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Lecture

Lecture 23.docx

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Department
Biology
Course
Biology 1001A
Professor
Tom Haffie
Semester
Fall

Description
Role of cytochrome oxidase in production of ROS - ● Cytochrome oxidase takes the electrons in the ETC and reduces O 2o make water ● If Cytochrome oxidase donated electrons one at a time, aerobic life would not exist as by adding one electron at a time, you would produce too many partially reduced 2 which is ROS ● However, cytochrome oxidase actually donates 4 electrons simultaneously; a complete reduction from O 2o H 2 ● Thus, cytochrome oxidase not a major source of ROS because of this Role of quinone pool in production of ROS - ● Quinone pool is the most common site of ROS production ● The reason is that there is so much 2 competing with downstream electron that some of the electrons from the pool leak and the2O is reduced by an electron creating superoxide ● SOD1 would take superoxide and catalyze reaction to form H 2 w2ich is then broken down by catalase How defects in mitochondrial function might lead to disease - ● Very subtle changes in the ETC structures, any mutation at all, can increase the possibility of electron leakage and cause higher ROS production as the electron does not reach cytochrome oxidase ● There are so many electrons going through the chain that there is bound to be a leak; efficiency will never be 100% Human diseases associated with mitochondrial dysfunction - ● Parkinson’s disease (certain forms) seem to be caused by mutation to one of the proteins that make up NADH dehydrogenase complex; the complex doesn’t work as perfectly as it should causing electron leak ● ALS - amyotrophic lateral sclerosis seems to be linked to a mutation to the SOD1 enzyme meaning that superoxide is not converted into H2O 2nd thus can do more harm ● Individuals with these dysfunctions leads to higher levels of ROS production How defects in cytochrome complex lead to increased oxygen toxicity in C. elegans - ● Mutation causes the cytochrome complex to just work not as well as it should; if mutation stopped function, ETC would be stopped and the worm wouldn’t be able to grow, mutation must be subtle ● If per cent oxygen is increased, survival drops much greater in the mutant than in wild type ● Even under normal oxygen conditions, survival in the mutants is lower Relationship between mitochondrial ROS and ageing - ● It seems that anything that decreases efficiency of ETC, thus leading to more electron leakage and more mitochondrial ROS production causes survival to be less ● More mitochondrial ROS causes death at younger age, less ROS causes survival till greater age ● Aging is linked to decrease in mitochondrial function ● There is a cycle where mitochondrial dysfunction causes DNAdamage (mitochondrial genome, not nuclear) which causes further mitochondrial dysfunction ● Mitochondria also has a major role in programmed cell death; mitochondria involved in intrinsic programmed cell death caused by changes in mitochondrial function ○ there are protein factors within the mitochondria which are released and activate the caspase ○ Triggers include metabolic triggers and increased ROS Evidence in support of ROS ageing hypothesis - ● There is a higher incidence in changes in specific amino acids of mitochondrial genome related to complex proteins among centenarians ● Exposure to high oxygen seems to accelerate aging in drosophila as those drosophila grown in hyperoxic conditions show similar mitochond
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