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DNA damage occurring in oocytes, if not repaired, can be lethal and result in reduced fecundity and loss of potential progeny. Oocytes are substantially larger than the average somatic cell, and thus considerable metabolic activity is necessary for their provisioning.
Degenerated oocytes are classified as damaged oocytes or oocytes without a zona pellucida. [6] Dysmorphic oocytes are oocytes with abnormal physical characteristics, for example multiple nuclei. [7] EFS is a condition occurring when no oocytes are produced from the mature follicle after ovulation is induced in cycles of in vitro fertilisation ...
When there is too much damage, apoptosis is triggered in order to protect the organism from potentially harmful cells.7 p53, also known as a tumor suppressor gene, is a major regulatory protein in the DNA damage response system which binds directly to the promoters of its target genes. p53 acts primarily at the G1 checkpoint (controlling the G1 ...
If a cell retains DNA damage, transcription of a gene can be prevented, and thus translation into a protein will also be blocked. Replication may also be blocked or the cell may die. In contrast to DNA damage, a mutation is a change in the base sequence of the DNA.
Nucleotide excision repair (NER) is a particularly important excision mechanism that removes DNA damage induced by ultraviolet light (UV). UV DNA damage results in bulky DNA adducts — these adducts are mostly thymine dimers and 6,4-photoproducts. Recognition of the damage leads to removal of a short single-stranded DNA segment that contains ...
Cell damage (also known as cell injury) is a variety of changes of stress that a cell suffers due to external as well as internal environmental changes. Amongst other causes, this can be due to physical, chemical, infectious, biological, nutritional or immunological factors. Cell damage can be reversible or irreversible.
The species with longer lifespans were found to have slower accumulation of DNA damage, a finding consistent with the DNA damage theory of aging. [119] In healthy humans after age 50, endogenous DNA single- and double-strand breaks increase linearly, and other forms of DNA damage also increase with age in blood mononuclear cells. [ 120 ]
Melanoma cells are commonly defective in postreplication repair of DNA damages that are in the form of cyclobutane pyrimidine dimers, a type of damage caused by ultraviolet radiation. [ 11 ] [ 12 ] A particular repair process that appears to be defective in melanoma cells is homologous recombinational repair. [ 12 ]