Lecture 22: Aging Flashcards
(39 cards)
life history trade offs
small clutch size, slow growth rate = longer lifespans and lower life history traits
large clutch size, fast growth rate = shorter lifespan and higher life history traits
tradeoffs
- larger clutch size = lower adult survival
- smaller clutch size = higher adult survival
Pace of life: “fast living”
- juveniles mature quickly
- short life span
- large number of offspring
- high mortality
- minimal parental care
examples of “fast living” species
rodents, marsupials
semelparity
- characterized by a single reproductive event, after which most adults die
- extreme level of “fast living”
example of semelparity
- antechinus marsupial
- 2 week mating season, body tissue disintegrates over time, and they die
pace of life: “slow living”
- juveniles mature slowly
- long life span
- few number of offspring
- low mortality
- high parental care
examples of “slow living” species
elephants
survivorship curves
Type I = species like humans and elephants exhibit high survival in early and middle life, with significant mortality in old age
Type II = species like lagomorphs (rabbits) have a constant rate of survival/mortality across their lifespan
Type III = species like frogs experience high early life mortality, but survivors tend to live much longer thereafter
disposable soma theory of aging
a biological theory proposing that organisms allocate energy between reproduction and bodily maintenance, influencing aging and lifespan
disposable soma theory of aging graph
A: more resources are devoted to growth and reproduction the expense of anti-aging repair mechanisms, leading to a shorter lifespan
B: resources allocated toward anti-aging repair rather than growth and reproduction, resulting in a longer lifespan
mechanisms of aging
oxidative damage and telomere shortening
oxidative damage
refers to harm caused by free radicals, which are unstable molecules that can damage cells and contribute to aging
telomere shortening
involves the gradual reduction of protective end caps on chromosomes (telomeres) with each cell division, limiting a cell’s lifespan
oxidative stress and free radical damage
- production of free radicals and hydrogen peroxide by mitochondria
- resulting oxidative stress can damage cellular structures like proteins and membranes
hydrogen peroxide
a reactive molecule produces during cellular metabolism that can contribute to oxidative stress
mitochondrial DNA damage and oxidative stress
- reactive oxygen species (ROS) generation: the mitochondria produce ROS as a byproduct of electron transport
- components involved: NADH, FMN, FeS, O2, Q, CIII, CIV, and H2O2
- formation of 8-oxodG and MDA: damage to mitochondrial DNA leads to the production of 8-oxodG fragments and malondialdehyde (MDA), contributing to oxidative stress
- ROS and H2O2 accumulate in the intermembrane space
free radicals
one electron in orbit, very unstable
antioxidants can
neutralize free radicals
ROS impact on membrane
- liquid peroxidation
- damage to membranes and lipoproteins
ROS impact on DNA
- DNA strand breaks
- mutations leading to cancer
ROS impact on proteins
- aggregation and fragmentation
- enzyme inhibition
ROS impact on membrane, DNA, proteins lead to
oxidative stress, disease and aging
relationship between longevity and H2O2 production
- species with longer life spans tend to have lower rates of H2O2 production