The Body’s Offense

University of Hawai‘i at Mānoa Food Science and Human Nutrition Program and Human Nutrition Program

While our bodies have acquired multiple defenses against , we also use free radicals to support its functions. For example, the uses the cell-damaging properties of free radicals to kill . First, immune cells engulf an invader (such as a bacterium), then they expose it to free radicals such as hydrogen peroxide, which destroys its membrane. The invader is thus neutralized. Scientific studies also suggest hydrogen peroxide acts as a signaling molecule that calls immune cells to injury sites, meaning free radicals may aid with tissue repair when you get cut.

Free radicals are necessary for many other bodily functions as well. The synthesizes its own hydrogen peroxide, which is required for the production of . Reactive oxygen species and reactive nitrogen species, which are free radicals containing nitrogen, have been found to interact with proteins in cells to produce signaling molecules. The free radical nitric oxide has been found to help dilate blood vessels and act as a chemical messenger in the brain. By acting as signaling molecules, free radicals are involved in the control of their own synthesis, stress responses, regulation of cell growth and death, and .

Sources of Free Radicals in the Environment

Substances and energy sources from the environment can add to or accelerate the production of free radicals within the body. Exposure to excessive sunlight, ozone, smoke, heavy metals, ionizing radiation, asbestos, and other toxic chemicals increase the amount of free radicals in the body. They do so by being free radicals themselves or by adding energy that provokes to move between atoms. Excessive exposure to environmental sources of free radicals can contribute to disease by overwhelming the free radical detoxifying systems and those processes involved in repairing oxidative damage.

Oxidative Stress

refers to an imbalance in any cell, tissue, or organ between the amount of free radicals and the capabilities of the detoxifying and repair systems. Sustained oxidative damage results only under conditions of oxidative stress—when the detoxifying and repair systems are insufficient. Free radical-induced damage, when left unrepaired, destroys lipids, proteins, RNA, and DNA, and can contribute to disease. Oxidative stress has been implicated as a contributing factor to cancer, (hardening of arteries), arthritis, diabetes, kidney disease, , Parkinson’s disease, schizophrenia, bipolar disorder, emphysema, and cataracts.

Aging is a process that is genetically determined but modulated by factors in the environment. In the process of aging, tissue function declines. The idea that oxidative stress is the primary contributor to age-related tissue decline has been around for decades, and it is true that tissues accumulate free radical-induced damage as we age. Recent scientific evidence slightly modifies this theory by suggesting oxidative stress is not the initial trigger for age-related decline of tissues; it is suggested that the true culprit is progressive dysfunction of metabolic processes, which leads to increases in free radical production, thus influencing the stress response of tissues as they age.


Learning Activities

Technology Note: The second edition of the Human Nutrition Open Educational Resource (OER) textbook features interactive learning activities.  These activities are available in the web-based textbook and not available in the downloadable versions (EPUB, Digital PDF, Print_PDF, or Open Document).

Learning activities may be used across various mobile devices, however, for the best user experience it is strongly recommended that users complete these activities using a desktop or laptop computer and in Google Chrome.

 

 

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The Body’s Offense Copyright © 2020 by University of Hawai‘i at Mānoa Food Science and Human Nutrition Program and Human Nutrition Program is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License, except where otherwise noted.

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