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BMB 401 > Exam 3 (Lectures 24-26) > Flashcards

Exam 3 (Lectures 24-26) Flashcards

1
Q

NAD+ is mainly used for…

A

oxidation that powers ATP synthesis

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2
Q

NADPH is used for…

A

reduction

able to reduce reactive oxygen species to remove them

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3
Q

NAD+ in the mitochondrial matrix

A

oxidizes substrates to produce reducing equivalents: NADH

happens in: TCA cycle and Fatty Acid Oxidation

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4
Q

NADH in the mitochondrial matrix

A

reduces electron carriers to power ATP synthesis

happens in: Electron Transport Chain

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5
Q

NADPH in the cytoplasm

A

reduces substrates in reductive synthetic reactions:

Fatty Acid Synthesis

Cholesterol Synthesis

Nucleotide Synthesis

Neurotransmitter Synthesis

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6
Q

Pentose Phosphate Pathway (Oxidative)

Reaction 1 Regulation

A

High NADPH/NADP+ inhibits G6PD

Low NADPH/NADP+ activates G6PD

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7
Q

High need Ribose 5-P

Low need NADPH

A

products from glycolysis Fructose 5-P and GAP to make Ribose 5-P

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8
Q

If equal amounts of NADPH and Ribose 5-P is needed both at the same time…

A

Only oxidative PPP is used to make NADPH and Ribose 5-P

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9
Q

High need of NADPH

Low need Ribose 5-P

A

use both OPPP and non-OPPP then send products to gluconeogenesis to make more G6P for PPP

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10
Q

High need in NADPH and ATP

A

OPPP and non-OPPP are used and sent to glycolysis to make pyruvate + ATP then TCA cycle to make more ATP

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11
Q

Deficiency of Glucose 6-P Dehydrogenase

A

caused by x-linked genetic mutation

increase susceptibility to oxidative injury => Hemolytic Anemia (lysis of RBC)

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12
Q

Oxidative Challenges

A

Oxidative Drugs: antibiotics, antimalarials, fever reducers

Favism: hemolytic anemia precipitated by fava bean ingestion

Infection: peroxides are made in macrophages mobilized in reponse to infection

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13
Q

Favism

A

from fava beans that contain active oxidants (vicine & convicine)

may afford some protection from death from malarial infection

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14
Q

What is Triacylglycerol (fats)

A

high energy fuel preferred by Liver and Heart

fuel by skeletal muscles

yields greater than ATP per Glycogen

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15
Q

Where does the catabolism of dietary fats begin?

A

in the small intestine where bile salts are released after a meal

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16
Q

Where are Bile Salts synthesized, stored, and released?

A

Synthesized in the liver using cholesterol

stored in the gall bladder

released in to the small intestine

17
Q

How many cycles are needed to break n-C Saturated Fatty Acid down completely to Acetyl CoA?

How many Acetyl CoA produced?

How many NADH and FADH2 produced?

A

N/2 - 1

N/2

N/2 - 1

18
Q

Fatty Acid Synthesis Reaction 1 Regulation

A

positively regulated by citrate

negatively regulated by AMP

19
Q

We can use Acetyl CoA to make…

A

fatty acids, ketone bodies, cholesterol, CO2, H2O, ATP

20
Q

Ketone bodies are preffered fuel for…

A

heart and renal cortex

can also be with brain under starvation condition

21
Q

Ketone Bodies Synthesis

A

in the fasting state, the liver used Acetyl CoA to make ketone bodies

22
Q

What are the ketone bodies?

A

acetoacetate, D-3-hydroxybutyrate can be used to make acetyl CoA for TCA or other cells

acetone - excreted by breathing out or urine

23
Q

What are the two sources of Cholesterol?

A

Dietary and indogenous produced by the liver

24
Q

Rank the lipoproteins in increasing density

A

Chylomicron > VLDL > IDL > LDL > HDL

25
Q

Physiological Role: Chylomicron

A

dietary fat transport

26
Q

Physiological Role: VLDL

A

endogenous fat transport

27
Q

Physiological Role: IDL

A

LDL precursor

28
Q

Physiological Role: LDL

A

cholesterol transport

29
Q

Physiological Role: HDL

A

reverse cholesterol transport

30
Q

Hypercholesterolemia

A

Long-term ingestion of dietary cholesterol far exceeds requirement

high cholesterol => decrease in LDL receptor synthesis

31
Q

Familial Hypercholesterolemia (FH)

A

FH/FH mutation: serum cholesterol is 3 to 5 times normal levels in childhood

FH/+ mutation: serum cholesterol is about twice normal levels by mid age

32
Q

Atherosclerosis

A

Hardening of the arteries

an inflammatory desease caused by LDL seeping past the endothelium and becoming inflammatory

33
Q

What are HDL’s protective effects?

A

reverse transport of cholesterol from circulating lipoprotein particles

reverse transport of cholesterol from foam cells

degredation of oxidized lipoprotein particle constituents trough an HDL-associated serum esterase

34
Q

ATP III: Metabolic Syndrome

A

>= 3 risk factors are present:

Abdominal obesity

high triacylglycerals

Low HDL-C

high BP

high fasting glucose

35
Q
A

BMB 401 (6 decks)

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