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Lecture

Lecture 24: "Oxygen & Ageing"

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Department
Biology
Course
Biology 1002B
Professor
Tom Haffie
Semester
Fall

Description
Biology Lecture No. 24: Oxygen & Ageing Wednesday April 4 , 2012 Introduction: -Ageing is defined as the progressive impairment of function with an increasing probability of death. There are many factors that determine lifespan among humans, these include: Environmental factors (where one lives), genetic factors (if one has certain genes expressed and certain ones not), and metabolic factors (the state of one’s mitochondria in relation to cellular respiration). -Apparently, developed countries are home to individuals with longer lifespans due to improved sanitation (especially with clean water) and advancements in health care, which modern-day humans rely on for the maintenance of their health. -There have also been various hypotheses discussed about ageing being linked to oxygen as the terminal electron acceptor in cellular respiration. The Paradox Of Aerobic Life: -It has been documented that many anaerobic organisms die when exposed to oxygen. This is profound because such organisms that grow by fermentation (relying heavily on glycolysis) are not just displaying inability to use oxygen, but induced death from oxygen exposure. -Certain hyperoxia treatments used to be a regular occurrence in hospitals in which patients would receive the maximum supply of oxygen (100%). Nowadays, pure O is never2used for procedures like newborn resuscitation. In the event that isochemia occurs, a reperfusion injury whereby tissue was depleted of oxygen for prolonged periods of time, providing 100% oxygen is detrimental to the patient. -The paradox of aerobic life is essentially that humans require oxygen to survive, but oxygen at the same time (in large quantities) can be very toxic as well. Reactive Oxygen Species (ROS): -The reduction of oxygen to water requires 4 electrons to reach completion. In this reduction reaction there are steps that yield partial forms of oxygen, which are deadly, by the administration of one electron at a time. -A single electron reduction of oxygen gives the ROS superoxide, which becomes hydrogen peroxide through the addition of an electron and 2 hydrogen ions, a hydroxyl radical by way of another electron and H ion, and finally water by adding one more electron and 2 other H ions.+ -These partially-reduced oxygen molecules are dangerous because they are strong oxidizing molecules. Superoxide especially can potentially pull electrons from DNA and proteins, oxidizing biologically important molecules. -That is precisely why the enzyme superoxide dismutase (SOD) drives the conversion of superoxide to hydrogen peroxide, whereby the catalase enzyme quickly converts hydrogen peroxide to water. -It is because these anaerobes (also known obligate anaerobic bacteria) lack these enzymes that minimize exposure to the formation of partially reduced oxidizing molecules that they suffer from exposure to oxygen as a result. The Mitochondria As A Main Source Of ROS: -The link between the respiratory electron transport chain and reactive oxygen species is, of course, the mitochondria. But where exactly along the chain are ROS made? It is not cytochrome oxidase that is the source of ROS as the enzyme actually holds on to individual electrons until four are totalled. It then donates all four of these electrons simultaneously to oxygen. -The major site for ROS is in fact the ubiquinone pool; where electrons are fed through, but that very easily accumulate. Approximately, for every 1000 electrons, 1 electron will be picked up by oxygen to form partially-reduced oxygen (superoxide, to be exact) from ubiquinone. This is why SOD1 (human version of SOD) is in great abundance in this area. -It is important to note that the paradox of aerobic life is an inevitable consequence of cellular respiration. That is to say, the formation and production of ROS is an unavoidable circumstance and it bound to happen. -There are a multitude of human illnesses that are the result of the condition of the respiratory electron transport chain. For example, there are forms of Parkinson’s disease that seem to be based on defects of NADH dehydrogenase. The enzyme is essentially still operational, but mutations to the gene lower the protein’s efficiency. -Other examples include patients of amyotrophic lateral sclerosis (ALS) which is related to defects in the SOD1 enzyme. Cytochrome Complex Mutation: -In a study observing the effects of mutation in the cytochrome complex of worms, the mutant worms (with a working, but less-effective cytochrome complex) would die. Wild types survive extremely well through increases in oxygen levels, but the mutants cannot deal with such high levels of oxygen; it is toxic to them. -There are molecules that can counteract ROS called antioxidants and if you pre-treat the mutants with antioxidants, than the mutants live as long as the wild type. Thus it can be said that mutations to the cytochrome complex affects the formation of ROS. The Mitochondrial ROS Theory Of Ageing: -This theory demonstrates the notion that ageing is linked to disease through the state of mitochondrial function. Alterations in mitochondrial function (especially with age) lead to elevations in mitochondrial dysfunction. This eventually leads to further formation of ROS
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