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Molecule Damage theory of Ageing Flashcards

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1
Q

what is the general molecular damage theory of ageing?

A

One class of theories of aging is based on the concept that damage, either due to normal toxic by-products of metabolism or inefficient repair/defensive systems, accumulates throughout the entire lifespan and causes aging

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2
Q

what does AGE stand for?

A

advanced glycation endproducts

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3
Q

what ageing disease has AGEs been implicated specifically in? (4)

A

osteoarthritis, vascular stiffening and various amyloidoses, diabetes

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4
Q

what type of sugars in glycation carried out by?

A

reducing sugars

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5
Q

how do AGE generally form?

A

they form as a result of glycation which involves the condensation of reducing sugars with free amino groups in lysine, hydroxylysine or arginine residues. A covalent bond is formed between the amino acid and the sugar and is proceeded by reactions which give rise to AGEs

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6
Q

what are the residues prone to AGEs?

A

lysine, hydroxylysine and arginine

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7
Q

as well as reducing sugars, what has also been implicated in AGE formation?

A

lipids - in rats

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8
Q

what influences AGE accumulation?

A

environment, smoking, age and gene

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9
Q

what are the different ways in which AGEs can exist on the protein?

A
  • adducts to the protein (simply joined to)

- protein protein crosslinks

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10
Q

what is important in terms of the quality and quantity of AGEs?

A

not only the quantity but also the type and location of the AGE contributes to the effect of AGE accumulation- even if the number of total sites is low, the localisation of a fet to reactive sites may be very harmful.

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11
Q

once formed, when are AGEs degraded?

A

only when the protein that they are attached to is degraded.

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12
Q

where is the highest area of AGE accumulation?

A

in areas of tissue that have a low turnover- long lived proteins such as crystallin in the lens and collagen in the ECM of connective tissues (cartilage, bone, tendom and skin)

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13
Q

what are the precise tissues in which AGE accumulation is rife?

A

in areas of tissue that have a low turnover- long lived proteins such as crystallin in the lens and collagen in the ECM of connective tissues (cartilage, bone, tendom and skin)

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14
Q

how is connective tissue affected by AGE?

A

its strength is dependent on the amount of intramolecular collagen crosslinks. in artciular cartilage, accumulation of AGE crosslinks results in increased stiffness and brittleness of the tissue, thereby rendering it more prone to mechanical stress and damage

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15
Q

what is the evidence for AGE accumulation over time?

A

• AGE formation -> cross linking between collagen fibres, which increase throughout life. This, e.g. reduces capacity of collagen to swell, makes it resistant to chemical corrosion.
• Diabetic show much greter increase in glycation of collagen- so high glucose levels increases this
- so if increased blood glucose levels (such as that in daibetics) is associated with increased flycation then the levels seen in older people should mean they have more glycation

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16
Q

what is the accumulation of AGEs correlated with? (give 2 precise examples)

A

increased tissue stiffness in arteries, lens, skin and tendon.Increased tissue brittleness following AGE accumulation was shown in human lens capsules and in rat cortical bone in the early 1990s

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17
Q

How can AGEs affect protein degradation and what disease has this property been linked to?

A

AGEs interfere with the susceptitbility of matrix protein towards proteolytic degradation- in alzeihmers- the pathological aggregates of amyloid fibrils are commonly modified by AGEs- AGE formation induces portein aggregaton by inducing refolding of initially globula albumin into amyloid fibrils

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18
Q

what is the evidence connecting AGE accumulation with osteoarthritis?

A
  • ## an in vivo model for OA demonstrated that the accumulation of AGE predisposes to the development of OA- those dogs with model:. Using the established dog anterior cruciate ligament transection model of OA, animals with enhanced AGE levels in articular cartilage showed a statistically significant increase in severity of OA compared with dogs with normal cartilage AGE levels
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19
Q

where has age related accumulation of AGE been shown and in what organism?

A

in humans!

  • cartilage, skin collagen and pericardial fluid
  • the age of human cadavers can be esitmated by the assesmen tof AGEs in the hippocampus
  • mice too
  • in drosophila
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20
Q

Has AGE treatment been shown to aleviate the symptoms of AGEs?

A

yes= Animal models and small trials in humans show that some of the adverse effects of AGEs upon the cardiovascular and renal systems can be reduced with AGE inhibitors or breakers and by dietary restriction of AGEs. In animal models, treatment with alagebrium (formerly ALT7-111), a thiazolium derivative that can break established AGE cross-links, has been shown to reverse arterial and myocardial stiffness and improve cardiac function (93) and reduce AGE deposition in the kidneys and improve renal function

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21
Q

what is the general principle of the damage ageing theory

A

that molecule damage= ageing but maintenance and repair (turnover) means increased longevity

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22
Q

what are the 3 mains kinds of wear and tear?

A

oxidation (free radical theory)
glycation
lipofuscin formation

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23
Q

what is the glycation reaction?

A

it involves a reducing sugar such as glucosr which undergoes a non enzymatic condensation reaction with the amino acid side chains of lysine , hydroxylysine or arginine. The CHO group of the sugar reacts with the NH2 group of the amino acid, a covalent bond forms between the C and the N. following a condensation reaction. this forms a schiff base. Then amadori rearrangement can occur to form an amadori product

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24
Q

why is it thought that AGEs increase with age?

A

because blood sugar levels of people increase with age- this means that the increased glucose levels in the plasma can result in the glycation of various proteins in the body. The evidence for the correlation of AGE production with high glucose levels comes from diabetic patients. These people have chronic increase glucose plasma levels and suffer from increased glycation and AGE formation is associated with many of the complications that arise in diabetes with the eyes, rheumatoid arthritis and osteoporoses. these diseases are also associated with ageing- diabetic people seem to have accelerated ageing- so maybe the chronic increase in glucose causes the increase in AGEs accumulation which results in the pathologies of ageing.

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25
Q

how can AGE formation induce osteoporesis?

A

structural impairment in collagen alters the osteoblast differentiation leading to bone remodeling and skeletal fragility

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26
Q

how can AGE accumulation case vascular stiffness? what is the pathology from this

A

by increasingg cross like between collagen and making it less flexible increases systolic hypertension

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27
Q

how can the interactions of AGE with RAGE (its receptor) induce oxidative damage and an inflammatory response?

A
  • AGE binding to RAGE and a sustained period of cellular activation can lead to inflammation: interaction go AGE with RAGE on macrophages in cause oxidative stress and and activation of the NF-Kb which stimulates the generation of proinflamtory cytokines. nd NF-Kb also stimulates TNF-a production with increases ROS production. The activation to NF-kB acts in a positive feedback mechanisms whereby RAE increases
  • binding of AGE adducts with RAGE in other tissues also increases ROS damage
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28
Q

what does NF-KB stimulate?

A
  • TNF-alpha which leads to ROS

- transcription of pro-inflammatory cytokines

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29
Q

on what cell can AGEs bind to stimulate an inflammatory response?

A

macrophages

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30
Q

what are the two overeateng ways th`at AGE accumulation can induce the pathologies of Ageing

A
  • perturbing protein functioning

- interact with RAGE to induce an inflammatory response

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31
Q

what molecule is affected by AGEs in the eye

A

crystallin

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32
Q

what percentage of the body’s total protein is collagen ?

A

20-30%

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33
Q

what is the molecule which forms protein-protein cross links?

A

glyoxal derived lysine dimer

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34
Q

how can AGEs be easily measured?

A

pentosidine formation- formed when an ARG and a Lys residue are linked by a pentose sugar- it produced a florescent product- measured easily

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35
Q

what is a key hinderance in undestanding the role of AGEs? how are there being tackled?

A

they are hard to measure. but using ELISA and pentosidine is circumventing this

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36
Q

what is the evidence that suggest AGE accumulation may be genetic?

A

monozygotic twins had higher correlation coefficients go AGEs than dizygotic

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37
Q

what is the general free radical theory of ageing

A

a free radical is a species which contains one or more unaired electrons. An example is superoxide. These cause damage because the unpaired electrons oxidise other proteins. When a protein is oxidised is normally can no longerr function. An accumulation of oxidative damage can hinder key functions and cause cells to die .
The theory of ageing is that, as we age, we accumulate more ROS because our cells become in efficient in recycling them through enzymes such as catalase and superoxide dismutase. This leads to an accumulation of molecular damage that manifest themselves as the pathologies of ageing

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38
Q

name 3 ROSs

A

superoxide, hydroxyl, and peroxyl.

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39
Q

what is an oxidising agent?

A

an agent which oxidises another chemical either by adding oxygen to it or takin an electron or hydrogen- this induces oxidative stress on the protein

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40
Q

what are the three types of oxidation that can occur in the cell?

A
  • protein oxidation which forms protein carbonyls
  • peroxidation of lipids which forms malonaldehyde
  • oxidation of DNA which forms 8-hydroxyguanine
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41
Q

what is a piece of experimental evidence which links protein oxidation with ageing?

A

as you age the carbonyl content of protein in tissues increases

42
Q

how have people tried to link the rate of living theory with the oxidative stress theory and why has it generally been rejected?

A

it is intuitive because oxidative species are a result of mitochondrial metabolism…..

43
Q

how do mitochondria produce reactive oxygen species?

A

The formation of superoxide occurs via the transfer of a free electron to molecular oxygen. This reaction occurs at specific sites of the electron transport chain, which resides in the inner mitochondrial membrane. ETC complexes I (NADH dehydrogenase) and III (ubisemiquinone) produce most of the superoxide (the electron leaks from the compolexes and bind to oxygen), which is then scavenged by the mitochondrial enzyme manganese superoxide dismutase (MnSOD) to produce H2O2

44
Q

what is he ROS produced by the mitochrondria transport chain?

A

superoxide (O2*-)

45
Q

how is superoxide recycled by the mitochondria?

A

the enzyme mangenese superoxide dismutase produces hydrogen peroxide from two hydrogens and two superoxides. catalase then takes two hydrogen peroxide molecules and forms 2 waters and a oxygen

46
Q

what are the two enzymes in evolved in recycling superoxide ?

A

mangenese superoxide dismutase and catalase

47
Q

do mitochondria contain catalse ?

A

yes but not in c.elegans

48
Q

how do mitochondria circumvent not having catalase t deal with hydrogen peroxide ?

A

they use an enzyme called glutathione peroxidase. This requires glutathione (GSH) as a coenzyme and converts H2O2 to water, thus completely detoxifying ROS.

49
Q

how are ROS generally formed?

A

as a byproduct of oxygen metabolism

50
Q

other than in mitochondria, where else can ROS be produced?

A

in the red blood cell via the binding and release of O2 and CO2 from carbon dioxide

51
Q

what evidence in support of the link between ROS and longevity has been found in c.elegans?

A

c.elegan mutants for IGf signalling are on livedare resistant to oxidative stress and selection of c.legenas mutants with increases resistance to a ROS generating compound lead to the identification of long-lived mutants.

52
Q

what is the best way to study the ROS theory ? and what are he 2 sub experiments of this? what is a good way to achieve this?

A

to manipulate levels of ROS and observe the resulting effects on ageing- to increase levels of ROS and see if it decreases life span or accelerates ageing, and the second is to lower ROS levels and see if it retard ageing. A good way of doing this is do manipulate the expression of enzymes which control ROS recycling

53
Q

what are the three main ways in which ROS’s involvement in ageing can be determined due to the increase of ROS with age? (A-C)

A

A- that ROS causes oxidative damage which causes ageing which causes degeneration and death
B- there is another primary cause for ageingg and that ROS also occurs wand can contribute to ageing in a minor way
C- there is a primary cause of ageing with causes degeneration disease and death and then this produced ROS

54
Q

If increasing ROS shortens lifespan then which of ABC does this support and how may this not be a wholly reliable conclusion?

A

this would mean that A or B is true, However, it could mean that you are decreasing lifespan in a way that is not physiological to normal ageing

55
Q

If increasing ROS does not affect lifespan then which of the ABC outcomes can be supported ?

A

C

56
Q

IF increases of lifespan are seen when yo reduce ROS, which of the ABC can be accepted and why is this not entirely reliable?

A

This would support A or B, but you could also argue that this increase in lifespan may be due to altered cell signalling as superoxide and hydrogen peroxide are involved in signalling pathways too

57
Q

if increases and decreases in ROS result in the supporting of A or B, what then must be done and how?

A

you must determined whether ROS is a primary cause of ageing or a secondaryy cause, this can be done y looking at the degree with with ROS manipulations alters life span

58
Q

at experiments have been carried out in flies which maniplate ROS production and what were their outcomes? How did this contrast some mouse experiments?

A
  • hey manipulated the expression of and copper and zinc containing superoxide dismutase (Cu/ZnSOD) in flies. They found moderate increases n lifespan were seen by the over expression of this or manganese SOD. This contrast mouse experiments which found that over expression of these in combination with catalase had no affect on lifespan. But one did find that catalase expression in the mitochondria increased lifespan. Mn-SOD heterozygous mice accrue 30–80% higher 8-oxodeoxyguanosine (8-OHdG), a product of DNA oxidation, with- out showing any effect on longevity
59
Q

what studies in mice have given rise to support or lack of evidence for the oxidative stress experiment?

A

some fond that expressing Cu/ZnSOD and MnSOD and catalase over expression in combination had no effect but one found that expressiong catalase in the mitochondria increased lifespan

60
Q

describe two experiments in the c.elegan which support the oxidative damage theory and highlight relative issues.

A
  • treatment of c.elegans with pro-oxidants such was hydrogen peroxide and redox cline agents such as paraquat- these causes a decrease in lifespan but this does not show whether there was a deceleration in the ageing process.
  • treating worms with antioxidants succh as vitamin E increased life in some studies but not in another. some anti oxidants also increase resistance to heat shock- could be a stress response that they trigger (some antioxidants have actually shortened lifespan)
61
Q

what were the results of experiments seeking to later the expression of peroxisomes in c.elegans?

A
  • deletions in SOD-2 and SOD-3 did not affect life span despite increased sensitivity to oxidative stress
  • one experiment did find that SOD-2 alone enhanced life span- but 4 found the opposite
  • the increase in lifespan of IGF-1 mutants was thought to be due to increase oxidative damage resistance- but deletion of sod-2 has no effect on the longevity of daf-2 mutants.
62
Q

why do some argue that investigating the oxidative damage theory in c.elegans is not wise?

A

some have argued that the c.elegans is a particularly stress resistance animal - it is exposed to to much stress naturally- changing oxygen levels, temperature, oxygen etc due to its subterranean habitat- maybe not a generic reaction to oxidative stress

63
Q

what is a piece of evidence showing that DNA oxidative damage does not affect longevity and in what organism?

A

Mn-SOD heterozygous mice accrue 30–80% higher 8-oxodeoxyguanosine (8-OHdG), a product of DNA oxidation, with- out showing any effect on longevity

64
Q

what would be the alternative theory to oxidative molecular damage being the main cause of ageing?

A
  • that there is a very high threshold of molecular damage that t needs t o be reached to hinder functioning- high levels of DNA oxidation is required in mice to hinder functioning
65
Q

what evidence is there in c.elegns that ROS does have an infuence on ageing?

A

over expression of SOD-1 caused a slight increase in lifespan

66
Q

what is a key problem with studying the effects of ROS on ageing?

A
  • it is very hard to directly measure the levels of superoxide of hydrogen peroxidase in vivo- and it is normally inferred indirectly from the effects on the resistance to oxidative stress.
67
Q

what is lipofuscin ?

A

it is a brown-yellow electron dense material known as cored pigment which accumulates in post-mitotic cells such as cardiac myocytes, skeletal muscle fibres, retinal pigment epithelial cells.

68
Q

where does lipofuscin accumulate?

A

in post mitotic cells: cardiac myocytes, skeletal muscle fibres, retinal pigment epithelial cells.

69
Q

what is the premise of lipofuscin’s contribution to ageing?

A

it accumulates in cells as the turnover mechanism s are prevented in cells with age

70
Q

why are lipofuscins linked to ageing?

A

hey accumulate in various tissue with age and they can be damaging

71
Q

which organelles normally get rid of old protein and lipids? (2)

A

lysosomes and proteasomes

72
Q

at are lysosomes?

A

they break don and recycle proteins and lipids they never either via macroautophagy or microautphagy

73
Q

what are proteosomes ?

A

they break down and recycle proteins, they target proteins which have been tagged ubiquitin

74
Q

why doe lipofuscins accumulate with age?

A

because there is increased molecular damage in the cell- causing more lysosomal breakdown and the tapping of lipfosucin in the lysosome

75
Q

why is lipofscin accumulate bad news?

A

it blocks cellular turnover and therefore increases levels of damaged macromolecules- the fluorescence of lipofuscin in retinal pigment epithelial cells contributes to macular degeneration

76
Q

how does lipofuscin contribute to lipofuscin?

A

the fluorescence of lipofuscin in retinal pigment epithelial cells contributes to macular degeneration

77
Q

what generally is the garbage catastrophe theory?

A

that damaged macromolecules accumulate which then stops turnover which causes more to accumulate and so on. this has been linked to alzheimers- amyloid plaques

78
Q

what is a piece of evidence that shows that activation of turnover (autophagy and proteasomal action) can increase lifespan?

A

in flies if you over express ATG8a, lifespan is increased but ageing is not decelerated
- in c.elegans over expression of a proteasome subunit increases lifespan.

79
Q

why are turnover processes such as autophagy and the action of proteosomes so important in post-mitotic cells?

A

because they do not divide and so can’t be replaced by mitosis- this means that they need to be able to dispose of damaged or faulty proteins and molecules within themselves to avoid death

80
Q

why have studies of the amounts of lipofuscin in different species supported the link between lipofuscin and ageing?

A

short live monkeys and long lived monkeys have the same amount of lipofuscin in their cardiac myocytes when their creative age is the same

81
Q

what does the accumulation of lipofuscin with age tell us about the recycling machinery?

A

it is inherently imperfect

82
Q

where do lipofuscins accumulate?

A

in the lysosomes

83
Q

what lysosomal enzyme has been particularly associated with lipofuscin accumulation?

A

cysteine proteases

84
Q

what is the theory about how lipofuscins develop and the reason for this and the effect this has on recycing machinery?

A

lipofuscins start to ccumulate immediately following birth, suggesting that the recycling machinery is inherently imperfect, it increases linearly over life. So the idea is that the lipofuscin eventually hinders the lysosomes from functioning rather than the lysosomes failing over time, therey resulting in the accumulation of lipofuscins.

85
Q

describe a piece of evidence which suggests that lipofuscins interfere with recycling machinery?

A

fibroblasts loaded have decreases proteosomal activity- lysosomes normally recycle proteosomes so if lysosomes are hindered lipofuscins then they can’t replace proteosomes and these can fail

86
Q

what is the general content of lipofuscins?

A

30-70% protein and 20-50% lipid

87
Q

what lipids are found in lipofuscins?

A

triglcerides, free fatty acids, cholesterol and phospholipids

88
Q

what are lipofuscins thought to arise from?

A

oxidative stress- oxidation makes cellular components undigestable

89
Q

what is the evidence for lipofuscins being caused by oxidative stress?

A
  • accelerated lipofusin formation was observed in fibroblasts and cardiac myocytes cultured at high (40%) ambient oxygen
  • redox active ron, a catalyst of oxidative reactions, increased lipofuscin accumulation in cultured human glial cells and rat cardiac myocytes
  • caloric restriction slows the accumulation of lipofuscin and is known to decrease oxidative reactions
90
Q

why do lipofuscins arise in lysosomes?

A

the material is undegradable so can’t be degraded by the lysosomes-

91
Q

what is the theory for how lipofuscins form in lysosomes as a result of oxidative stress? what is the organelles that, when degraded, poses the biggest threat to lipfuscin formation?

A

ROS (mainly H2O2, which is produced in mitochondria by dismutation of O •􏰁) easily diffuse into 2 lysosomes that contain various autophagocytosed mac- romolecules under degradation as well as redox-active low-molecular weight iron. The latter would be released from a variety of metalloproteins during their intralysosomal degradation. The interaction between H2O2 and iron would result in the generation of HO• engendering the cross-linking of surrounding macromolecules and result- ant lipofuscin formation. when mitochondria are re

92
Q

why is the accumulation of lysosomes a bad thing?

A

they block cellular turnover- this causes an increase in cellular ‘garbage” thus starts a vicious cycle which can cause cel death and degeneration- alzheimers and parkinsons

93
Q

is lipofuscin accumulation reversible ?

A

you can retard it by slowing ROS production but unlikley that you can reverse it- some claim that an antioxidant called Centrophenoxine can reverse sit but more studies show that it can just slow

94
Q

so what is the link between lipofuscin and the molecular damage theory?

A

it is a byproduct of ROS production and the oxidative stress theory

95
Q

what is the name a drug that can be used to target AGE accumulation?

A

alagebrium, can break established AGE cross-links,

96
Q

what effects have AGE-RAGE interactions between implicated in?

A

RAGE -AGE interactions have been implicated in proinflammation in the endothelial cells, proinlfammation in fibroblasts and ROS and proinflammation in phagocytes

97
Q

what are the three main types of AGEs

A

pentosidine, glucosepane, methylgloxdal lysine dimer

98
Q

can AGEs be consumed?

A

yes- CML

99
Q

what age associated diseases are related to AGE accumulation in the eye?

A

cararacts and macular degeneration

100
Q

what age associated diseases of the cardiovascular system are associated with AGE accumulation?

A

atherscletoric lesions (contain high concentrations of AGE)

  • systolic hypertension
  • vascualr stiffenin (via collagen cross links and binding to the ECM,)
  • heart failure as a result of cardiac stiffening
101
Q

what age associated diseases of the liver are associated with AGE accumulation?

A

liver failure

102
Q

what is the key thing to rememer about lipofuscin in the wear and tear theory?

A

it is caused by increased ROS damage- hence growing fibroblasts at an ambient temp or 40% increases lipofuscin formation- it is a demonstration of wear and tear

Biology Of Ageing (8 decks)

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