Term
| What are some of the common phospholipids? |
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Definition
phosphatidylserine
phosphatidylethanolamine
phosphatidylcholine
phopsphatidylinositol
diphosphatidylglycerol |
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Term
| How is phosphatidate formed? |
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Definition
It comes from Dihydroxyacetone phosphate (produced in glycolysis).
DAP is reduced to glycerol 3-phosphate.
Fatty acid from Acyl-CoA is added to C1 and C2 of glycerol 3-phosphate forming phosphatidate. |
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Term
| How is phosphatidate used in the synthesis of phospholipids? |
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Definition
Two enzymes will act on phosphatidate:
phosphatidate phosphohydrolase (produces diacylglycerol and Pi)
phosphatidate:CTP cytidyl transferase (produces CDP-diacylglycerides and PPi).
All of the phosphoglycerides can be synthesized from phosphatidate via CDP-diacylglyceride. |
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Term
| How is phosphatidylcholine synthesized? |
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Definition
Phosphatidyl choline can be made by
i) three N-methylations of phosphatidylethanolamine using S- adenosylmethionine;
ii) CDP-diacyl-glyceride reacting with the free hydroxyl of choline;
iii) CDP-choline reacting with diacyl glycerol. |
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Term
| How is phosphatidylethanolamine synthesized? |
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Definition
PE can be made by
i) the decarboxylation of phosphatidylserine (PS)
ii) base exchange between the serine of PS and ethanolamine (reversible reaction - the reverse is used to make PS)
iii) the CDP ethanolamine reaction with 1,2-diacylglycerol |
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Term
| What is the remodeling pathway and why is it important? |
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Definition
sn-1-palmitoyl and sn-2-oleolyllecthin react to form sn-1-palmitoyllysolecithin using phospholipase A2.
sn-1-palmitoyllysolecithin can then either react with itself (1 pathway) or palmitoyl CoA (2nd pathway) to form dipalmitoyllecithin (dipalmitoylphosphatidylcholine)
Disaturated-PC is the largest component of human lung surfactant. |
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Term
| What is respiratory distress syndrome? |
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Definition
The respiratory distress syndrome (RDS) is a major cause of neonatal morbidity and mortality in many countries
It accounts for approximately 15—20% of all neonatal deaths in Western countries and somewhat less in the developing countries.
The disease affects only premature babies and its incidence varies directly with the degree of prematurity.
Premature babies develop RDS because of immaturity of their lungs, resulting from a deficiency of pulmonary surfactant.
The maturity of the fetal lung can be predicted antenatally by measuring the lecithin/sphingomyelin (L/S) ratio in the amniotic fluid.
The mean L/S ratio in normal pregnancies increases gradually with gestation until about 31 or 32 weeks when the slope rises sharply. |
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Term
| How is the L/S ratio related to respiratory distress syndrome? |
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Definition
L/S ratio = lecithin/sphingomyelin ratio
The ratio of 2.0 that is characteristic of the term infant at birth is achieved at the gestational age of about 34 weeks. In terms of predicting pulmonary maturity, the critical L/S ratio is 2.0 or greater.
The risk of developing RDS when the L/S ratio is less than 2.0 has been worked out: for an L/S ratio of 1.5—1.9, the risk is approximately 40%, and for a ratio less than 1.5 the calculated risk of developing RDS is about 75%.
Diabetes delays development of the fetal lung. Fetuses of mothers with diabetes mellitus need to have a L/S ratio of 3.4 to indicate a fully mature lung; the risk of developing RDS is high with L/S ratios less than 2.0. |
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Term
| What enzymes degrade intact phospholipids? |
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Definition
Phospholipase A1 degrades at the carboxyl group attached to C1
Phospholipase A2 degrades at the carboxyl group attached to C2
Phospholipase C kicks off the phosphate group attached to C3
Phospholipase D kicks off the side group (serine, choline,inositol, ethanolamine etc.)attached to the phosphate
They all work independently only on intact phospholipids only
They can create products like IP3 and DAG that are important 2nd messengers |
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Term
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Definition
sphingolipids are sphingosine containing lipids. they have sphingosine as opposed to glycerol as the alcohol portion. These include:
sphingomyelin (ceramide phosphocholine)
cerebrosides (ceramide monohexoside)
globosides (ceramide oligosaccharide, without N-acetyl neuraminic acid, NANA)
gangliosides (ceramide oligosaccharide, containing one or more NANA)
sulfatides (globosides which are sulfated). |
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Term
| How does ganglioside nomenclature work |
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Definition
Example
Ganglioside Gm2
m = mono (d = di, t= tri and so on)
2 tells you the type of structure (#'s 1-3) |
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Term
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Definition
A series of reactions starting with palmitoyl-CoA and serine.
requires pyridoxal phosphate and Mn2+ |
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Term
| How is ceramide important? |
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Definition
It is the immediate precursor of sphingomyelin
Ceramide reacts with phosphatidlycholine to form sphingomyelin
Ceramide is also used to form cerebrosides, gangliosides, globusides, and sulfatides |
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Term
| What is the enzyme deficiency of Tay-Sachs and what accumulates? |
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Definition
Hexosaminidase A is deficient
Gm2 ganglioside accumulates |
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Term
| What is the enzyme deficiency of Fabry's disease and what accumulates? |
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Definition
alpha-galactosidase is deficient
Globotriaosylceramide accumulates |
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Term
| What is the enzyme deficiency of Krabbe's disease and what accumulates? |
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Definition
beta-galactosidase is deficient
galactosylceramide accumulates |
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Term
| What is the enzyme deficiency of Gaucher's disease and what accumulates? |
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Definition
beta-glucosidase is deficient
glucosylceramide accumulates |
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Term
| What is the enzyme deficiency of Niemann-Pick disease and what accumulates? |
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Definition
sphingomyelinase is deficient
sphingomyelin accumulates |
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Term
| How is sphingolipid synthesis regulated? |
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Definition
It is only regulated by the availability of the carbohydrates needed.
things like hormones and ATP do not serve as regulators |
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Term
| Explain prostaglandin synthesis |
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Definition
Phospholipase A2 can convert phospholipids into arachidonic acid. This step is inhibited by ant-inflammatory steroids (like cortisol)
Cyclooxygenase converts arachidonic acid to prostaglandins. This step is inhibited by aspirin, idomethacin, and phenlybutazone (non-steroidal ant-inflammatory compounds)
There are two types of Cyclooxygenase. COX-1 is constitutively expressed and COX-2 is inducible |
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Term
| How are prostaglandins, prostanoids, and leukotrines produced? |
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Definition
| They are produced from arachidonate, eicosapentaenoate (EPA found in fish oil), and 8,11,14-eicosatrienoate |
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Term
| What is the importance of leukotrienes? |
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Definition
They are powerful constrictors of bronchial and intestinal smooth muscle and they increase capillary permeability.
They are unique from other eicosanoids because they can survive for hours in tissue (as opposed to minutes)
They are mediators of allergic reactions and assoc. with anaphylatic shock |
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Term
| How do thromboxane A2 and prostacyclin relate |
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Definition
They are eicosanoids with opposite effects
Thromboxane A2
- promotes platelet aggregation
- decreases formation of cAMP
- causes vasoconstriction
Prostacylcin (PGI2)
- inhibits platelet aggregation
- increases formation of cAMP
- causes vasodilation |
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Term
| How do PGE2 and PGF2 relate? |
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Definition
They are prostaglandins with opposite effects
PGE2
- causes vasodilation
- relaxes smooth muscle
- used to induce labor
PGF2
- causes vasoconstriction
- causes smooth muscle contraction
- stimulates uterine contractions |
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