Lipids 2 Flashcards

1
Q

1st Lipid Functions

A

The vast bulk of cellular lipids (not counting triglycerides) serve as bilayer structural components.

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2
Q

2nd lipid function

A

Lipids, especially acidic phospholipids, can serve as modulators of the activity of both soluble and membrane-bound proteins.

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3
Q

3rd lipid function

A

Phosphatidylinositol serves as part of the tether of GPI-anchored membrane proteins.

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4
Q

4th lipid function

A

Ether-linked glycerophospholipids, such as platelet activating factor, can act as molecular signals.

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5
Q

5th lipid function

A

Derivatives of phosphatidylinositol act as intracellular second messengers in signal transduction pathways involved with many aspects of cellular regulation.

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6
Q

6th lipid function

A

Fatty acid metabolites, the eicosanoids, act as potent, short-lived hormone-like molecules.

  • ecosatetranoic acid (arachidonic acid)
  • imflamation
  • pain
  • fever
  • blood clotting affected
  • uterine contractions
  • sleep cycle
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7
Q

phospholips release

A

arachidonic acid (20:4)

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8
Q

what are 2 pathways

A

Cyclic: prostaglandins and thromboxanes

linear:
- leukotrienes

-Lipoxins
Hepoxilins
Epi-lipoxins

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9
Q

precursor to prodce 2 series… how to determine subscript

A

number of unsaturated bonds’

  • 2 series can be derived:
    • same as # of unsaturated
    • # of unsaturated -2
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10
Q

What can we make from palminate?

name essential FA

A

palmitate- stearate - Oleate

we cannot desaturate it beyond Oleate acid

-plants saturate it to make Linoleate acid (essential)

linolate- gamma linoleate –Elongation to Eicosatrienoate - desaturation to Arachodonate

Other path:
linoleate - alpha linoleate- other polyunsat FA’s

-other essential FA is alpha- linolenate

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11
Q

omega carbon is which

A

the last one

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12
Q

delta # is position of saturated bond from:

A

omega carbon

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13
Q

not high yield:

how are elongation steps carried out?

A

The elongation steps, carried out in the smooth ER and mitochondria, involve the addition of acetyl groups from Coenzyme A (instead of ACP, as with stearate synthesis).

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14
Q

what is a- linoleate

what is gamma linoleate

A

a-linolenate is an w-3 fatty acid

gamma-linolenate is an w-6 fatty acid

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15
Q

w-3 fatty acid

A

90% reduction in Sudden Cardiac Death

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16
Q

plants can change which omega FA?

A

9 to 6

6 to 3

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17
Q

phospholipase if it cleaves FA at position 1

A

Phospholipase A1

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18
Q

phospholipase if it cleaves FA at position 2

A

Phospholipase A2

  • sn2 position (related to ecosanoids)
  • releases FA
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19
Q

phospholipase if it cleaves head group

A

Phospholipase D

20
Q

phospholipase if it cleaves phosphohead group

A

phospholipase C

leaves diacylglycerol

21
Q

rate limited step of ecosanoid synthesis

A

releasing of FA by phospholipase A2

-also targeted step of anti- imflamatory action of glucocorticoids

22
Q

if phospholipase C cuts first what happens

A

minor pathway:

followed by diacylglycerol lipase to release the same thing arachidonic acid

23
Q

cyclooxygenase (COX)

A

arachadonate is converted into PGH2 by a bifunctional enzyme, cyclooxygenase (COX). The conversion is a two step process. First molecular oxygen is introduced to produce PGG2 and then the peroxidase activity produces PGH2.

24
Q

PGH2 is precursor for what

A

PGH2 is the precursor for the production of the prostaglandins and thromboxanes.

25
Q

what blocks COX

A

The action of COX is blocked by aspirin and other NSAIDs.

26
Q

Aspirin is what

A

Aspirin as a nonsteroidal antiinflammatory drug

  • blocks 1st reaction of COX
  • irreversible rxn
27
Q

how does aspirin work on COX

A

serine residue acetylates OH to O-C=O-CH3

28
Q

tylenol, ibuprofen, and Naproxen

A

other nsaids are reversible

29
Q

COX1

A

House keeping

  • renal blood flow
  • protects from gastric acids
  • vascular homeostasis
30
Q

Cox2

A

inducible in response to imflamation mediators

31
Q

aspirin inhibits which isomer

A

both COX1 and COX 2

32
Q

2nd gen NSAIDS

A

target COX 2 (VALINE VS ISOLEUCINE)

drug cant get pass isoleucine but it can pass valine

  • Celecoxib
  • Rofecoxib

300 times more inhibition of COX 2 compared to COX 1

33
Q

Thromboxin A2

A

strong platelet activity (made by platelets)

34
Q

tylenol

A

may affect COX 3

35
Q

prostacyclin

A

prevents clots from forming clots

36
Q

aspirin shifts to prostacyclin side how

A

platelets irrevesible block platelet forming (no nucleus)

  • more thromboxane synthase

endothelial cells have nucleus so they can make new cyclooxygenase

  • more prostacyclin synthase
37
Q

pain relief

A

not explained ( many other pathways)

38
Q

omega 3 FA

A

release more pentainoic acid

  • gives rise to PG H3
  • PGI3

ALSO many other mechanism TAG’s etc

39
Q

Leukotriene biosynthesis begins with

A

the action of 5-lipoxygenase.

40
Q

LTB4 promotes:

A

LTB4 promotes inflammation. Implicated in chronic inflammation associated with atherosclerosis.

41
Q

cysteinyl-leukotrienes

A

LTC4, LTD4, and LTE4

-important mediators of immune-mediated inflammatory reactions of anaphylaxis.

42
Q

Treatments for asthma include

A

antileukotriene agents that inhibit 5-lipoxygenase or the binding of the activator protein

43
Q

lipoxins have opposing action to:

A

Interestingly, lipoxins have opposing action to LTC4. They inhibit bronchial spasms and have anti-inflammatory properties.

44
Q

A new class of lipoxins are:

how are they different?

what is their synthesis triggered by?

what actions do they have?

A
A new class of lipoxins, epi-lipoxins,
differ in their stereochemistry.

Their synthesis is triggered by aspirin.

They also have potent anti-inflammatory actions, further explaning the efficacy of aspirin

45
Q

The Newest Players

A

Resolvins and Protectins

  • Potent anti-inflammatory action
  • Derived from the 20:5 and 22:6 w-3 fatty acids by a pathway involving aspirin-acetylated COX2 followed by 5-lipoxygenase. In the absence of aspirin-triggered COX2, EPA and DHA are acted on by 15-lipoxygenase to generate other anti-inflammatory agents.
  • It has been suggested by some that a dietary supplement of w-3 fatty acids, taken with aspirin, may reduce the clinical symptoms of several disease states, including inflammatory disorders (such as arthritis), cardiovascular disease, asthma, and certain cancers.