It may be surprising to learn that the same chemical reactions that control how quickly your food spoils can also be the cause of cancer, Alzheimer’s disease, or diabetes. These “autoxidation” reactions occur when a reactive molecule, often containing oxygen and commonly called a “reactive oxygen species,” interacts with another molecule in a cell, producing a result called a free radical. In most atoms, electrons are organized in pairs, while in a radical, a single unpaired electron is present, leading to a high reactivity. Moreover, whenever the radical interacts with another molecule, it produces another radical as a result, leading to a chain reaction that only stops when two radicals cancel each other out. Each molecule that interacted with the radical during the chain reaction is damaged, so initiation of a single one of these events can cause significant damage to cells. A common target of reactive oxygen species is the fat (or lipid) molecules making up the outer border of the cell (the plasma membrane). The products of these reactions can then cause further damage to the cell, even to the point of causing cell death (an underlying cause of dementia, aging, food spoilage, etc.) or mutating the DNA (which can cause cancer). Scientists believed that one major reaction pathway was at work to cause damage, but experiments at Lawrence Berkeley National Laboratory in California have revealed that we may not understand how these reactions occur quite as well as we thought.

Chemists knew that autoxidation of lipids could occur when a reactive oxygen species steals a hydrogen atom from a lipid, creating a free radical. However, experiments have also previously shown the creation of some molecules that couldn’t occur using this mechanism. By using a technique called mass spectrometry, these scientists were able to carefully identify all the final products from these autoxidation reactions with various model lipid molecules, as well as the presence of an intermediate molecule that, up until now, was only found in reactions that occur with ozone in the upper atmosphere (a “Criegee intermediate”). Importantly, adding alcohols that react with these intermediates decreases the rate of autoxidation, suggesting that not only do these Criegee molecules contribute to the reaction pathways but actually make up a significant portion of it. The alcohol here mimics the effect of an antioxidant, which works to inhibit the destructive tendencies of free radicals by reacting with them before they can do damage instead, but this of course relies on understanding of what types of free radicals are present, how they are formed, and how they interact.

While such a discovery is interesting from a scientific standpoint and suggests that such Criegee molecules could be far more common than previously believed, the implications could be much more widespread. Now that we know that Criegee intermediates are present, our antioxidant treatments can become much more effective: we can develop better drugs and therapies to prevent these sources of tissue damage, reduce the effects of aging, and keep our food from spoiling for longer.

Managing Correspondent: Andrew T. Sullivan

Press Articles: Scientists discover new clue behind age-related diseases and food spoilage,” Science Daily

New Clues To Age Related Diseases & Food Spoilage,”

Original Journal Article: Evidence that Criegee intermediates drive autoxidation in unsaturated lipids,” PNAS


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One thought on “A Radical New Mechanism for Cell Damage

  1. It’s fascinating how much we are learning every day. As someone who works in a memory care facility, there is so much sadness, confusion, and anger that surrounds Alzheimer’s dementia. I try to stay as up-to-date on this topic as I can, hoping that we find more and more answers to how we can prevent and treat it.

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