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Biochem > Lipids > Flashcards

Lipids Flashcards

1
Q

what are lipids?

A

hydrophobic molecules include;
phospholipids
glycophospholipids, isoprenoids, eicosenoids

all come from Acetyl CoA

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2
Q

Phospholipids

A

major comp of cell membranes

glycerophospholipids (glycerol backbone)
sphingolipids (ceramide)

alcohol attached via phosphodiester bond to DAG (diaclyglycerol)

can be sat / unsat
diff head groups

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3
Q

cardiolipin

A

unusual glycerophospholipid:
two phosphatidic acids eterified to an additional glycerol molecule

found only in inner mito mem (part of ETC0

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4
Q

plsmalogens

A

glycerophospholipid;
fatty acid at C1 of glycerol is attached via an ether linkage (rather than ester)

most common plsamalogens:
phsphatidalenthanolamine & phsphatidalcholine
30% of glycerphospholipids in brain
reduced levels ~ Alzheimer’s disease

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5
Q

platelet activating factor

A

ether glycerophospholipid
fatty acid chain on C2 replaced by an acetyl group

platelet aggregation and degranulation, inflammation, analphylaxis

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6
Q

trans vs cis double bond

A

trans wont put a kink in the fatty acid tail

nature of tails affects fluidity of membrane

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7
Q

C1

C2

A

C1 generally saturated tail

C2 unsaturated tail

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8
Q

sphingophospholipids

A

long chain amino alcohol sphingosine as backbone

sphingomyelin is major sphingosine

  • choline head group
  • myelin sheath
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9
Q

glycerophospholipids are derived from

A

phosphatidic acid

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10
Q

what is phosphatidic acid synth from?

A

2 fatty acyl tails + glycerol-3-phosphate (from DHAP)

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11
Q

formation of phosphatidylcholine (PC)

A
  1. deP Phosphatidic acid -> DAG + CDP-Choline
  2. Methlylation of PE ->PC
    - PC has 3 methyl grps
    - SAM - S-adenosyl-methionine (methly donor) req 3
  3. Phosphatidylserine -> PC
    - decarboxylational; phosphatidylserine DC (PLP)
    - or base transfer; phosphatidyl-ethanolamine-serine transferase

Choline; diet or lipid turnover

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12
Q

phosphatidlethanolamine (PE)

A

deP Phosphatidic acid -> DAG + CDP-ethanolamine

Ethanolamine; diet or lipid turnover

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13
Q

Phosphatidyl inositol (PI)

A

DAG is activated by UDP

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14
Q

Phosphatiditylserine (PS)

A

base exchange between serine and PE

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15
Q

sphingolipid synthesis

A
  1. palmitoyl CoA + Serine
    enz; serine palmitoyl transferase
    req NADPH
  2. Spinganine (1 tail) - > Dihydroceramide
    enz; Ceramid synthase
  3. Dihydroceramide -> Ceramide (2 tail)
  4. ceramide sphingomyelin
    -transfer of the choline fr PC
    -> enz: sphingomyelin synthase
    <- enz: sphingomyelinase (SMase)
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16
Q

phospholipase

A

degrade glycerophospholipids by hydrolize phosphodiester bonds
activate 2nd messengers

-release 1 tail = lysophospholipid (good detergent - alter solubility)
- acyl chains released = intermediates;
PL-A2 -> arachidonic acid -> syn of prostaglandins, leukotriees, thromboxanes

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17
Q

Phospholipase C

A

PL -C; act by Gprotein coupled receptors, alpha-adrenergic R acts on PIP2 -> DAG + IP3
IP3 -> Ca release
DAG -> act PK-C (also act by Ca)

NE or EP
Constriction of blood vessels - sm mm

18
Q

Phospholipase A 2

A

release hydrocarbon tail at 2nd C -> the unsat FA

PL - A2 alpha - specific for those with arachidonic acid
-> generation of prostaglandins, leukotrienes, etc

19
Q

sphingomyelinase

A

degrade sphingophospholipids
remove phosphorylcholine = > ceramide
(ceramide further degraded into sphiingosine and free FA)

SMase classified by pH optima

Niemann-Pick disease

20
Q

lysosomal acid SMase

A

Neimann-Pick (A,B) disease, AR
lipid buildup in cells
A - more severe, neuro defects, death early
ashkenazi jews
B - 5% fuction, lipid dep in liver
C & D - transporter problem -> build up of lipids inside cells

21
Q

glycosphingolipids

A

derived from ceramide (like sphingolipids)
No phosphoester moiety
Polar portion = monosaccharide or oligos attached via O-glycosidic linkage
classified as neutral or acid

22
Q

neutral glycosphingolipids

A 
neutral charge
single sugar (glucose or galactose = glucocerebroside/galactocebroside) or oligosaccharide (globoside)

most common found in mem = galactocerbroside

glucocerbrosides = precursors of more complex glycosphingolipids

23
Q

acidic glycosphingolipids

A

neg at phys pH due to:
1. N-acetyleneuraminic acid (NANA aka silaic acid) (note: attached via CMP-NANA)
= gangliosides - ganglion cells of CNS
2. Sulfate = sulfatides

24
Q

gangliosides

A

acidic glycosphingolipids w NANA attached

Gm - 1 NANA, cholera toxin interacts here
Gd - 2
Gt - 3
Gq - 4

carb portion stick out from cell surface; communication, bacteria use them as receptor for toxins

25
Q

sulfatides

A

cerebrosides containing sulfated galatosyl residues

sulfate donor; (PAPS) 3 phosphoadenosine 5 - phosphosulfate
attached to 3 OH of galactose

26
Q

where are glycosphingolipids synthesized and how

A

golgi
sequential attachment of UDP-sugars by glycosyl transferases to the glucose
(similar to glycogen syn)

27
Q

degradation of glycosphingolipids: where how

A

endocytosed into lysosomes

lysosomal hydrolases - remove sugars 1 at a time -> ceramide
ceramide -> sphingosine + FA

normal; balance bet syn & deg = constant amt of glycosphingolipids in membrane

1 hydrolase deficient / absent -> buildup of glycosphingolipids in lysosomes

28
Q

lipidoses

A

buildup of glycosphingolipids in lysosome due to deficiency/absence of a lysosomal hydrolase

29
Q

Tay-sachs

A

lipidoses
defect; hexosaminidase A -> buildup of Gm2
(gangliosides)

rapid, progressive, fatal neurodegen
blindness, cherry red macula, mm weakness, seizures

30
Q

Gaucher disease

A

Gaucher diesease = enz beta-glucosidase (aka glucocerbrosidase) -> buildup of glucocerbrosides

most common lysosomal storage disease
hepatospienomegaly
osteoporosis of long bones
CNS inovl in rare infantile/ juvenile forms

31
Q

eiconsinoids

A

include: prostaglandins, thromboxanes, leakotrienes

PG/TX - platelet agg, ovulation, gastric acid sec, gastric mucous formation, vasocon/relax
LK - allergic response, asthma, netrophil & eosinophil function, airway dia

all derived from 20C omega-6 FA
- most cases = arachidonic acid - der from linoleic acid, released from mem phospholipids via PL A 2

32
Q

Prostaglandins and thromboxanes synethesis

A

PGH synthase (2 catalytic act); takes Arachadonic acid:
1. fatty acid cyclooxygenase (COX) - forms the intermediate PGG2
req O2
2. Peroxidase - converts PGG2 -> PGH2
req glutathione

PGH2 -> converted to a number of diff things dep on cell type (aka the enzymes present)

33
Q

COX 1

A

const expressed in all tissue

34
Q

COX 2

A

inc induced cytokines/ inflammatory response

35
Q

COX inhibitors

A

NSAIDS - non-selective COX inhib
ant-inflammatory (blocks COX-2)
side-affects; stomach upset bc of COX 1 inhibition (dec mucous sec)

36
Q

selective COX-2 inhib

A

celecoxib

only COX assoc w anti-inflam response
should have no side-effects
may have adverse cardiovascular effects -> unpredicted side effects

37
Q

TXA 2

A

platalet agg

38
Q

PGI 2

A

inhibits platelet aggregation

endothelial cells

39
Q

how do prostaglandins/thromboxanes exert their effects?

A

via specific G-protein coupled receptors (GCPRs) in target cells

PGI 2 - syn by endothelial cells, ihibits platelet aggregation

TXA2 - syn by platelets and triggers aggregation

Result = limit platelet aggregation to site of injury

40
Q

aspirin

A

COX - 1 irreversible (fround in platelets)
COX - 2 reversible

Platelets - anucleated so can’t produce more proteins, so shuts doesn platelet TXA2 production and aggregation

low-dose aspirin therapy more or less platelet specific

41
Q

leukotriene synthesis

A

enz; 5-lipoxygenase (5-LOX);
arachadoinc acid -> leukotriene A4 (LTA4)
(intermmediate = 5-hydroperoxyeicosatetranoic acid, 5 HPETE)

not Cyclic (unlike prostaglandins and thromboxanes)
exert effects via GPCR
many contain conj cysteine residue (fr glutathione) = Cysteinyl leukotrienes
- these are the slow-reacting substance of anaphylaxis (SRS-A) - asthma
- inhib of 5-LOX & antagonists of CysLT-1 tx for asthma

Biochem (13 decks)

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