Completed Cells, Biochemistry & Physiology

Mitochondrial oxidative damage and human diseases

In plain English

AI plain-English summary

Every minute, the mitochondria inside your cells churn out free radicals—reactive molecules that can damage the cells from within. This damage, called oxidative stress, is linked to cell death in diseases like Parkinson’s, Alzheimer’s, Friedreich’s ataxia, and diabetes. Scientists know that mitochondria are both the main source of these free radicals and the gatekeepers of cell death, but the exact chain of events from radical to damage to disease remains unclear. This project aims to fill that gap. The researchers have developed a way to deliver novel molecules directly into mitochondria. Some of these molecules are antioxidants designed to neutralise free radicals on the spot. Others are tools to track exactly how radicals harm mitochondrial components and trigger cell death. If successful, the work will clarify the fundamental mechanisms of oxidative damage in human disease. That understanding could eventually lead to new therapies that reduce mitochondrial oxidative stress—potentially slowing or preventing cell death in neurodegenerative conditions. For now, the research is fundamental science: it will not produce a treatment tomorrow, but it may reveal the molecular targets that future drugs must hit.

View original technical description
A number of human diseases are associated with increased cell death caused by free radicals. These include degenerative diseases such as Parkinson's disease, Friedreich's ataxia and diabetes. Free radicals are reactive by-products of normal metabolism that damage cell components thereby disrupting normal function and leading to cell death. Mitochondria are the major source of free radicals within cells. These free radicals are formed as mitochondria consume the oxygen we breathe to make energy available to the cell. Mitochondria are also central to determining how cells die, consequently free radical damage to mitochondria is an important cause of cell death. We have developed procedures to target novel molecules to mitochondria. The hope is that these new molecules will enable us to elucidate the mechanisms by which free radicals damage mitochondria and increase cell death in human diseases. Some of these molecules are antioxidants that should block the effects of free radicals. Therefore this approach may also lead to novel therapies to decrease mitochondrial oxidative stress in human diseases such as Alzheimer's Disease and Parkinson's Disease.

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Researchers

Michael Murphy (Principal Investigator)

Related Research

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The role of mitochondrial oxidative damage in ageing: a chemical intervention approach

Original classification

Intramural

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