Kuksal, Nidhi (2018) Examination of the importance of reactive oxygen species release from complex I in ischemia-reperfusion injury. Masters thesis, Memorial University of Newfoundland.
[English]
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Abstract
Recent work has indicated that respiratory Complex I may be the sole source of reactive oxygen species (ROS) during ischemic-reperfusion (IR) injury. However, evidence collected by several groups, including ours, has demonstrated that Complex III and Krebs cycle enzymes are also high capacity sites for ROS production. Here, the ROS producing capacity of Complex I was examined in hearts subjected to IR injury. Using mice deficient in Complex I (NDUFS4⁺/⁻), the respiratory chain was found to be the main source of ROS in cardiac and liver mitochondria. However, Complex III was found to be the major source, producing ~50% of the total ROS, while Complex I accounted for ~30%. Partial deletion of Complex I sensitized hearts towards reperfusion injury, increasing infarct size, which correlated with higher ROS production. Collectively, these results refute the claim that Complex I is the sole source of ROS following IR injury.
Item Type: | Thesis (Masters) |
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URI: | http://research.library.mun.ca/id/eprint/13605 |
Item ID: | 13605 |
Additional Information: | Includes bibliographical references (pages 107-127). |
Keywords: | Complex I deficiency, Ischemic reperfusion injury, NDUFS4-/- mice, Role of Complex I in IR injury, ROS release |
Department(s): | Science, Faculty of > Biochemistry |
Date: | October 2018 |
Date Type: | Submission |
Library of Congress Subject Heading: | Reperfusion injury—Pathophysiology |
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