release is a key factor in nonalcoholic steatohepatitis pathogenesis,,

HEPATOLOGY, Issue 3 2009
Koji Fujita
The specific mechanisms of nonalcoholic fatty liver (NAFL) and nonalcoholic steatohepatitis (NASH) pathogenesis remain unknown. In the present study we investigated the differences between NAFL and NASH in terms of liver lipid metabolites and serum lipoprotein. In all, 104 Japanese subjects (50 men and 54 postmenopausal women) with histologically verified NAFL disease (NAFLD) (51 with NAFL, 53 with NASH) were evaluated; all diagnoses were based on liver biopsy findings and the proposed diagnostic criteria. To investigate the differences between NAFL and NASH in humans, we carefully examined (1) lipid inflow in the liver, (2) lipid outflow from the liver, (3) very-low-density lipoprotein (VLDL) synthesis in the liver, (4) triglyceride (TG) metabolites in the liver, and (5) lipid changes and oxidative DNA damage. Most of the hepatic lipid metabolite profiles were similar in the NAFL and NASH groups. However, VLDL synthesis and lipid outflow from the liver were impaired, and surplus TGs might have been produced as a result of lipid oxidation and oxidative DNA damage in the NASH group. Conclusion: A growing body of literature suggests that a deterioration in fatty acid oxidation and VLDL secretion from the liver, caused by the impediment of VLDL synthesis, might induce serious lipid oxidation and DNA oxidative damage, impacting the degree of liver injury and thereby contributing to the progression of NASH. Therefore, dysfunctional VLDL synthesis and release may be a key factor in progression to NASH. (HEPATOLOGY 2009.) [source]

Effects of primary testicular damage on sperm DNA oxidative status and embryonic and foetal development

ANDROLOGIA, Issue 5 2009
F. Dimitriadis
Summary We evaluated the development of embryos generated from the fertilisation of oocytes with spermatozoa isolated from animals with primary testicular damage (PTD). Embryos derived in vivo or in vitro from oocytes fertilised with spermatozoa produced by PTD rats that had undergone surgical treatment for the PTD (group A1), or PTD rats (group A2), or control rats (group B) were cultured and transferred to recipients. At the end of the experimental period, the fertilisation potential of each rat was assessed in vitro (IVF trials). Sperm 8-oxodG/dG ratio (a marker of DNA oxidative status) was significantly larger in group A2 than in groups A1 and B. Blastocysts of the group A2 transferred to recipients demonstrated a significantly larger loss before implantation than transferred blastocysts of groups A1 or B. In addition, the proportion of implanted blastocysts that could not complete the intrauterine development was significantly larger in group A2 than in groups A1 and B. This study reveals a post-fertilisation detrimental effect in animals with PTD on the capacity of oocytes (fertilised either in vitro or in vivo) to develop in vitro and implant after transferring them to recipients probably attributable to sperm DNA oxidative damage. [source]