MEDRADSC 3U03 Lecture Notes - Lecture 3: Genetic Disorder, Heteroduplex, Ataxia Telangiectasia

• School: McMaster University
• Department: Medical Radiation Sciences
• Course: MEDRADSC 3U03
• Professor: Cathy Hayward

Document Summary

There are a tremendous number of factors which influence cell killing. Effect results from the repair of sub-lethal damage that occurs during a long radiation exposure. With low let radiation, dose-rate is one of the principle factors at determining biologic consequences of the absorbed dose: as the dose-rate is lowered, and exposure time extended, the biologic effect of the dose is reduced. As dose-rate is reduced the slope of the curve becomes progressively more shallow. Mammalian cells experience an average of 100,000 dna lesions/day: replication errors, chemical decay of bases, attack by ros, exposure to mutagens (i. e. ir) Ionizing radiation can induce: base damage, single-strand breaks, double-strand breaks, sugar damage, dna-dna and dna-protein crosslinks. Cells have developed specialized pathways to sense, respond to and repair these different types of damage. Reversal of damage: specific enzymes for specific (common) damage, e. g. alkyl transferase. Base excision repair: single nucleotide (apurinic/apyrimidinic) Nucleotide excision repair (ner: patch excision.