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Class Two Flashcards

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1
Q

what is a monosaccharide

A

single carbohydrate molecule aka simple sugar

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2
Q

monosaccharide general formula

A

CnH2nOn

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3
Q

bond between two sugar molecules

A

glycosidic linkage

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4
Q

glucose + fructose

A

sucrose

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5
Q

galactose + glucose

A

lactose

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6
Q

characteristics of a glycosidic linkage

A

covalent bond

formed in a dehydration reaction (requires enzymatic catalysis)

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7
Q

difference between alpha and beta glycosidic linkages

A

alpha: anomeric C is pointing down (below the plane)
beta: anomeric C is pointing up (above the plane)

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8
Q

what is glycogen

A

polysaccharide

energy storage for animals, thousands of glucose units joined together

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9
Q

what is starch

A

same as glycogen but for plants

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10
Q

what is cellulose

A

polymer of cellobiose

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11
Q

how to turn polysaccharides → monosaccharides? is it favoured?

A

hydrolysis

thermodynamically favoured

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12
Q

why is hydrolysis of polysaccharides important?

A

allows for the monosaccharides to enter metabolic pathways & be used for energy by the cell

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13
Q

mammalian enzymes can’t hydrolyze…? and what is the exception?

A

B-glycosidic linkages

can digest lactose with lactase

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14
Q

lactose malabsorbers

A

people without lactase (most people naturally stop making this enzyme after breast feeding)

their lactose ends up in the colon → causes gas + diarrhea

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15
Q

why is the high activation energy of polysaccharide hydrolysis relevant

A

use enzymes as gatekeepers - when we need it, we use it

if the Ea was very low, the polysaccharides would hydrolyze spontaneously - very unstable

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16
Q

the oxidation of glucose is accompanied by..

A

the reduction of high energy-electron carriers

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17
Q

what is NAD+

A

nicotinamide adenine dinucleotide

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18
Q

what is FAD

A

flavin adenine dinucleotide

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19
Q

how do NAD+ and FAD work

A

they accept high-energy electrons during redox reactions (forming NADH and FADH2)

they are later oxidized when they deliver the electrons to the ETC

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20
Q

main function of NAD+ and FAD

A

generation of the proton gradient that is used to generate ATP

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21
Q

glucose is oxidized to produced CO2 and ATP in a 4 step process..

A

glycolysis, pyruvate dehydrogenase complex, Krebs cycle & electron transport/oxidative phosphorylation

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22
Q

what happens in glycolysis

A

glucose molecule is oxidized + split into 2 pyruvate molecules

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23
Q

net surplus from glycolysis

A

2 ATP (ADP + Pi) and 2 NADH (NDH+ + H+)

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24
Q

first step of glycolysis

A

phosphorylation of glucose (ATP → ADP: phosphate goes to glucose)

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25
Q

enzyme required for the first step of glycolysis

A

hexokinase

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26
Q

2nd & 3rd steps of glycolysis

A

isomerization of G6P → F6P

phosphorylated again (ATP → ADP) to F1,6bP

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27
Q

enzyme required for the 3rd step of glycolysis

A

phosphofructokinase

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28
Q

how much energy for each glucose molecule in glycolysis

A

4 ATP and 2 NADH

(half for each pyruvate molecule)

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29
Q

what do you NEED to start glycolysis

A

a bit of ATP

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30
Q

what catalyses the first step of glycolysis & how is it inhibited?

A

hexokinase (phosphorylation of glucose → G6P)

G6P feedback inhibits hexokinase

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31
Q

when is NADH produced & how many steps? (glycolysis)

A

aldehyde is oxidized to a COOH

only happens in one step!

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32
Q

when is ATP converted to ADP in glycolysis

A

everytime a phosphate is added to a substrate

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33
Q

when is ADP made into ATP in glycolysis

A

every time a phosphate comes off a substrat

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34
Q

why is the step with PFK important

A

transfer of the phosphate group is thermodynamically favourable so its basically irreversible

once you get to this step, you’re committed to glycolysis

F1,6bP is only used in glycolysis

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35
Q

what is the biochemical valve of glycolysis

A

PFK

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36
Q

what is the committed step of glycolysis

A

conversion of F6P → F1,6bP (with PFK)

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37
Q

what happens to F1,6bP

A

split into 3 carbon molecules that is converted to pyruvate with the production of NADH and ATP

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38
Q

PFK and ATP relationship

A

ATP is an allosteric regulator of PFK

high levels of ATP → slowed glycolysis

too little ATP (or none) → no glycolysis (it is still a reactant)

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39
Q

limited NAD+ stimulate or inhibit glycolysis

A

inhibition - need NAD+ as a substrate to produce NADH

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40
Q

anaerobic conditions & NAD+

A

all the NAD+ gets converted to NADH

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41
Q

importance of fermentation

A

regenerates NAD+ in anaerobic conditions - allows glycolysis to continue in the absence of oxygen

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42
Q

how does fermentation work

A

use of pyruvate as the acceptor of the high energy electrons form NADH

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43
Q

examples of NADH as the high energy electron acceptor

A

reduction of pyruvate to ethanol (beer making)

reduction of pyruvate to lactate in muscle cells

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44
Q

why is there a limit to anaerobic respiration

A

the ethanol and lactate produced builds up + acts like a poison

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45
Q

how does liver deal with lactate from muscle

A

exported from muscle cell to liver

when oxygen becomes available, liver converts lactate back to pyruvate (makes NADH)

excess NADH is used to make ATP in oxidative phosphorylation

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46
Q

where does glycolysis occur

A

in the cytoplasm

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47
Q

where does the PDC occur

A

innermost compartment of the mitochondria - the matric

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48
Q

where does the Krebs cycle occur

A

innermost compartment of the mitochondria - the matrix

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49
Q

oxidative decarboxylation

A

molecule is oxidized to release CO2 and produce NADH

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50
Q

pyruvate → activated acetyl unit

A

activated = not free floating, attached to coenzyme A

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51
Q

CoA-SH bond

A

the bond between sulfur and the acetyl group is high energy → makes it easy for it to transfer the acetyl fragment into the Krebs cycle

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52
Q

how is acetyl-CoA formed

A

pyruvate + coenzyme A → oxidized → acetyl-CoA

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53
Q

what is a prosthetic group

A

a cofactor that is tightly bound to an enzyme

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54
Q

prosthetic group in PDC

A

thiamine pyrophosphate (TPP) - at one of its active sites

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55
Q

what is the thiamine in thiamine pyrophosphate

A

vitamin B1

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56
Q

what happens if the PDC and Krebs cycle is shut down

A

glycolysis would increase to try to maintain ATP levels

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57
Q

what would happens in thiamine deficiency

A

PDC and Krebs cycle = shut down

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58
Q

overview of Krebs cycle

A

takes the 2 carbon unit from acetyl-CoA, combines it with oxaloacetate to release 2 CO2, NADH & FADH2

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59
Q

acetate fragment of acetyl-CoA + oxaloacetate →

A

citrate (2 + 4 → 6 carbon)

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60
Q

where is OAA derived from

A

previous round of Krebs cycle (recycled)

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61
Q

first stage of Krebs cycle

A

oxaloacetate + acetyl CoA + H20 → citric acid + CoA-SH + H+

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62
Q

second stage of Krebs cycle

A

citrate is further oxidized to release CO2 and produced NADH with each oxidative decarboxylation

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63
Q

product of stage 2 of Krebs cycle

A

succinyl-CoA

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64
Q

what happens in the third stage of Krebs

A

succinyl-CoA is turned into OAA so the cycle can continue

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65
Q

what does GTP do in the third stage of Krebs

A

a high energy phosphate bond is produced directly as GTP

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66
Q

what does GTP eventually do

A

transfer its high energy phosphate bond to ADP to make ATP

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67
Q

FADH2 vs NADH

A

similar but FADH2 produces less ATP

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68
Q

after the Krebs cycle, what are the remaining products

A

glycolysis: 2 ATP and 2 NADH per glucose (net)

PDC: 2 NADH per glucose

Krebs: 6 NADH, 2FADH2 and 2 GTP per glucose

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69
Q

characteristics of the outer membrane of mitochondrion

A

smooth + contains large pores formed by porin proteins

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70
Q

characteristics of the inner membrane of mitochondrion

A

impermeable even to small molecules (H+)

densely folded into cristae

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71
Q

where are the enzymes of PDC/Krebs cycle located

A

matrix

72
Q

where are the enzymes of the ETC and oxidative phosphorylation found

A

bond to the inner mitochondrial membrane

73
Q

2 main goals of ETC/OP

A

deoxidize all the electron carriers reduced in the previous steps

store energy in the form of ATP

74
Q

where are the NADH from glycolysis found and where do they have to go

A

found in the cytoplasm, need to go to the matrix so they can donate electrons to the ETC

75
Q

how is the proton gradient set up in prokaryotes

A

by membrane bound ATPase

76
Q

differences between OP in eukaryotes vs prokaryotes

A

eukaryotes use their inner mitochondrial membrane for OP

prokaryotes don’t have mitochondria - they use their cell membrane

77
Q

what is oxidative phosphorylation

A

oxidation of high energy electron carriers (NADH & FADH2) coupled to the phosphorylation of ADP → ATP

78
Q

what is an ETC

A

group of 5 electron carriers

79
Q

what are cytochromes

A

3/5 of the electron carriers on the ETC

large, embedded din the inner membrane & have heme groups

80
Q

NADH dehydrogenase

A

first carrier in the ETC, receives electrons from NADH (which is oxidized to NAD+)

81
Q

NADH dehydrogenase aka..

A

coenzyme Q reductase

82
Q

ubiquinone

A

receives electrons from NADH dehydrogenase

small + mobile

83
Q

ubiquinone aka..

A

coenzyme Q

84
Q

cytochrome C reductase

A

receives electrons from ubiquinone

aka B

one of the big ones

85
Q

cytochrome C

A

receives electrons from cytochrome C reductase

86
Q

cytochrome C oxidase

A

aka C

last member of the ETC

87
Q

what do the large membrane bound proteins in the ETC do

A

pump protons out of the matrix into the intermembrane space

88
Q

each molecule of NADH provides the energy to produce __ ATP molecules

A

2.5

10 protons for 4 ATP

89
Q

each molecule of FADH provides the energy for __ ATP

A

1.5

90
Q

what does the glycerol phosphate shuttle do

A

brings the NADH from glycolysis in the cytoplasm → mitochondria

91
Q

where is the NADH shuttled

A

directly to ubiquinone (like FADH2)

92
Q

cytosolic NADH vs matrix NADH ATP

A

cytosolic: makes 1.5 molecules
matrix: makes 2.5

93
Q

why do prokaryotes make more ATP from each glucose

A

they don’t have to transport their cytosolic NADH (takes up energy)

94
Q

ATP yield from eukaryotes vs prokaryotes

A

eukaryotes = 36 ATP/glucose

prokaryotes = 38 ATP/glucose

95
Q

why does gluconeogenesis occur

A

dietary sources of glucose are unavailable & no glycogen or glucose from the liver

96
Q

first step of gluconeogenesis

A

CO2 + pyruvate → pyruvate carboxylase → oxaloacetate

*need ATP hydrolysis for this process

97
Q

2nd step of gluconeogenesis

A

oxaloacetate is decarboxylated & phosphorylated to form PEP

*this process needs PEP carboxykinase (PEPCK)

98
Q

what does fructose-1,6-biphosphatase do

A

catalyzes the removal of a phosphate group

fru-1,6-bisP → fru-6-P

99
Q

what does glucose-6-phosphatase do

A

glu-6-P → glucose

irreversible process

100
Q

why is the dephosphorylation of glucose-6-P required

A

so glucose can be released from the liver

phosphorylated glucose is charged and cannot cross the cell membrane

101
Q

what does gluconeogenesis

A

4 ATP, 2 GTP and 2 NADH

102
Q

what is reciprocal control

A

the same molecule regulating 2 enzymes in opposite ways

seen in glycolysis and gluconeogenesis

103
Q

heavily regulated enzymes in glycolysis/gluconeogenesis

A

PFK and F-1,6-BPase

104
Q

how are PFK and F-1,6-BPase regulated

A

allosterically regulated by glycolytic intermediates that activate one enzyme while inhibiting the other

105
Q

examples of enzymes that exert reciprocal control

A

AMP and F-2,6-BP

106
Q

how does F-2,6-BP work

A

stimulates PFK (which stimulates glycolysis)

inhibits fru-1,6-bisPase (inhibits gluconeogenesis)

107
Q

insulin effects on F-2,6-bP

A

stimulates it → stimulates PFK → stimulates glycolysis

108
Q

glucagon effects on F-2,6-bP

A

inhibits it → inhibits fru-1,6-bisPase → inhibits gluconeogenesis

109
Q

how is glycogen made

A

glucose-6-P → phosphoglucomutase → glucose-1-P

glu-1-P is activated with UTP to form UDP-glucose which is added to the growing glycogen polymer by glycogen synthase

110
Q

why does skeletal muscle lack glucose-6-P

A

keeps the glucose phosphorylated and unable to leave the muscle cell

111
Q

insulin simulates..

A

glycolysis and glycogenesis

112
Q

purpose of the pentose phosphate pathway

A

diverts glucose-6-phosphate from glycolysis to form NADPH, ribose-5-P and glycolytic intermediates

113
Q

what is formed during the oxidative phase of PPP

A

NADPH and ribose-5-P

114
Q

what is formed during the non-oxidative phase

A

glycolic intermediates

115
Q

G6PDH in the PPP

A

primary point of regulation

the product (NADPH) acts via negative feedback to inhibit the enzyme

116
Q

deficiency of G6PDH

A

limits the ability of RBCs to eliminate ROS → cell death & renal/hepatic complications

117
Q

3 roles of lipids

A

in adipose cells, triglycerides store energy

in cellular membranes, phospholipids constitute a barrier between intracellular & extracellular environments

cholesterol is the building block for hydrophobic steroid hormones

118
Q

soaps are..

A

the sodium salts of fatty acids

amphipathic (hydrophobic & hydrophilic regions)

119
Q

what is saponification

A

soap is produced by base-catalyzed hydrolysis of triglycerides from animal fat into fatty acid salts (soaps)

120
Q

why do fat molecules have more energy content than carbohydrates

A

fats are much more reduced → oxidizing them releases more energy

121
Q

most common phospholipids in eukaryotic cells

A

phosphatidylcholine and phosphatidylethanolamine

122
Q

role of phosphatidylcholine

A

lipid component of lung surfactant → reduces surface tension

123
Q

role of phosphatidylinositol

A

signal transmission across cell membranes

124
Q

what is squalene and why is it important

A

triterpene (6 isoprene units)

utilized in the manufacture of steroids & earwax

125
Q

example of a terpenoid

A

Vitamin A

126
Q

example of a polycyclic amphipath

A

cholesterol

127
Q

where are the receptors for steroid hormones found

A

located within cells

128
Q

what is a sphinolipid

A

structured the same as phospholipids but the backbone is sphingosine instead of a glycerol

129
Q

significant sphingolipid in humans

A

sphingomyelin - component of the myelin sheath around neurons

130
Q

what is a wax

A

long chain fats esterified to long chain alcohols

extremely hydrophobic, form waterproof barriers

131
Q

what are fat soluble vitamins

A

absorbed with dietary fat and stored in adipose/liver

132
Q

what are the 4 fat soluble vitamins

A

A D E K

133
Q

characteristic of the 4 fat soluble vitamins

A

ring structures

134
Q

vitamin A

A

terpenoid, essential for vision/growth

135
Q

vitamin D

A

derived from cholesterol, regulates calcium and phosphate

136
Q

vitamin E

A

group of compounds (tocopherols, methylated phenols)

antioxidant

137
Q

most active vitamin E

A

alpha-tocopherol

138
Q

vitamin K

A

coenzyme for the activation of clotting proteins

139
Q

characteristics of prostaglandins

A

belong to the group of molecules known as eicosanoids

have a 5 membered ring

140
Q

roles of prostaglandins

A

regulate SM contraction, BV diameter

decrease acid secretion and increase mucus secretion

141
Q

how are fatty acids activated

A

fatty acid + ATP → acyl adenylate

acyl adenylate + HS-CoA → acyl CoA + AMP

142
Q

end result of fatty acid (beta) oxidation

A

acetyl-CoA

143
Q

why does ketogenesis occur

A

generation of ketone bodies

when glycogen stores are exhausted and blood glucose falls a lot

144
Q

what are ketone bodies generated from

A

acetyl-CoA

145
Q

when can ketogenesis occur when there IS enough glucose

A

if the glucose is present but cannot enter the cell (type 1 diabetic with no insulin shots)

146
Q

diabetic ketoacidosis

A

acidic ketone bodies

fatigue, confusion and fruity breath

147
Q

what is the committed step of fatty acid synthesis

A

activation of acetyl CoA in a carboxylation reaction

148
Q

what can individual AAs be broken down into

A

an amine and a carbon skeleton

149
Q

what can come from an amine (broken down from AA)

A

urea and nitrogen containing compounds (nucleotide bases)

150
Q

what can come from a carbon skeleton (broken down from AA)

A

glucose and acetyl CoA

151
Q

how are fatty acids activated

A

addition of coenzyme A (need 2 ATP)

152
Q

fatty acid oxidation - acetyl CoA

A

breaks off the fatty acid and goes to the Krebs cycle

153
Q

how many times does a fat go through the beta oxidation cycle

A

1 less than the number of 2-carbon units

154
Q

what happens if there is a double bond (fatty acid oxidation)

A

isomerase shifts the double bond to the right place

155
Q

why do unsaturated fats give off less energy

A

no FADH2 created since a double bond isn’t created

156
Q

where does fatty acid synthesis take place

A

cytosol of liver cells

157
Q

how to turn acetyl CoA to malonyl CoA

A

add HCO3- (just need another C)

process takes 1 ATP

158
Q

first step of fatty acid synthesis

A

acetyl CoA attaches to ACP subunit of fatty acid synthase → acetyl ACP & CoA

malonyl CoA + ACP → malonyl ACP + CoA

159
Q

maximum length of fatty acid during synthesis

A

16 Cs

160
Q

where does fatty acid oxidation occur

A

mitochondrial matrix

161
Q

linked to __ in fatty acid oxidation

A

CoA

162
Q

linked to __ in fatty acid synthesis

A

ACP

163
Q

coenzymes involved with fatty acid oxidation

A

NAD+ and FAD

164
Q

coenzymes involved with fatty acid synthesis

A

NADPH

165
Q

fatty acid oxidation goal

A

generate ATP

166
Q

fatty acid synthesis energy

A

requires ATP

167
Q

formation of ketone bodies

A

acetyl CoA → acetoacetate → hydroxybutyrate and acetone

*all three are ketone bodies

168
Q

basic amino acids have a ___ charge

A

+1

169
Q

acidic amino acids have a ____ charge

A

-1

170
Q

side chain of asparate contains..

A

a carboxylate group

171
Q

GTP is in the family of..

A

nucleotides

172
Q

actin is a ____

A

microfilament

173
Q

what cleaves peptide bonds

A

proteases

174
Q

DNA mutation that results in a change to the nucleotide sequence but no change to amino acid primary structure

A

silent

175
Q

chromosomes are proofread and repaired following duplication in which stage of the cell cycle

A

G2

Biology - MCAT (11 decks)

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