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Lecture 23.docx

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Western University
Biology 1002B
Denis Maxwell

Lecture 23: Oxygen and Aging 1. What are the major forms of reaction oxygen and how are they formed (see Figure 6.25). + -  O2+ 4H + 4e 2H O 2  SOD = superoxide dismutase  The intermediates are very toxic and reactive 2. Role of cytochrome oxidase in production of ROS  Donates electrons to oxygen  Donate one electron at a time o Produce partially reduced forms of oxygen o No aerobic respiration due to too much ROS o Therefore selective advantage to donate 4 electrons at a time 3. Role of quinone pool in production of ROS  Oxygen accepts electrons at reduced Q to make superoxide o Oxygen in matrix of mitochondria compete with cytochrome complex  So much oxygen, bound to get electron leak from Q  SOD converts superoxide to hydrogen peroxide and destroys mitochondria 4. How defects in mitochondrial function might lead to disease  Produce less energy since mitochondria isn’t as efficient  Any defects would increase electron leak and produce ROS 5. Human diseases associated with mitochondrial dysfunction  ALS (amyotrophic lateral sclerosis) – mutation to SOD 1 enzyme (not as efficient) o Cannot get rid of ROS  Some Parkinson’s diseases – NADH dehydrogenase defect (complex I electron leak) 6. How defects in cytochrome complex lead to increased oxygen toxicity in C. elegans  Mutation causes cytochrome complex to work as not efficiently as its wildtype  The more oxygen in the environment, the cells with the mutation do not survive as well o Even in normal (21% oxygen) conditions, they don’t last that long 7. Relationship between mitochondrial ROS and ageing  Aging linked to decrease in mitochondrial function  In complex I, V, rRNA, ATP synthase o Higher incidences of specific changes to amino acid sequence o Complex II, III, IV are unaffected/unchanged o Complex I – 40 proteins/genes with 2 amino acid changes  Correlation between specific mitochondrial genotype and longevity  Intrinsic program cell death is triggered by changes in the mitochondria o Metabolic triggers and ROS activates cascade (CED-3) o Mitochondria is the metabolic hub o Hyperoxia – too much oxygen  Gives swirling phenotype (damaged mitochondria)  Too much ox
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