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Lab Report Example

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Lab Report DNA in the living cell is subject to damage by both endogenous and exogenous agents. The endogenous sources of DNA damage include the Reactive Oxygen Species (ROS) formed during oxidative metabolism, aldehydes derived from lipid peroxidation, some oestrogen metabolites, and many metabolites that can act as methylating agents (De Bont and van Larebeke, 2004)…
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Download file to see previous pages DNA double-strand breaks (DSBs) represent the most dangerous type of DNA damage since a single DSB is capable of causing cell death or disturbing the genomic integrity of the cell (Jackson and Bartek, 2009). DSBs are difficult to repair and extremely harmful (Khanna and Jackson, 2001). DSBs generally form when two single-strand breaks (SSBs) occur in close proximity, or when a SSB or certain other lesions are encountered during DNA-replication (Jackson and Bartek, 2009). Ionising radiation (IR) and chemotherapeutic compounds used in cancer also generate DSBs. Mediated by DSBs, DNA lesions develop as a result of recombination between different loci (Kongruttanachok et al., 2010). Thus, a cell constantly faces the risk of DNA damage caused exogenously as well as from an incorrect incorporation of base pairs occurring during normal replication. The chemical changes occurring in the DNA structure, therefore, must be corrected in order to preserve the encoded genetic information. Mechanisms of DNA damage repair exist which involve systems that detect DNA damage, signal its location and bring about the repair. The DNA-damage responses (DDR) are physiologically very important as each of the nearly 1013 cells in the human body experiences innumerable DNA lesions per day (Lindahl and Barnes, 2000). Nuclear Excision Repair (NER) is a repair mechanism in the cell to deal with DNA damage caused exogenously by UV rays and ionizing radiation, besides other types of chemical alteration to the DNA (Wood, 1997). Mismatch repair (MMR) is an evolutionarily conserved DNA damage fixing process that is employed by the cell when base pairs are added incorrectly during replication (Kunkel and Erie, 2005). At least ten different DNA repair processes are operative in higher organisms (Reed, 2010). Platinum-based compounds e.g., cisplatin, oxaliplatin, satraplatin etc. interfere with the repair mechanisms to effect programmed cell death, or apoptosis. For example, cisplatin when introduced into the nucleus, forms adducts (Fichtinger-Sherpman, et al., 1985). The formation of the bulky adducts causes torsional strain on the DNA strand prompting the cell to invoke the NER and/or the Mismatch repair enzymes. However, the repair mechanisms are generally unable to effectively correct the damage as the platinum adduct is a non-native structure, and this leads to permanent DNA damage causing apoptosis of the potentially defective cell (Agarwal et al., 1998). The inactivation of repair processes could have wide-ranging consequences, both beneficial and detrimental. In the context of the former, DNA damage and repair has been the major target of anticancer therapy. Serious attempts are being made to modulate these processes in order to improve their efficacy in the treatment of cancer (Reed, 2010). While DSBs are processed by a number of DNA repair pathways depending partly on the phases of the cell cycle, NER is the only mechanism known to remove bulky DNA adducts, including those formed by platinum-based anticancer drugs, from human cells (Readon et al., 1999). A majority of DSBs are repaired by non-homologous end-joining repair (NHEJ) mediated by either ...Download file to see next pagesRead More
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