Block 3 PLs and SLs Flashcards

1
Q

What’s the difference between a glyceroPL and a sphingoPL?

A

Glycerol or sphingosine as backbone

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2
Q

What are the components of a glyceroPL?

A

Glycerol backbone, head group (small polar with OH ester linked to PO4), FA 1 (mostly sat), FA 2 (PUFA)

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3
Q

Where are PLs synthesized?

A

Cytosolic face ER, then transported to final destination

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4
Q

What is phosphatidic acid?

A

PA; simplest phosphoglyceride (X=H), precursor of all others

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5
Q

What are PLs formed from? Give examples.

A

PA esterified to alcohol (polar); PS (serine), PE (ethanolamine), PC/lecithin (choline), etc.

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6
Q

What is a lysophosphoglyceride?

A

If either R1 or R2 is removed (e.g. lysolecithin)

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7
Q

What is cardiolipin? What is the function?

A

2 molecules esterified PS; has 3 glycerols, 4 FFAs, in IMM; proton trap buffering pH near PM in IMM

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8
Q

What happens when cardiolipin is peroxidated?

A

Apoptosis triggered; CL oxygenase -> perox unsat acyl chain -> cytC pore -> binds IP3 -> Ca release ER -> more cytC release

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9
Q

What are ether PLs?

A

FA attached at C1 in ether not ester; sat (alkyl) or unsat (alkenyl) alc in sn-1 position

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10
Q

What type of PLs are plasmalogens? Where are they found?

A

Alkenyl ether PLs, 20% mammal glyceroPLs; myelin has ethanolamine plasmalogens, heart mm choline plasmalogens

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11
Q

What is platelet activating factor (PAF)?

A

1-alkyl-2-acetyl-PC; potent platelet agg, degran; mediates acute inflamm & ana shock; neutros, dust cells -> superoxide anion; TM signaling -> act PLipase -> PL degradation

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12
Q

What is surfactant?

A

DPPC; secreted by type 2 pneumocytes; 2 saturated palmitic acid v risk for ROS oxidation; also contains PtGlycerol, chol, surfactant proteins Sp-A,B,C

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13
Q

What is respiratory distress syndrome?

A

Hyaline membrane disease in infants, inadequate lung maturation in premies; increased PC/SPH ratio in amniotic fluid indicates lung maturation (>2); 15% neonatal deaths in Western countries

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14
Q

What is respiratory failure?

A

In adults, damaged/destroyed surfactant-producing pneumocytes b/c immunosuppressive meds or chemo drugs

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15
Q

Why are PA and CTP important in glyceroPL synthesis?

A

PA is precursor of most, CTP required as activator of polar head groups or hydrophobic tail

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16
Q

How is PA synthesized?

A

Liver: glycerol -> Gly3P
Liver, adipose: glucose -> DHAP -> Gly3P + 2 FaCoA = PA
PL -> PLase D -> PA

17
Q

What is the product of CTP activating polar head or hydrophobic tail?

A

Head: PA -> DAG + CTP-head -> glyceroPL = PC, PE
Tail: PA -> CDP-DAG + head group -> glyceroPL = PI, CL

18
Q

How are PE and PS interconverted?

A

Reversible, Ca-activated “base exchange” of free serine for ethanolamine of PE; to make PS for membrane synthesis

19
Q

How is membrane PS converted to PC?

A

PS decarboxylated to PE, undergoes 3 methylations (donor SAM) -> PC + SAH

20
Q

What aa is required to make PC? What is the salvage pathway?

A

Methionine (essential, often deficient)

CDP-choline pathway for PC synth because activates free choline for reincorporation into membrane lipids

21
Q

What are the 3 sources of choline?

A

Liver synth (need Met, Bvit); recycled choline (during turnover PC, SM, ACh reincorporated via salvage); dietary (PC/lecithin in meat, eggs, veg; def = brain dev, memory)

22
Q

What is a phospholipase? What do the major classes do?

A

Degrade glyceroPLs
A1/2 remove FA from C1/2
C cleaves PDE bond b/t C3 & P
D cleaves PDE bond b/t P and polar head

23
Q

What are products of PLA2? Why is this important?

A

FFA and lysoPL (amphipathic detergents); major mech for cytotoxicity bee/snake venoms; contribute to PL synth (membrane remodel), release AA for eicosanoid synth, major mech removal damaged PUFA

24
Q

What are the different types of PLA2?

A

Cytosolic: releases AA for eicosanoid synth, act by ^ [Ca], P by MAPK ^ activity
Ca-ind intracellular: turnover/remodeling cellular PLs
Secretory: extracellular, response to sepsis/inflam, high [ ] in arthritic synovial fluid
Pancreatic: digestive, secreted as zymogen

25
Q

Describe the structure of a sphingolipid.

A

Backbone of sphingosine, 1 FA (palmitic 16:0, stearic 18:0, or nerving 24:1), polar head of phosphocholine (SphPL) or carb (glycolipid)

26
Q

What are the physiological roles of SLs?

A

ABO, receptors for intercellular comm, SM major in nervous tissue, more sat than PLs = specialized membrane domains, ceramide 2nd mess signals apoptosis/differentiation

27
Q

How does SM affect chol?

A

Chol intx with SM in PM bc highly sat LCFA + sphingoid base -> gel phase domains (+ chol -> liquid) caveolae and rafts with PKC, LDL-R, eNOS, etc.

28
Q

How is SM degraded?

A

SMase is lysosomal, deficient in Niemann-Pick type 1 (type A most severe)

29
Q

What are symptoms of Niemann Pick type 1?

A

SMase def; enlarged liver and spleen due to lipid, severe mental retardation, death in early childhood

30
Q

What are glycolipids? What’s the difference between cerebrosides and gangliosides?

A

GL: one or more sugars + ceramide (replace phosphocholine as head)
C: ceramide + 1 sugar
G: ceramide + complex, branched carb chain