Compound lipids

Dedicated to all Zoologists

1. II- Compound lipids: They composed of fatty acids + alcohol+
other substance which may be phosphorous (phosphlipids), proteins
(lipoproteins), sugar (glycolipid)
(1)Phospholipids
Phospholipids are classified according to alcohol content into:
1- Glycerophospholipids: alcohol is glycerol
2- Sphingophospholipids: alcohol is sphingosine

2. I- Glycerophospholipids
OR

3. The most common glycerophospholipids are:
1- Phosphatidic acid:
it is the simplest phosphlipid and doesn’t have specific functions
2- Lecithin: It is formed of glycerol, two fatty acids, phosphate and
choline which is a nitrogenous base. It is phosphatidic acid +
choline so it is called phosphatidylcholine
Lecithin Phosphatidic acid

4. Cephalins: Their chemical structure is exactly as lecithin but they
differ only in the base which may be:
a)Ethanol amine so called: phosphatidyl ethanol amine
b) Serine and so called phosphatidyl serine
Phosphatidyl serine

5. Phosphatidyl Serine is an important
phospholipid which supports cell
integrity
- Found in high concentrations in
the brain, levels of which decline
with age.
- It is essential for normal neuron
structure and function and may play
a critical role in maintaining
concentration and memory

6. Phosphatidyl ethanolamine (cephalin)
Sources: brain tissues.

7. Phosphatidyl inositol: structure not required
It is one of cell
membrane lipids
(but less common)
In addition it plays a
role in cell
signaling

8. 2-Sphingophospholipids
Sphingomyelin: it is a sphingophospholipid
Not contain glycerol but contain alcohol called : sphingosine,
Fatty acid is attached to amino group of sphingosine and
phosphorylcholine (phosphate + choline) is
attached to the last OH group.
Sources: present in high amount in brain and nerve tissues.

10. Q: Classify each lipid

11. Phospholipids
Phospholipids are lipids containing phosphate. They also contain alcohol
(glycerol or sphingosine), fatty acids and base (choline, ethanolamine or
serine). See the structures
Sources: Exogenous: from diet e.g. eggs
Endogenous: In all cell.

Plasma levels: The average total phospholipids are about 200
mg/dl (60% lecithins, 25% cephalins and 15% sphingomyelins)
Digestion and absorption: begins in the intestine
Phospholipids either absorbed as such or are hydrolyzed by certain
pancreatic phospholipases as follow:
•Phospholipase A
1
: Act on ester bond in position 1: removes the first
fatty acid from lecithin or cephalin producing lysolecithin or
lysocephalin.

12. •Phospholipase A
2
(PLA2)): act on position
2 removes the second fatty acid from
lysolecithin or lysocephalin.
•Phospholipase C (phosphodiesterase): act
on linkage between the glycerol and
phosphate giving free glycerol and
phosphate+base (phosphoryl base)
•Phospholipase D (phosphatase): act on
linkage between phosphate and base giving
free phosphate and free base.

13. PLA2 releases arachidonic acid from C2 of glycerol.
Arachidonic acid enter in synthesis of prostaglandins and
leukotriens which causes inflammation.
PLA2 are commonly found in mammalian tissues as well as
insect and snake venom. Due to the increased presence and
activity of PLA2 resulting from a snake or insect bite,
aracidonic acid is released from the phospholipid membrane .
As a result, inflammation and pain occur at the site of insect
bite.

14. CH
2
O-COR
1
CHOCOR
2
CH
2O-P-O-X
PhospholipaseA
1
CH
2OH
CHO-COR
2
CH
2O-P-O-X
PhospholipaseA
2
CH
2
OH
CHOH
CH
2O-P-O-X
O
R
1
COOH
O
R
2
COOH
Freeglycerol+P+base
PhospholipaseC(phosphdiesterase)
PhosphlipaseD
(phosphatase)
Degradation of phospholipids:
Lysolecithin
or
lysocephaline

15. •If phospholipids absorbed as it is, they are usually absorbed with
triglycerides and cholesterol. All are bound to protein to form
chylomicrons (mainly TG + phospholipids + cholesterol +
apoprotein).

16. Functions of phospholipids:
1- Enter in the structure of cell membranes
2- Help triglycerides transport (enter in the synthesis of chylomicron) .
3- Blood clotting: Cephalins enter in the formation of thromboplastin
which is necessary for blood clotting.
4- Phospholipids act as lipotropic factors i.e. prevent accumulation of
fats in liver hence prevent fatty liver.
5- Phospholipids in bile make cholesterol soluble. Their deficiency
leads to cholesterol gallstones (see image A).
6- Dipalmitoyl lecithin act as lung surfactant, prevent alveolar collapse
and allow air passage (see image B).

17. Image A) Choleserol gallstones

18. Phospholipid bilayer

20. Image B: alveolar collapse in absence of surfactant
(lecithin)

21. Synthesis of Phospholipids: Liver is the site of synthesis
(A) Synthesis of lecithin (phosphatidyl choline) and cephalins
(phosphatidyl ethanolamine and phosphatidyl serine):
Their synthesis needs

1- Glycerol activated by ATP (by glycerokinase) giving 3-
glycerophosphate.
2- Two fatty acids activated by CoA (by thiokinase) giving acyl
CoA (active FA).
3- Choline (for synthesis of lecithin), ethanolamine or serine (for
synthesis of cephalines) activated by CTP to give CDP choline or
CDP ethanolamine or CDP serine.

22. A)
CH
2
-OH
CH-OH
CH
2
-OH
Glycerol
glycerokinase
ATP
ADP
CH
2
-OH
CH-OH
CH
2
-O-PO
3
3-glycerophosphate
B)
2RCOOH
Fattyacid
2CoASH
thiokinase
2RC-SCoA
O
-2CoA
CH
2-O-CO-R
1
CH-O-CO-R
2
CH
2
-O-PO
3
Phosphatidicacid
Phosphatase
p
i
CH
2O-CO-R
1
CH
2
-O-H
CH
2
O-CH
3O-R
2
1,2diacylglycerol(DAG)
CDP-choline
Lecithicin
Acyl CoA
C)
Lecithin
Synthesis of Lecithin

23. B) Synthesis of sphingomyelins (not required, cancelled):
Sphingomyeline is formed of sphingosine base, fatty acyl CoA, phosphate and
choline. (Remembr structure, first lecture).
Steps of synthesis: see figure
1- Palmitic acid is activated by CoA to give palmitoyl CoA.
2- Combination of palmitoyl CoA with serine to form sphingosine base.
3- Then sphingosine reacts with acyl CoA to form ceramide
4- Ceramide then reacts with lecithin (phosphatidyl choline) to form
sphingomyelin and diacylglycerol.
Degradation of phospholipids:
- Lecithin and cephalins are degraded by plasma phospholipases A
1
, A
2
, C and D.
(as before).
-Sphigomyelin is degraded by sphingomyleinase

24. Niemann-Pick disease: in children
It is one of lipid storage disease in which harmful
quantities of fatty substances, or lipids, accumulate in the
spleen, liver, lungs, bone marrow, and brain
Niemann-Pick disease results from genetic absence of
sphingomyelinase enzyme (the enzyme that breakdown
excess sphingomylein). The absence of this enzyme leads
to accumulation of sphingomyelin in liver and spleen
leading to enlargement of these organs and may cause
reduced appetite, abdominal distension and pain, and the
enlarged spleen may trap platelets and other blood cells,
leading to reduced numbers of these cells in the
circulation. The disease is fatal in early life.
Sphingomyelin accumulation in the brain results in
unsteady gait (ataxia), slurring of speech and difficult
swallowing (dysphagia). More widespread disease
involving the cerebral crortex cause dementia and
seizers.

25. CH
3(CH
2)
12CH
2CH
2C-CoA+OH-CH
2-CH COOH
O
NH
2
Serine
PamitoylCoA
CO
2
CH
3
(CH
2
)
12
CH
2
CH
2
C-CH-CH
2
-OH
O
NH
2
CoA
Ketosphinganine
1-reductionofketogroupintoCHOH,
2-oxidationofCH
2
CH
2
intoCH=CH
CH
3
(CH
2
)
12
CH=CHCHCH-CH
2
-OH
HONH
2
RC-CoA acylCoA
O
CH
3(CH
2)
12CH=CHCHCH-CH
2-OH
Sphingosine
HO
HNC=O
Ceramide
Phosphatidylcholine
CH3(CH2)12CH=CHCHCH-CH2-O-P-O-CH2CH2N(CH3)3
HO
R
HNC=OO
OH
Sphingomyelin
Not
required