By Steven Akman, Regen Drouin, Gerald Holmquist (auth.), Miral Dizdaroglu, Ali Esat Karakaya (eds.)
Damage to DNA by means of either exogenous and endogenous resources is more and more considered as hugely vital within the initiation and development of melanoma and within the occurance of alternative pathological occasions. DNA harm brought on by reactive oxygen-derived species, also referred to as oxidative DNA harm, is so much the widespread kind encountered through cardio cells. Mechanistic stories of carcinogenesis point out an incredible function of this sort of harm to DNA. there's additionally powerful proof to aid the function of oxidative DNA harm within the getting older method. DNA harm is adverse in vivo through fix structures. If now not repaired, DNA harm could lead on to harmful organic effects. for this reason, the fix of DNA harm is considered one of many crucial occasions in all lifestyles types. in recent times the sphere of DNA fix has flourished as a result of new findings on DNA fix mechanisms and the molecular foundation of melanoma. an in depth wisdom of mechanisms of DNA harm and service, and the way person fix enzymes functionality could lead to manipulation of DNA fix in cells and eventually to a rise of the resistence of human cells to DNA-damaging brokers. This quantity covers the latest devlopments during this examine box and comprises contributions from scientists operating within the fields of biochemistry, molecular biology, enzymology, biomedical technology, and radiation biology.
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Additional resources for Advances in DNA Damage and Repair: Oxygen Radical Effects, Cellular Protection, and Biological Consequences
In the Fenton mechanism, oxidative stress could cause release of catalytic copper or iron within cells which could then bind to DNA. Metal ions are naturally occurring metal constituents of the cell nucleus (Pezzano 1980, Bryan et al 1981). Generation of OR' by reaction of H 20 2 with the transition metal ions already bound onto the DNA would lead to strand breakage, base modification and deoxysugar fragmentation. In the nuclease activation mechanism, oxidative stress leads to the inactivation of Ca 2+-binding 22 O.
Pratt (1993). Ind. Health 9: 63-75. B. G. M. G. So (1980). Degradation of deoxyribonucleic acid by a I, I O-phenanthrolinecopper complex: the role of hydroxyl radicals, Biochemistry 19: 5987-5991. K. A. E. R. S. Sigman (1981). Cleavage of DNA by the phenanthroline-copper ion complex. Superoxide mediates the reaction dependent on NADH and hydrogen peroxide, J. Am. Chem. Soc. 103: 3582-3584. D. M. Schaefer, Q. Liu, C. -C. Yin (1995). Supranutritional administration of vitamins E and C improves oxidative stability of beef, J.
It is possible that under certain conditions the BLM-Fe(III)-02 - might decompose to yield 02'-' and BLMFe(III)-02H- to release OR (Sugiura et al. 1982, Petering et al 1990). Hydroxyl radical is not necessarily the major DNA damaging species in the bleomycin system. The bleomycin-iron(III) complex by itself is inactive in inducing damage in DNA. Oxygen and a reducing agent or hydrogen peroxide are required for the damage to DNA to occur. DNA cleavage by bleomycin releases some free bases and base propenals in amounts that are stoichiometric with strand cleavage (Burger et al 1981, Giloni et al 1981).