PHOSPHOLIPID, GLYCOSPHINGOLIPID, AND EICOSANOID METABOLISM Flashcards

(50 cards)

1
Q

are a class of lipids that are essential components of cell membranes.
They are amphipathic molecules.
Major components of biological membranes

A

Phospholipids

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2
Q

Two classes of phospholipids:

A

Glycerophospholipids
Sphingophospholipids

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3
Q

(contain glycerol backbone)

A

Glycerophospholipids

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4
Q

(contain sphingosine)

A

Sphingophospholipids

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5
Q

Serine + PA →

A

phosphatidylserine (PS)

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6
Q

Ethanolamine+PA→

A

phosphatidylethanolamine (PE) (cephalin)

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7
Q

Choline + PA →

A

phosphatidylcholine (PC) (lecithin)

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8
Q

Inositol + PA →

A

phosphatidylinositol (PI)

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9
Q

Glycerol + PA →

A

phosphatidylglycerol (PG)

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10
Q

an important component of myelin that protects and insulates nerve fibers

A

Sphingomyelin

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11
Q

are a major component of lung surfactant

A

Phospholipids

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12
Q

a phospholipid that is found in relatively large amounts in mitochondrial membranes.

is a precursor of cardiolipin, a phospholipid that is unique to mitochondria

A

Phosphatidylglycerol

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13
Q

Phosphatidylserine (PS) is synthesized from phosphatidylethanolamine (PE) and free serine in a base exchange reaction catalyzed by the enzyme ___

A

phosphatidylserine synthase.

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14
Q

Defects in phospholipid synthesis can lead to a variety of diseases, including

A

respiratory distress syndrome (RDS)

acute respiratory distress syndrome (ARDS)

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15
Q

Phosphoglycerides are degraded by ___, a group of enzymes that hydrolyze the phosphodiester bonds of phosphoglycerides.

A

phospholipases

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16
Q

Phospholipases are also responsible for ___, which is a process of removing and replacing fatty acids on phospholipids.

A

remodeling phospholipids

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17
Q

Sphingomyelin is degraded by __

A

sphingomyelinase

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18
Q

a lysosomal enzyme that hydrolyzes the phosphodiester bond between the phosphate group and the choline group on sphingomyelin.

A

sphingomyelinase

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19
Q

is a lysosomal storage disease caused by a deficiency of sphingomyelinase.

A

Niemann-Pick disease

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20
Q

most severe form of the disease and is characterized by rapid and progressive neurodegeneration.

A

Type A Niemann-Pick disease

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21
Q

less severe and does not cause damage to the nervous system.

A

Type B Niemann-Pick disease

22
Q

are molecules that contain both carbohydrate and lipid components.
They are derivatives of ceramides.
Act as: Blood group antigens, cell surface receptors for bacteria/viruses

23
Q

are composed of a ceramide backbone and a carbohydrate head group

A

Glycosphingolipids

24
Q

Glycosphingolipids TYPES

A

Neutral glycosphingolipids
Acidic glycosphingolipids

25
do not have a net charge at physiological pH.
Neutral glycosphingolipids
26
have a net negative charge at physiological pH.
Acidic glycosphingolipids
27
____ are the most complex acidic glyco- sphingolipids. They contain one or more sialic acid residues attached to the carbohydrate head group.
Gangliosides
28
These are a group of genetic disorders in which glycosphingolipids accumulate in cells and tissues.
Lipid storage disorders:
29
Glycosphingolipids are thought to play a role in the development of neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease.
Neurodegenerative diseases
30
Cancer: ___ can be used as tumor markers to diagnose and monitor cancer.
Glycosphingolipids
31
Synthesis of glycosphingolipids: occurs primarily in the
Golgi apparatus.
32
___ can recognize both glycosphingolipids and glycoproteins as substrates.
Glycosyltransferases
33
Glycosphingolipids are degraded in ___.
lysosomes
34
are organelles that contain enzymes that can break down a variety of molecules.
Lysosomes
35
can lead to lysosomal storage diseases.
Defects in glycosphingolipid degradation
36
are a group of genetic disorders in which specific molecules accumulate in cells due to deficiencies in lysosomal enzymes
Lysosomal storage diseases
37
It is caused by a deficiency of the enzyme hexosaminidase A, which breaks down the molecule GM2 ganglioside. typically appear in the first few months of life and include blindness, deafness, seizures, and muscle weakness.
Tay-Sachs disease
38
It is caused by a deficiency of the enzyme hexosaminidase A and B. Symptoms: similar to those of Tay-Sachs disease, but they typically appear earlier in life and are more severe.
Sandhoff disease:
39
This is a genetic disorder that affects the way the body metabolizes fat. It is caused by a deficiency of the enzyme glucocerebrosidase, which breaks down the molecule glucocerebroside. symptoms, including hepatosplenomegaly (enlargement of the liver and spleen), skeletal deformities, and bleeding disorders
Gaucher disease
40
It is caused by a deficiency of the enzyme galactocerebrosidase, which breaks down the molecule galactocerebroside. Symptoms: typically appear in the first few months of life and include irritability, stiffness, seizures, and developmental delays.
Krabbe disease
41
This is a group of genetic disorders that affect the way the body metabolizes cholesterol. It is caused by a deficiency of one of several enzymes that break down cholesterol and other lipids.
Niemann-Pick disease
42
This is a rare genetic disorder that is X-linked, meaning that it affects males more often than females. It is caused by a deficiency of the enzyme alpha-galactosidase A, which breaks down the molecule globotriaosylceramide (Gb3) symptoms, including a redpurple skin rash, kidney and heart failure, and burning pain in the extremities
Fabry disease
43
It is caused by a deficiency of one of several enzymes that break down the molecule sulfatides. Sulfatides build up in the myelin sheath, which is the protective coating that surrounds nerve fibers.
Metachromatic leukodystrophy
44
Disorfer that affects the way the body metabolizes ceramides. It is caused by a deficiency of the enzyme acid ceramidase, which breaks down ceramides. symptoms, including painful and progressive joint deformity, subcutaneous nodules of lipid-laden cells, and a hoarse cry.
Farber disease
45
are a class of signaling molecules derived from arachidonic acid. They are produced by a variety of enzymes, including cyclooxygenases (COX-1 and COX-2), lipoxygenases (LOXs), and epoxygenases.
Eicosanoids
46
The first step in the synthesis of prostaglandins and thromboxanes is the conversion of arachidonic acid to prostaglandin endoperoxide H2 (PGH2) by __
COX-1 or COX-2.
47
family of lipid mediators that promote platelet aggregation and vasoconstriction.
Thromboxanes
48
The most important thromboxane is ___ it is produced by activated platelets and plays a key role in blood clot formation
thromboxane A2 (TXA2). TXA2
49
are a family of lipid mediators that play a role in inflammation and allergic reactions.
Leukotrienes
50
are a family of lipid mediators that play a role in a wide range of physiological and pathophysiological processes.
Prostaglandins