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Biochem 2 Exam 2 > ROS - Free Radicals > Flashcards

ROS - Free Radicals Flashcards

0
Q

Oxygen toxicity results from what?

A

It results from reactive oxygen species and free radicals.

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1
Q

What are the two faces of oxygen

A

It supports life, but also bears toxicity

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2
Q

What are free radicals and why are they harmful?

A

Free radicals are atomic or molecular species which are extremely reactive because they have an unpaired electron.

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3
Q

What do ROS and free radicals initiate?

A

Cell injury

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4
Q

Detoxification mechanisms overlap with what system?

A

The antioxidant system. Detoxification is one of the biggest generators of ROS.

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5
Q

How are ROS generated?

A

One-electron transfers generate ROS

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6
Q

Why don’t we want free iron floating around in the blood?

A

Iron (Fe2+) and also copper (Cu1+) combine with H2O2 to create OH* (hydroxyl radical: the “bad actor”) and OH-. This is the Fenton reaction.

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7
Q

Where is the superoxide anion (O2-)produced?

A

It is produced in the electron transport chain, among other sites. It generates other ROS, but CAN NOT diffuse far from the site of origin.

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8
Q

Hydrogen peroxide (H2O2) is NOT a free radical, so how is harmful?

A

It can generate free radicals by reaction with a transitional metal (i.e. Fe3+ or Cu1+). It can also diffuse into and through cell membranes.

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9
Q

What is the most reactive species in attacking biological molecules and how is produced?

A

OH* (Hydroxyl radicals). They are produced by H2O2 in the presence of Fe2+

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10
Q

What is produced by bacteria during the respiratory burst to destroy invading organisms?

A

HOCl (Hypochlorous acid)

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11
Q

What are endogenous sources of free radicals in the body?

A

COX, LOX, Cytochrome P450, desaturases, xanthine oxidase - from enzyme activity, electron transport chain, and phagocytic respiratory burst.

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12
Q

What are exogenous sources of free radicals?

A

UV radiation, drugs (doxorubin), and air pollutants

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13
Q

Why is CoQ10 the biggest offender of free radical formation?

A

It is abundant, it is small, and unprotected.

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14
Q

What other area of the ETC is a potential source of interaction for ROS?

A

The complexes that utilize metals (Fe, Cu)

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15
Q

What is the key enzyme that creates HOCl, and causes destruction of the surface of bacteria through the respiratory burst? And which phagocytic cell secretes this enzyme?

A

Myeloperoxidase; neutrophil

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16
Q

Lipids are susceptible to free radical damage. Oxidation involves the removal of _________ _________ from a/an _____________ fatty acid.

A

hydrogen radicals; unsaturated

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17
Q

Which type of unsaturated fatty acids are the MOST susceptible to oxidative damage and why?

A

Polyunsaturated fatty acids (PUFA); because they have more double bonds

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18
Q

Oxidation products form with what two other biosynthetic products?

A

amino acid residues and DNA

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19
Q

Free radical damage to PUFA can involve what two reactions?

A
  1. ) decomposition to bifunctional aldehydes and/or a,B-unsaturated aldehydes which can form adducts or crosslink other biomolucules (this gives more binding sites).
  2. ) reacting with sulfhydryl groups on enzymes
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20
Q

What are the four stages of the mechanisms for free radical damage of lipids?

A

Initiation, propagation, degradation, and termination

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21
Q

What is the reaction taking place during initiation?

A

LH reacts with OH* (the bad actor) and creates a L* and H2O

22
Q

What is the reaction taking place during propagation and where will it go next?

A

The L* reacts with O2 to create LOO* which can continue on to either termination or propagation/degradation.

23
Q

If the LOO* interacts with antioxidants, it will follow which path and ultimately become what?

A

It will follow the termination pathway to become non-radical products or stable radicals.

24
Q

If the LOO* follows the propagation pathway, what other pathway will it interact with and what will be the outcomes?

A

LOO* will interact with LH leaving the L* to continue back through the cycle of propagation, and the LOOH will degrade to 4-HNE, malondialdehyde, ethane/pentane and other products.

25
Q

How do cells protect themselves against free radical damage/oxygen toxicity (the first line of defense).

A

Antioxidant enzymes: glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT).

26
Q

What are the other free radical scavengers (the second line of defense)?

A

Endogenous: Uric acid & CoQ10
Exogenous: Vitamin E & Vitamin C

27
Q

What is the third line of defense that mediates oxidative damage?

A

Repair de novo excision

28
Q

What is the fourth line of defense leading to diseases and aging?

A

Adaptation

29
Q

How do ROS/RNS/ROCl lead to oxidative stress?

A

They cause disturbance of redox balance

30
Q

How does oxidative stress lead to oxidative damage?

A

There is an oxidation of biological molecules

31
Q

What are the cellular and tissue locations of antioxidants?

A

Cellular: mitochondria, peroxisomes, and cytosol
Tissue: liver, adrenals, and kidneys

32
Q

What metal is associated with cytosolic SOD?

A

Cooper and Zinc

33
Q

What metal is associated with mitochondrial SOD?

A

Manganese

34
Q

What metal is associated with GSH peroxidase?

A

Selenium

35
Q

Absorption of Vit C occurs where and by what means?

A

Distal small intestine; through a sodium dependent ascorbate transporter (SVCT1)

36
Q

How do other cells acquire Vit C?

A

They use either SVCT2 or GLUT 1 & GLUT 3 transporters.

37
Q

What is the primary scavenger/antioxidant that neutralizes radical oxygen and nitrogen species, peroxides, and superoxide?

A

Ascorbate

38
Q

Ascorbate is a free radical, why is it okay to have in the body?

A

It is free to move around the body, but it is VERY stable.

39
Q

What is required for the regeneration of the reduced form of Vit C?

A

Reducing agents: NADH, glutathione and an enzyme (NADH reductase, dehydroascorbate reductase, or thioredoxin reductase)

40
Q

Any antioxidant taken in too high of quantities can lead to pro-oxidant, what is an instance of this with Vit C?

A

High dose Vit C can lead to kidney stones and diarrhea as a result of oxalic acid.

41
Q

Where does Vit E come from?

A

It refers to a mixture of tocopherols and tocotrienols (vitamer). It is made from isoprenes and is an intermediate in biosynthesis of cholesterol.

42
Q

What specific part of Vit E is selectively extracted in the liver?

A

a-tocopherol

43
Q

How does Vit E function as an anti-oxidant?

A

It accumulates in membranes and lipoproteins for protection, and it donates electrons to free radical species to neutralize them (terminates membrane lipid oxidation through single electron transfers, forming a stable tocopherol species).

44
Q

How does a redox cycle regenerate reduced Vit E from reduced Vit C?

A

Vit E gets exposed to Vit C on the surface of membranes and a thiol cycle resets the radical scavengers to their reduced form.

45
Q

Maintaining RBC membranes depends upon the production of what two products?

A

NADPH and ATP from glycolysis.

46
Q

What is the purpose of NADPH in the removal of ROS?

A

NADPH reduces glutathione which ultimately removes the ROS

47
Q

What is an action of ROS?

A

It creates cross-linked hemoglobins, which shortens RBC life cycles.

48
Q

What enzymatic deficiency is the MOST COMMON genetic enzyme deficiency? And with which condition does it co-localize?

A

Glucose-6-phosphate dehydrogenase; it co-localizes with malaria

49
Q

What is the danger with having a G-6-P dehydrogenase deficiency?

A

It produces anemia and excessive destruction of RBCs

50
Q

What are some oxidant stressors that increase ROS in RBCs?

A

Infection, drugs (primaquine - anti-Malaria drug), and fava beans (vicine)

51
Q

What are the 3 isoforms of NOS?

A

eNOS - endothelial, nNO - nervous system, and iNOS - inducible by WBC

52
Q

How are NOS damaging of tissues?

A

Nitric oxide (NO) diffused through membranes (much like H2O2), HONO2 targets thiols and aromatic residues in proteins, and it reacts slowly with Vit C.

Biochem 2 Exam 2 (7 decks)

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