DNA Repair Mechanisms

DNA repair is a collection of processes by which a cell identifies and corrects damage to the DNA molecules that encode its genome. In human cells, both normal metabolic activities and environmental factors such as radiation can cause DNA damage, resulting in as many as 1 million individual molecular lesions per cell per day. (1)

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DNA damage resulting in multiple broken chromosomes

 

Many of these lesions cause structural damage to the DNA molecule and can alter or eliminate the cell’s ability to transcribe the gene that the affected DNA encodes.

Other lesions induce potentially harmful mutations in the cell’s genome, which affect the survival of its daughter cells after it undergoes mitosis. As a consequence, the DNA repair process is constantly active as it responds to damage in the DNA structure.

When normal repair processes fail, and when cellular apoptosis does not occur, irreparable DNA damage may occur, including double-strand breaks and DNA crosslinkages (interstrand crosslinks or ICLs).[2][3]

a b Acharya, PV (1971). “The isolation and partial characterization of age-correlated oligo-deoxyribo-ribonucleotides with covalently linked aspartyl-glutamyl polypeptides”. Johns Hopkins medical journal. Supplement (1): 254–60. PMID 5055816.

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a b Bjorksten, J; Acharya, PVN; Ashman, S; Wetlaufer, DB (1971). “Gerogenic fractions in the tritiated rat”. Journal of the American Geriatrics Society. 19 (7): 561–74. doi:10.1111/j.1532-5415.1971.tb02577.x. PMID 5106728.

This can eventually lead to malignant tumors, or cancer as per the two hit hypothesis.

The rate of DNA repair is dependent on many factors, including the cell type, the age of the cell, and the extracellular environment. A cell that has accumulated a large amount of DNA damage, or one that no longer effectively repairs damage incurred to its DNA, can enter one of three possible states:

1an irreversible state of dormancy, known as senescence

2cell suicide, also known as apoptosis or programmed cell death

3unregulated cell division, which can lead to the formation of a tumor that is cancerous

The DNA repair ability of a cell is vital to the integrity of its genome and thus to the normal functionality of that organism. Many genes that were initially shown to influence life span have turned out to be involved in DNA damage repair and protection.[4]

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Browner, WS; Kahn, AJ; Ziv, E; Reiner, AP; Oshima, J; Cawthon, RM; Hsueh, WC; Cummings, SR. (2004). “The genetics of human longevity”. Am J Med. 117 (11): 851–60. doi:10.1016/j.amjmed.2004.06.033. PMID 15589490.

 

 

 

 

 

 

 

2015 Nobel Prize in Physiology (Medicine)

The 2015 Nobel Prize in Chemistry was awarded to Tomas Lindahl, Paul Modrich, and Aziz Sancar for their work on the molecular mechanisms of DNA repair processes.[5][6] There are two types: nucleotide excision repair and base excision repair.

DNA Repair Mechanisms

More on this topic

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Reference and Precision Notes

1 Lodish H, Berk A, Matsudaira P, Kaiser CA, Krieger M, Scott MP, Zipursky SL, Darnell J (2004). Molecular Biology of the Cell (5th ed.). New York: WH Freeman. p. 963.

5 Broad, William J. (7 October 2015). “Nobel Prize in Chemistry Awarded to Tomas Lindahl, Paul Modrich and Aziz Sancar for DNA Studies”. New York Times. Retrieved 7 October 2015.

6 Staff (7 October 2015). “The Nobel Prize in Chemistry 2015 – DNA repair – providing chemical stability for life” (PDF). Nobel Prize. Retrieved 7 October 2015.

 

 

 

 

 

 

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