Mitochondrial Dysfunction Lab Report

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Mitochondrial-targeted peptide counters effects of mitochondrial dysfunction by increasing glutathionylation in aging mice
Sheuli Chowdhury

Abstract

Introduction
Within the field of cellular science, there is general agreement that the mitochondria play a significant role in the process of aging. The mitochondrial theory of aging proposes that oxidative damage to mitochondria leads to mitochondrial dysfunction and tissue degeneration with age1. However, the role of mitochondrial oxidative stress in this process remained controversial. Researchers have studied the association between disorders affecting the mitochondria and impaired redox balance, and a key correlation was determined between redox inhibition of mitochondrial function and age-related energy deficits.
Within the last year, a new hypothesis emerged which suggests that aged tissues experience a more oxidized redox environment due to greater H2O2
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Throughout the entire process, the treadmill was set a 10° uphill angle with consistently increasing speeds. For two days following the actual test date, mice were trained to run on the treadmill in an acclimation period. On the first day, the treadmill was set at 0 m/min for one minute so that the mice could be exposed to the treadmill lanes and motivational shocking grid which produced one small electric shock every second. Following this minute, the treadmill moved at a rate of 10 m/min at a 0° incline for two minutes. On the following day, the treadmill was set to a 10° incline and increased gradually in speeds up to 30 m/min. On the day of the actual test, mice were run at a maximum rate of 30 m/min at a 10° incline until failure. The time of failure was manually determined and recorded, and the mouse would be allowed to rest. This experiment was repeated for every mouse before the after the SS-31