programmed cell death - cells between fingers/toes die
- 1/2 of neurons created never make connections, eventually die
- required for proper development
- necrosis - cells that die due to injury, releases contents into extracellular fluid
- apoptosis - cell programmed to die shrink/shrivel, remains taken up by other cells
- bax proteins starts apoptosis by binding to permeable pores of mitochondria
- bcl-2 prevents cell death by preventing damange from free radicals (highly reactive atomic fragments)
- antioxidants - proteins, other molecules that destroy free radicals
aging theories - puberty is safest time to live
- accumulated mutation hypothesis - oldest general theory about aging
- accumulation of mutations >> lethal death
- OH group tends to be added to guanine base as cells age
- effects of radiation-induced mutations after Hiroshima/Nagasaki bombings show no correlation between aging and mutations
- telomere depletion hypothesis - older cells have shorter telomeres
- telomere - repeated TTAGGG sequence
- portion of telomere cap lost w/ each replication
- cancer cells avoid telomeric shortening
- adding to telomeric caps increased number of times cells could perform DNA replication
- wear-and-tear hypothesis - cells wear out, get damaged through age
- damage over time limits cell’s ability to work properly
- free radicals - atomic fragments containing an unpaired electron, produced by oxidative metabolism, can damage cells
- glycation - process that causes glucose to link to proteins, reducing flexibility
- gene clock hypothesis - people over 100 years of age more likely to have mutated C150T mitochondrial DNA
- Werner’s syndrome - causes premature aging, found on chromosome 8, affects helicase enzyme in DNA repair
- current aging theories - still no true mechanism for counting
- connection found between aging, signaling from insulin-like receptors
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