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Ageing - Coggle Diagram

- - - - Aerobic respiration
        
        Metabolism
        
        Immune response
        
        Obesity
        
        Diabetes
        
        Exercise
        
        Injury
    - - Air pollution
        
        Asbestos
        
        Radioactive emissions
        
        Tobacco smoke
        
        UV radiation
        
        Trace elements - Fe, Cu
  - - - lipid peroxides -
        involved in atherogenesis
      - lipid peroxides
        break down to dialdehydes
        which modify
        proteins & nucleic acid bases
    - - may lead to formation of antibodies
        against modified protein
      - oxidised amino acids may catalyse
        further formation of oxygen radicals
    - - may cause heritable mutations
        (in germ cells)
      - may induce cancer
        (in somatic cells)
  - - - iron copper
        
        manganese
        
        cobalt
        
        nickel
        
        zinc
        
        cerium
        
        chromium
  - - - Copper bound by
        ceruloplasmin
      - Metal ions bound by
        metallothionein
      - Iron bound by
        transferrin, haemosidierin, ferritin
    - - ascorbic acid
        (vit c)
      - Polyphenolics
        (flavanoids, flavanones,
        anthocyanins, resveratrol,
        catechins)
      - a-tocopherol
        (vit e)
      - Carotenoids
        (B-carotene, lycopene,
        zeaxanthin, capsanthin, l
        utein)
      - Some antioxidants may be
        pro-oxidants - cause oxidative damage
        
        β-carotene may be an antioxidant at low partial pressure of oxygen but
        pro-oxidant at high partial pressure of oxygen
        
        Iron
        
        Vitamin C
        
        Vitamin E
    - - Catalase
      - Glutathione peroxidase
      - Superoxide dismutases
- - - - maintain telomere length
        
        preserve cell function
        (can't completely restore
        telomeres)
  - - - due to successive cell divisions
        where telomeres progressively shorten
        
        When the cell can
        no longer divide
        
        it permanently arrests the cell cycle
        (cellular senescence)
        
        triggers cell death programmes
        (apoptosis or autophagy)
- - - - Research began in the 1930s to determine
        the effect of restricted growth on life span –
        (rats lived longer on energy restricted diets)
        
        Is this due to
        
        reduced dietary intake?
        
        restricted growth?
        
        restriction of specific macro- or micro-nutrients?
        This is an area of research interest
      - Calorie restriction delays
        
        many physiological ageing processes
        
        the onset and progression of most diseases of old age
        (in rodents)
      - Since max life duration of rat is about 3yrs,
        longevity studies may be completed in 5 years.
        However, in humans the lifespan is 100+ years
        so not been possible to carry out well-controlled
        life-long studies to establish the effects of calorie restriction
    - - Dietary restriction may reduce the concentration of tissue oxidative damage biomarkers (ie. peroxidation of membrane lipids, protein carbonyl formation, oxidative damage to DNA bases)
      - many sites and enzymes within cells where FR generated but mitochondria considered to produce the majority of cellular reactive oxygen species (ROS) during normal metabolism
        
        A chronic reduction in mitochondrial ROS production has only been demonstrated in response to dietary restriction regimes in isolated mitochondria or cells using an in vitro approach. However, these methods are frequently conducted under non-physiological conditions, specifically with respect to oxygen levels, substrate concentration, and the presence of inhibitors of complexes of the electron transport chain
      - The majority of longevity genes in humans are involved in the insulin/insulin-like growth factor (IGF) pathway