Biology 1002B Lecture Notes - Superoxide Dismutase, Cytochrome C Oxidase, Hyperoxia

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Published on 21 Apr 2013
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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- 2H2O
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 oxygen could accelerate aging
8. Conditions that increase life span
Optimal amount of oxygen
Specific mitochondria genotype
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Document Summary

Lecture 23: oxygen and aging: what are the major forms of reaction oxygen and how are they formed (see figure 6. 25). The intermediates are very toxic and reactive: role of cytochrome oxidase in production of ros. Oxygen accepts electrons at reduced q to make superoxide: 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: 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: human diseases associated with mitochondrial dysfunction. Als (amyotrophic lateral sclerosis) mutation to sod 1 enzyme (not as efficient: cannot get rid of ros. Some parkinson"s diseases nadh dehydrogenase defect (complex i electron leak: 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.

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