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Flashcards in pathways Deck (23)
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1

Function: Provide blood glucose (liver). Provide glucose to produce energy for muscle contractions (muscle).

Substrates: Glycogen, Free phosphates

Products: free glucose and g-1-p or g-6-p

glycogenolysis (glycogen degradation)

2

Control Enzyme: glycogen synthase

Regulation: Insulin/Glucagon ratio and amount of glucose present (liver), epinephrine can also inhibit. Muscle insulin level (muscle).

Compartment: cytosol tissues: liver and muscles

Glycogenesis

3

Control: debrancher enzyme, glycogen phosphorylase

Reg: G phosphorylase, also epi has an effect. (Phosphorylation activates control enzyme.) In muscle, GNL is regulated via activation of glycogen phosphorylase by [AMP], [Ca2+],presence of epi C: Cytosol

Glycogenolysis (glycogen degradation)

4

Functions: To make NADPH (used for detoxification [ie. glutathione synthesis] and Reductive Biosynthesis [ie. fatty acid synthesis]) and Ribose 5 phosphate (nucleotide synthesis) .

Pentose Phosphate Pathway

5

Irreversible PPP Pathway.

Oxidative

6

Pathway synthesizes ribose 5-phosphate.

Non oxidative PPP

7

Functions: Produce energy and produce substrates for other anabolic pathways.

Substrates: Glucose (or G-6-P),ADP,NAD+

Product: ATP, pyruvate

Aerobic Glycolysis

8

2 primary control enzymes: Isocitrate dehydrogenase and a-Ketoglutarate dehydrogenase

Regulation: ATP/ADP ratio and the rate of ATP use

Compartment(s): Mitochondrial matrix Tissues: all except rbc

TCA/Kreb/ETC

9

What happens to citrate in the TCA cycle?

Isomerized by aconitase to isocitrate

10

What are the electron carriers of the ETC?

NADH, FADH2, coenzyme Q, cytochrome C, O2

11

NADH & FADH2 are reducing or oxidizing agents?

strong reducing agents

12

Water-soluble electron carriers

NADH

13

electrons passed from succinate to FAD in TCA cycle, electrons are transferred from FADH2 to three Fe-S centers and then to Q, two protons are taken up to from QH2

Complex II:succinate dehydrogenase

14

FMN (riboflavin) accepts electrons and protons from NADH+H to become FMNH2, FMNH2 contains an iron/sulphur center which takes two hydrogen and transfers them to coenzyme Q = QH2 (4 protons transferred into intermembrane space of mito)

Complex I:NADH Dehydrogenase action

15

Q bind CytoB and heme accepts e-, e- transferred to CytoC1, CytoC1 (membrane bound) transfers e- to CytoC (water soluble/mobile) which can diffuses and donate it's electrons to complex IV, 4 protons pumped

Complex III: cytochrome C oxidoreductase

16

iron atoms of the heme groups in the cytochromes and copper atoms are oxidized and reduced as electrons flow from cyto C to O2 to make water, 2 protons pumped

Complex IV: cytochrome oxidase

17

Where does superoxide USUALLY come from?

leaks from complex I

18

What type of metabolic pathway is Gluconeogenesis?

ANABOLIC
* generates glucose from non carb carbon substrates

19

What type of metabolic pathway is Glycogenesis?

ANABOLIC
* generates glycogen from glucose molecules

20

What type of metabolic pathway is Glycolysis?

CATABOLIC
* converts glucose to pyruvate

21

What type of metabolic pathway is Citric acid cycle?

CATABOLIC
* converts CHO, fat, protein into CO2 and water

22

This pathway synthesizes ribose 5-phosphate.

PPP Non oxidative pathway

23

This is where NADPH, ribulose 5-phosphate, and CO2 are generated. This pathway is a substrate for glutathione reductase, fatty acid synthesis, cytochrome P450 monooxygenases, and deoxynucleotide synthesis.

PPP Oxidative pathway