Temperature Flashcards
poikilotherms
body temp fluctuates with ambient environmental temps
- as temp inc-> MR inc
- as temp dec-> MR dec
ectotherms
heat input is obtained from outside organism
- lower vertebrates and invertebrate
homeotherms
maintain relatively constant body temp despite changes in ambient temp
- dec temp after critical temp-> inc MR
- inc MR-> inc heat production to maintain a constant body temp
endotherm
where animals use internal metabolic heat production
- birds and mammals
thermoneutral zone
- at high temp within this range, MR are lower than expected
- at lower temp, they’re higher than expected
- at critical temp, theres a point where MR must inc in order to maintain a constant temperature
MR of poikilotherms in Antarctic vs tropics
MR are about the same
- MR are similar in the different species at their respective ambient temp
- MR still inc with inc temp
how do enzymes get around effects of temperature
1) change in enzyme concentration
2) change in type of enzyme
3) modulate enzymes
how do enzymes adapt to be more efficient
- changes in catalytic efficiencies (Vmax = Kcat[E])
- via enzyme-substrate affinities
- inc Vmax= inc enzyme efficiency
0 Vmax greater in cold adapted species, activation energy lower too
Catalytic efficiency (Kcat)
how efficient is the enzyme in converting substrate to product per unit time
- enzymes from cold adapted apecies are more catalytically efficient–> lower activation energies (greater Kcat= greater Vmax)
enzyme-substrate affinities
cold adapted species have lower Km values–> greater substrate affinities–> more of that reaction will occur
modulate enzymes
- change in substrate concentrations
- change in Km and/or catalytic efficiencies
- cofactors
- microenvironments, pH, ion, membrane composition
- general modulation, positive or negative (ex; ATP, metabolic products, etc)
- Temperature (Km is temp dependent, Km dec with dec temp, to a point then it inc again)
isozymes
same enzyme, diff structure–> can be altered with temp diff (ex: one active in cold, one active in warm)
freeze damage
- primarily due to cell dehydration
- most animals cannot withstand freexing
- intracellular ice is lethal
- most freezing is extracellular but this causes damage due to dehydration of cell
cell dehydration
desiccation results in low water inside cell–> call volume dec–> solutes precipitate out–> membranes rupture–> protein denaturing occurs–> protein-protein interaction occurs
mechanisms to escape injury due to subzero temps
- behavioral avoidance
- rapid cold hardening
- cold acclimatization (avoid ice: inc supercooling ability, for freeze susceptible species; become freeze tolerant)
- developmental preparedness
what animals have a problem with freezing
animals that will freeze and animals that won’t
- isosmotic to sea water won’t freeze unless all SW freezes
- hyperosmotic to FW won’t freeze
- salt water teleost are hyposmotic to SW-> their FP are above SW-> have a problem with freezing
- terrestrial organisms encountering subzero temps may freeze
marine teleost
freezing
- supercool to -1.9 degrees C
- OK if don’t come into contact with ice
- behavioral avoidance: migration to deeper water
- use antifreeze proteins to depress FP
Antifreeze proteins
how does it work, what does it produce
- don’t depress FP by colligative means
- directly binds to ice (adsorbs to ice) and prevents further ice growth
- produce a thermal hysteresis (a difference between the melting point and freezing point of a solution
Thermal Hysteresis Proteins
AFPs = THPs
- coat ice seed crystal
- possess ice binding domain (IBM)
- through adsorption-inhibition, a non-colligative freezing point depressive activity ensues
- can dec FP belowS SW, without inc blood osmolarity
- produced in response to short photoperiod
seasonal regulation of AFP
growth hormone prevents production of transcription factors necessary to produce antifreeze–> GH not present = antifreeze can be produced (winter)
terrestrial environments
- more severe temps
- need cold acclimatization and other overwintering adaptations
- 2 strategies: supercooling and freeze tolerant
methods to inc supercooling ability
1) production of Polyols
2) Antifreeze proteins
3) removal of ice nucleating agents
Polyols
- Polyhydroxy alcohols
- called small MW antifreezes
- dec FP on colligative basis
- dec supercooling point on colligative basis
- inc osmolarity
- regulated by low temp switching of biosynthetic pathways
removal of Ice nucleating agents
- must be done to allow for supercooling
- ex: emptying gut in anticipation of winter
- eliminating any nucleating macromolecules
- masking ice nucleators
- AFPs may mask INAs
Successful supercooling
- involves all 3 methods to dec SCP
- polyols
- AFPs
- removal or masking of INAs
- with freeze susceptible species, freezing is lethal-> must remain supercooled in freezing temps
- supercooling is unstable, duration is a challenge
Freeze hardy species
- various invertebrate, especially insect, some lower vertebrates
- produce cryoprotectants and other chemicals which prevent desiccation
- In these species, the temp at which they freeze (SCP) is higher than their lower lethal temps
freeze tolerant methods
- produce cryoprotectants: Polyols
- may produce ice nucleating agents
- may use AFPs to inhibit recrystallization
0 inc blood bound water
cryoprotectants
- small mw cryoprotectants
- dec water loss by reducing osmotic gradient and inc viscosity
- helps maintain cell volume
- acts as solvent like water
- dec amount of ice at a given time
- dec osmotic stress
Ice nucleating proteins
- like antifreeze proteins
- some species produce proteins that will nucleate ice at relative high subzero temps–> allows them to control rate of freezing (limits osmotic shock)
recrystallization
during the melt, the growth of large ice crystals at expense of smaller ones
- slow thaws can cause membrane damage
- large ice crystals can shear membranes
- AFPs can block or limit the extent or recrystalization
mechanisms of heat gain
- metabolic heat production
- conduction (gain or loss)
- Radiation (gain or loss)
conduction
transfer of heat between two objects in contact
convection
transfer of heat to a fluid in movement
radiation
electromagnetic radiation emitted/recived
mechanisms of heat loss
- conduction (gain or loss)
- radiation (gain or loss)
- Evaporation (mostly heat loss)–> cutaneous and respiratory
to maintain constant body temp…
heat gain=heat loss
Metabolic heat+/- heat conduction +/ heat radiation +/- heat evaporation and +/- heat of storage
mechanisms of heat control
- metabolic rate
- insulation
- vascular control
- evaporation
- behavior
behavioral mechanisms
- migrations
- basking
- aggregation
- evaporation
heat in Aquatic organisms
- no evaporation
- Coefficient of K is very high for water–> lots of heat loss
- heat exchange between gills and tissues
- countercurrent heat exchangers at swim muscles
Cardiovascular control for aquatic organisms
shunting blood flow through heat exchangers or periphery, inc blood flow through rete mirabile to inc heat loss at higher temps
mechanisms of thermogenesis in homewotherms
- inc voluntary activity
- shivering
- non-shivering thermogenesis
- brown adipose tissue -
non-shivering thermogenesis
- involves Na+/K+ active transport
- ATP is used up and excess energy foes to heat–> inc gradients
Thyroid hormone
turns on Na+/K+ ATPases to generate heat
- also inc MR independently
Brown Adipose Tissue (BAT)
- only in mammals
- sole purpose is for heat production
- high number of mitochondria
- high cytochrome–> consumes oxygen at great rate–> heat production (uncouples oxidative phosphorylation)
- accumulated seasonally and in new borns
- site of nonshivering thermogenesis
Where is BAT found
around body organs and upstream from them so the blood flows from BAT to organs
neural control of BAT
- epinephrine produced by adrenal meulla
- works via cAMP
purpose of BAT
- uncouples oxidative phosphorylation which produces ATP–> energy goes to heat
- turns on ATPases
- cycling of carbon sources and ATP splitting–> heat
- proton transport system
- Uncoupling Protein 1 (UCP1) aka thermogenin in inner membranes of medulla
adaptations of homeotherms to high temp
- heat dissipation
- condution (seasonally vary insulation)
- peripheral vasodilation–> inc heat loss
- don’t normally dec MR with inc temp but behavioral activity may dec
- evaporation (respiratory surface)
- perspiration–> sweat glands in mammals
- heat storage
problem with panting
- causes hyperventilation–> respiratory alkalosis (gives off a lot of CO2, throws of acid base balance
- involves muscular activity
problem with perspiration
loss of salts and water
temperature sensors
- peripheral sensors
- core body temp sensors (monitor organs)
- CNS (temp sensitive regions)
- Hypothalamus= master control–> itself temp sensitive, receives input from everything else
hypothalamus acts like thermostat
- temp set points(when temp goes above these compensation is initiated)
1) shivering
2) nonshivering thermogenesis
3) hormonal *thyroid hormone and epinephriine in BAT)
fevers
what is it
- set points are reset to higher temp by proteins called pyrogens (released be leucocytes)
- temp regulating systems don’t kick in
salicylates
- in asprin
- reset set poin temp back where it should be
are fevers functional
- fight disease
- inc WBC mobilization
- inc lyphocyte activity
behavioral fever in fish
bacterically infected fish will choose higher temp in a thermal gradient
hibernation and daily torpor
- high energetic cost to maintain constant body temp in cold
- set points changed from 37C to 2-3C
- if temp goes near freezing animals will wake up
entry into torpor
- T ambient below critical temp
- dec MR-> dec Tbody
- inc fat accumulation
during hibernation and torpor
- dec heart rate
- dec MR
- repiration and ventilation rates are sporadic
- dec T body
- dec functions
process of arousal
- considerable energy expenditure
- vital organs warm fastest
- BAT
- violent shivering
- inc T body
control of entry into hibernation/daily torpor
-photoperiod
- temp
- lack of food
- circannual rhythms
duration of hibernation/ daily torpor
arrousal at temp 0, requires BAT
