Lecture 22: Aging Flashcards
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
peroxidation index vs maximum life span of species
- long-lived species tend to have lower peroxidation indexes, suggesting reduced membrane damage
what we lose with age
- telomeres: end caps that protect the chromosome
relationship between age and telomere length in birds
- all species (zebra finches, barn swallows, and Adelie penguins) exhibit a negative correlation between age and telomere length, emphasizing that telomeres shorten as birds age
rates of telomere shortening predicts life span
- species with slower rates of telomere shortening tend to live longer, both in maximum and average lifespans
body size x maximum lifespan across various animal species
- the larger the body size, the longer the maximum lifespan
- the naked mole rate has smaller body size and lives longer than expected
- humans are larger in size and live longer than expected
- elephants are very large and show a long lifespan
naked mole rat
- can live up to 29 years
- social animals, living in colonies
- polygamous: multiple mates
what adaptations do naked mole rates have that allow them to live so long?
- adaptations
comparison of hydrogen peroxide production in the mitochondria of mice vs mole rate in different tissues including the heart, skeletal muscle, kidney
heart tissue: naked mole rats produced significantly more H2O2 in heart mitochondria compared to mice; might seem unusual as higher H2O2 levels are typically associated with oxidative stress, but naked mole rates
skeletal muscle tissue: mice show higher H2O2 production than naked mole rates in skeletal muscle mitochondria; this aligns with the naked mole rat’s well known lower metabolic rate and efficient oxidative processes
kidney tissue: mice again have higher H2O2 production in kidney mitochondria relative to naked mole rats
reduction process of the electron transport chain: enzymes that play a pivotal role in protecting cells from oxidative stress by neutralizing reactive oxygen species
superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT)
superoxide dismutase (SOD)
converts harmful superoxide radicals into hydrogen peroxide and oxygen effectively reducing the damage caused by these reactive molecules
glutathione peroxidase (GPX)
further detoxifies hydrogen peroxide into water using reduced glutathione (GSH), a key antioxidant
catalase (CAT)
breaks down hydrogen peroxide into water and oxygen, preventing accumulation that could harm cells
telomerase
enzyme that rebuilds the protective caps (telomeres) on chromosomes, preventing them from shortening during cell division
telomerase activity in mice
decreases with age, leading to shorter telomeres and aging related effects
