LECTURE 31 Flashcards

CHECK ON LEARNING

1
Q

enzymes are considered _____?

A

catalysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

enzymes do this to spontaneous reactions?

A

accelerate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what do enzymes do to the transitional state so that the reaction can occur?

A

lowering the energy state

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how do spontaneous reactions occur more rapidly?

A

increase substrate

decrease product energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

how do enzymes accelerate the reactions?

A

by stabilizing the transitional state with van der waals, electrostatic and hydrogen bonds decreasing the activation energy

bring substrate molecules into close proximity with each other

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what is total activity in reference to enzyme activity?

A

specific activity x amt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

how is the specific activity of enzymes measured?

A

international units

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

how does activity get changed for an enzyme?

A

change amount of enzyme present

change specific activity of existing enzyme molecules via feedback inhibition, regulatory proteins, enzyme phosphorylation, proteolytic activation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what is a common example of regulatory proteins?

A

calmodulin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

name the two examples of enzyme phosphorylation?

A

kinases

phosphorylation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what is the significance of K1? K2 and K3?

A

KI is a measure of the rate of formation of ES

causes ES to disappear

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what is the measure of affinity? what is this known as?

A

the rate of disappearance of ES (K2+K3) and divided by the rate of formation of ES (K1)

michaelis constant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what does low Km mean?

A

low Km means high affinity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

high affinity means what kind of Km?

A

low Km

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

low affinity means what kind of Km?

A

high km

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Km is the substrate concentration that produces what type of velocity?

A

half maximal velocity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

how is enzyme kinematics graphed?

A

double reciprocal or lineweaver burke plot

18
Q

how do high and low affinity enzymes look on a double reciprocal plot?

A

Vmax is the same for each, high affinity enzyme has a lower Km so -1/km will be a larger negative number

19
Q

this type of inhibitor competes for binding at the active site?

how is affinity and Km affected?

A

competitive inhibitor

affinity is decreased and km is increased

20
Q

this type of inhibitor binds at sites other than the active site, so they don’t change affinity for substrate, what happens to the rate of the reaction of Vmax?

A

decrease Vmax

21
Q

what is needed to help facilitate enzyme catalyzed reactions?

A

cofactors or coenzymes, i.e. vitamins

22
Q

what is the job of the cells?

A

sense
survive
respond
reproduce

23
Q

any response by a cell is a change in what?

A

total activity

total activity=specific activity x amount

24
Q

what does signaling mean for a cell? what are the examples?

A

information is being transferred from one place to another and that it brings about a response

direct electrical communication
chemical signals

25
Q

t/f, chemical signals are faster than electrical signals?

A

f, slower than electrical

26
Q

what are the three examples of chemical signals, name any subclasses?

A

neurotransmitters
hormones like polypeptides (insulin, somatotropin, IGF-1, FSH) and steroids (cortisol, estradiol, aldosterone)
local signals like paracrine (NGF, histamine, PGs, Kinins) and autocrine (adenosine)

27
Q

what is the response like for the polypeptides and steroids?

A

faster onset
short acting

slow onset
long acting

28
Q

these hormones alter the specific activity primarily, faster onset, shorter duration response

A

polypeptides (insulin, somatotropin, IGF-1, FSH)

29
Q

these hormones alter gene expressions primarily, so slower onset and longer duration response

A

steroids (cortisol, estradiol, aldosterone)

30
Q

these local signals are released by one cell and affect neighboring cells. Onset and duration varies

A

paracrine (NGF, histamine, PGs, Kinins)

31
Q

these local signals affect the behavior of the cell that released them; fast onset and duration varies

A

autocrine (adenosine)

32
Q

what type of hormone are the hydrophilic signals?

A

polypeptide hormones

33
Q

T/F, lipophilic signals are polypeptide hormones? how are these signals associated with total activity?

A

steroid hormones

total activity=specific activity (hydrophilic signals) x amount (lipophilic signals)

34
Q

what are examples of paracrine?

A

histamine

PGs
Thromboxanes
Leukotrienes
aka “eicosanoids”

35
Q

which of the eicosanoids are being constantly released? what are the eicosanoids made from?

A

PGs

arachidonic acid cleaved from membrane phospholipids by phospholipase A2 stimulated by:

epinephrine
bradykinin
thrombin
angiotensin II

36
Q

so we know eicosanoids come from arachidonate, what are the enzymes used to make them?

A

lipooxygenase to produce HPETE to produce LTs

cyclooxygenase to produce PGG then peroxidase to produce PGH, both activities fall under the same enyzme (PG synthase) then on to PGs and TBs (via thromboxane synthase)

37
Q

what is cyclooxgenase inhibited by?

A

aspirin, ibuprofen and indomethacin

38
Q

what do thromboxanes promote?

A

vasoconstriction and platelet aggregation

39
Q

what do prostaglandins promote?

A

platelet aggregation

40
Q

what do leukotrienes promote?

A

bronchoconstriction and vascular permeability

41
Q

what inactivates PGs responses?

A

15-hydroxyprostaglandin DHase (metabolizes eicosanoids) and cyclo oxygenase (destroys self)