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PA20351 > Proteases, reactive oxygen and nitrogen species > Flashcards

Proteases, reactive oxygen and nitrogen species Flashcards

1
Q

What are proteases derived from?

A

Plasma zymogens, tissue cells and activated leukocytes.

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2
Q

What do proteases have a central role in?

A

Host defence, removal of damaged tissue, initiating repair and inflammation.

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3
Q

What effect do kinins have?

A

They cause vasodilation, increased permeability and pain.

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4
Q

What is the complement?

A

A larger protein consisting of 10 amino acids.

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5
Q

What does the complement system cause?

A

Leukocyte activation, chemotaxis, mast cell degranulation, bacterial opsonisation and lysis.

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6
Q

What are plasma proteases activated by?

A

Tissue injury, antibody complexes and foreign surfaces.

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7
Q

What do the complement components assemble to form?

A

A pore that helps to lyse target cells.

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8
Q

What is the C3b component of the complement important in?

A

It is a ligand for integrins on the neutrophil surface - it has a dual function.

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9
Q

What is thrombosis?

A

The generation of clotting factors via the protease cascade.

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10
Q

What is the clotting cascade important in?

A

Thrombosis, platelet activation and activating kinin and complement pathways.

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11
Q

What is angioedema?

A

Deep cutaneous and musosal swelling of the lips, tongue, larynx GI that lasts for days.

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12
Q

What is urticaria?

A

An outbreak of swollen, pale red bumps that appear on the skin suddenly. Angioedema is a form of this.

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13
Q

What is the cause of angioedema?

A

Mast cell degranulation.

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14
Q

How can angioedema be treated?

A

H1 antagonists.

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15
Q

What are some of the other forms of angioedema?

A

Histamine-independent forms such as drug induced or hereditary.

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16
Q

What are some of the causes of hereditary angioedema that have been identified?

A

Several gene defects such as increased complement or bradykinin activation resulting in a decrease in protease inhibitors and increased kininogenase.

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17
Q

What can hereditary angioedema be treated with?

A

Exogenous C1 inhibitor and bradykinin receptor antagonist.

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18
Q

What is an example of a bradykinin receptor antagonist?

A

Icatibant.

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19
Q

How are can angioedema be induced?

A

Induced by angiotensin converting enzyme inhibitor (ACE).

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20
Q

How can drug induced angioedema be caused?

A

ACE inhibitors block ANGII synthesis, which is useful in hypertension, but they block bradykinin degradation

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21
Q

What happens if ACE inhibitors are used in patients?

A

There will be elevated levels of bradykinin which will result in increased inflammation, as bradykinin is usually inactivated by ACE.

22
Q

Why are ACE inhibitors used to lower blood pressure?

A

ACE is responsible for metabolising angiotensin 1 to 2, which elevates blood pressure - blocking this can decrease blood pressure.

23
Q

What happens if an animal is immumised against specific collagen?

A

You can induce a type of arthritis.

24
Q

What are the families of proteolytic enzymes?

A

MMP, serine proteinases, cysteine proteinases and aspartate proteinases.

25
Q

What is cartilage made up of?

A

Collagen and proteoglycans.

26
Q

What happens to tissue in rheumatoid arthritis?

A

Cartilage proteoglycans are lost rapidly so there is loss of joint function and resulting pain.

27
Q

What happens to proteoglycans in rheumatoid arthritis?

A

As they have an open structure they are highly accessible and therefore sensitive to breakdown by several proteinases.

28
Q

What happens to collagen in rheumatoid arthritis?

A

It is lost more slowly than proteoglycan, but causes the loss of function of cartilage as a smooth surface. It is broken down by MMPs (collagenases).

29
Q

What are matrix metalloproteinases?

A

MMP - they break down collagen and other matrix proteins. They are a major class of enzymes that degrade cartilage.

30
Q

What conditions do MMPs need to function?

A

They are active at neutral pH and contain and require Zn2+ ions.

31
Q

What are MMPs inhibited by?

A

Tissue inhibitors of metallo-proteinases, TIMPs.

32
Q

What is the usual balance between MMPs and TIMPs?

A

There is usually a balance to provide a turnover to repair for restoration. If this balance is wrong there is tissue damage.

33
Q

What is the domain structure of MMP?

A

There is a propeptide, catalytic, hinge and C-terminal region.

34
Q

What is MMP activated by?

A

Removal of propeptide by other proteases such as elastase or plasmin and chemicla modification of propeptide by RONS.

35
Q

What is the C-terminus of MMP important in?

A

Substrate specificity and regulation.

36
Q

What drugs can be used in inflammation?

A

Synthetic MMP inhibitors.

37
Q

What are peptidomimetics?

A

Small hydroxamic acid-based molecules based on collagen structure. They are effectively used to inhibit MMP activity, but lack specificity and act on most metalloenzymes.

38
Q

What can tetracycline derivatives be used for?

A

Reducing MMP synthesis and activity - doxycycline is used for the treatment of periodontal and skin disease.

39
Q

What are serpins?

A

Serine protease inhibitors.

40
Q

What are serpins inactivated by?

A

Oxidation.

41
Q

What proteinases break down matrix proteins?

A

Elastin, laminin, chondroitin sulfate and proteoglycans.

42
Q

What are some of the adverse effects of MMP inhibitors?

A

Musculoskeletal syndrome, lack of specificity.

43
Q

What are reactive oxygen and nitrogen species (RONS) produced by?

A

Infiltrating leukocytes and tissue resident cells.

44
Q

What is H2O2 inactivated by?

A

Catalase.

45
Q

What does NADPH catalyse the formation of?

A

Superoxide.

46
Q

What is H2O2 metabolised to form?

A

Hydroxyl radical OH-, hypohalous acids such as HClO.

47
Q

What is respiratory burst?

A

When leukocytes phagocytose and release reactive oxygen species.

48
Q

What is hypoxia?

A

A condition when the body is deprived of adequate oxygen supply at tissue level.

49
Q

How do oxidant levels vary in rheumatoid arthritis patients?

A

There is increased oxidant and decreased antioxidant levels - a disturbed balance in inflammatory diseases.

50
Q

What effects do RONS cause?

A

They activate inflammatory gene transcription (NFKB, further inflammation), they cause amino acid modifications, matrix modifications, DNA damage and cell apoptosis and necrosis.

51
Q

What amino acid modifications occur due to RONS?

A

Inactivation of serpins, modification of latent MMPs, making host proteins immunogenic.

52
Q

Was there an association between disease and antioxidant intake found in studies?

A

No - no association.

PA20351 (11 decks)

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