1-1 (done perm) Flashcards
(36 cards)
(Triangle G not) does not predict what
why
behavior of rxn under physio condition
[ ] are rarely close to 1 M in cell
what is the thing that is calculated for physio condition then?
net (triangle G) for pathway
As long as sum of (triangle G) in a pathway is “”, the rxn can proceed
negative
Most ATP is produced how
via aerobic metabolism in mitochondria
mito
- starting pt FOR
- ending “”
st=biosynthesis
end=degradative
in net rxn in aerobic bio system is “” of substrates
oxidation
reduced def
oxidized “”
another def
red=MORE e
ox=FEWER e
red=gains bond to H OR loses bond to oxygen
ox=gains bond to oxygen OR loses bond to H
respiratory quotient def
RQ of 1 suggests that substrate utilization is mostly (fat/carb)
less than 1?
C02 produced divided by (02 consumed)
1-carb
less than 1-fat/protein
what’s the dif bt ATP, ADP, and AMP
ATP=3 P’s
ADP=2 P’s
AMP=1 P
most cells contain mitochondria - exception is
RBC
which membrane has HIGH protein content
inner membrane
energy carrying molecules are (reduced/oxidized)
reduced
presence of ADP (up/down) regulates oxidative phosphorylation
UP
what is complex 1 called (in ETC)
NADH dehydrogenase
the ensuing complexes (in the ETC) are called
cytochromes
ATP synthesis via ETC is called
chemiosmotic mec
for each molecule of NADH, # ATP are synthesis
3
how efficient is ETC (%)
about 40%
what’s the role of UCP
result
create protein leak (protons flow DOWN gradient without ATP being produced) SO there is greater heat production
UCP1 is called ?
function
thermogenin
heat production in brown fat of mammals
read: adults don’t have a lot of UCP1
-
Anaerobic vs aerobic ATP dif
An-2 ATP
Ae-38 ATP
energy is stored in muscles HOW (give eq)
rxn catalyst
how does this change under ANaerobic conditions
ATP + creatine -> ADP + phosphocreatine
CPK
PC donates phosphate to ADP (aka PC becomes source of ATP during ANaerobic conditions)
damaged muscle releases “” into serum (this is how we know person has myocardial infarction)
CPK-MB