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Deoxyribonucleic acid damage

Walker, G.C. (1984). Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia colt Microbiol. Rev. 48 60-93. [Pg.236]

Analysis of Deoxyribonucleic Acid Damage Using the Comet Assay Two... [Pg.604]

Kappen LS, Goldberg IH (1983) Deoxyribonucleic acid damage by neocarzinostatin chromo-phore strand breaks generated by selective oxidation of C-5 of deoxyribose. Biochemistry 22 4872-4878... [Pg.462]

Raehek LI, Musiyenko SI, LeDoux SP, Wilson GL. Palmitate indueed mitoehondrial deoxyribonucleic acid damage and apoptosis in 16 rat skeletal musele eells. Endocrinology. 2007,148(l) 293-299. [Pg.116]

Cohen JJ, Catino DM, Petzold SJ, Berger NA (1982) Activation of poly (adenosine diphosphate ribose) polymerase by SV40 minichromosomes effects of deoxyribonucleic acid damage and histone HI. Biochemistry 21 4931-4940... [Pg.122]

Podgorodnichenko, V. K., Poverenny, A. M., Mazin, A. L. Antigenic determinants of deoxyribonucleic acids damaged by ultraviolet radiation. Molekulyamaya Biol. [Pg.38]

No results indicating genotoxicity were observed in in vitro studies that examined six organophosphate ester hydraulic fluids for gene mutation, deoxyribonucleic acid (DNA) damage, or chromosomal aberrations in eukaryotes (see summarized data in Table 2-11). [Pg.219]

DNA effects Damage to DNA (Deoxyribonucleic acid) by a chemical or material may result in genotoxic effects such as mutations, which in turn may lead to carcinogenicity. Damage to DNA causes the cell to manufacture new DNA to compensate for the loss or damage. This can be assessed by evaluating the formation of newly synthesized DNA. Unscheduled DNA Synthesis... [Pg.178]

Administration of single oral doses of 90 or 120 mg/kg mirex by gavage to female Sprague-Dawley rats resulted in induction of hepatic ornithine decarboxylase activity there was, however, no evidence of significant damage to deoxyribonucleic acid (DNA) as measured by alkaline elution (Mitra et al. 1990). [Pg.98]

Deoxyribonucleic acid (DNA) serves as a template for the synthesis of nucleic acids. Ribonucleic acid (RNA) executes protein synthesis and thus permits cell growth. Synthesis of new DNA is a prerequisite for cell division. Substances that inhibit reading of genetic information at the DNA template damage the regulatory center of cell metabolism. The substances listed below are useful as antibacterial drugs because they do not affect human cells. [Pg.274]

Nitrenium ions, particularly the arylnitrenium ions, have been proposed as intermediates in deoxyribonucleic acid (DNA) damaging reactions that can ultimately convert a normal cell into a cancer cell. Carcinogenesis is a complex phenomenon. [Pg.597]

Dean, C.J., Feldschreiber, P., Lett, J.T. (1966). Repair of X-ray damage to the deoxyribonucleic acid in Micrococcus radiodurans. Nature (London) 209,49-52. [Pg.146]

Rasmussen, R.E. Painter, R.E. (1964). Evidence for repair of ultra-violet damaged deoxyribonucleic acid in cultured mammalian cells. Nature (London) 203, 1360-1362. [Pg.148]

Arsenic has been shown to induce oxidative stress (Shi, Shi and Liu, 2004 Hughes and Kitchin, 2006). Oxidative stress is a result of an imbalance between reactive oxygen species and the ability of a cell s antioxidant defense apparatus to respond. Oxidative stress can result in the damage of proteins, lipids, RNA, and deoxyribonucleic acid (DNA). In addition, since oxidant species have a role in cell signaling, a state of oxidative stress could potentially alter signaling within and between cells. [Pg.262]

Figure 7.5 Example of a chimeric oligonucleic acid and its modification. Chimeric RNA-DNA hybrids are used for correction of point mutations in target genes. One strand of this oligonucleic acid is composed of O-methyl-RNA (outline) with an interruption of 5 bases of deoxyribonucleic acid. X and Y are target residues for correction. In the complementary strand, there is a DNA nick, and T residues loop both ends. 3 -exonuclease and FEN-1 may act on the nick, PARP-1 possibly binds to and is activated by the nick, resulting in activation of damage response pathways. In the modified version, the 3 end is replaced by ribonucleic acids. The 5 end is extended, and the flipped back RNA tail is added. Thus, the nick is expected to be resistant to 3 -exonuclease and FEN-1. In addition, PARP-1 may not be activated by such a nick. Figure 7.5 Example of a chimeric oligonucleic acid and its modification. Chimeric RNA-DNA hybrids are used for correction of point mutations in target genes. One strand of this oligonucleic acid is composed of O-methyl-RNA (outline) with an interruption of 5 bases of deoxyribonucleic acid. X and Y are target residues for correction. In the complementary strand, there is a DNA nick, and T residues loop both ends. 3 -exonuclease and FEN-1 may act on the nick, PARP-1 possibly binds to and is activated by the nick, resulting in activation of damage response pathways. In the modified version, the 3 end is replaced by ribonucleic acids. The 5 end is extended, and the flipped back RNA tail is added. Thus, the nick is expected to be resistant to 3 -exonuclease and FEN-1. In addition, PARP-1 may not be activated by such a nick.
Deoxyribonucleic acid (DNA) has limited chemical stability. As a result, oxidative damage, hydrolysis, and nonenzymatic DNA methylation occur in vivo at significant rates (L6). Thus, another aspect of this theory is that of intrinsic somatic mutations and the ability of cells to repair the damage to both mitochondrial and nuclear DNA. Indeed, mammalian cells have an elaborate system of DNA repair enzymes which become less efficient with time. Thus, failure to repair damaged DNA or to "misrepair it could lead to gene inactivation or possible excision of... [Pg.4]


See other pages where Deoxyribonucleic acid damage is mentioned: [Pg.244]    [Pg.244]    [Pg.487]    [Pg.228]    [Pg.297]    [Pg.13]    [Pg.895]    [Pg.86]    [Pg.334]    [Pg.197]    [Pg.64]    [Pg.186]    [Pg.191]    [Pg.52]    [Pg.11]    [Pg.155]    [Pg.95]    [Pg.450]    [Pg.460]    [Pg.464]    [Pg.500]    [Pg.75]    [Pg.5]    [Pg.116]    [Pg.228]    [Pg.33]    [Pg.27]   
See also in sourсe #XX -- [ Pg.452 ]

See also in sourсe #XX -- [ Pg.316 , Pg.320 , Pg.324 ]




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