10.6 – The Body’s Offense Mechanism, Free Radicals, and Oxidative Stress
Learning Objective
- Be able to understand the body’s offense mechanism
While our bodies have acquired multiple defenses against free radicals, we also use free radicals to support its functions. For example, the immune system uses the cell-damaging properties of free radicals to kill pathogens. 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 thyroid gland synthesizes its own hydrogen peroxide, which is required for the production of thyroid hormone. 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 metabolism.
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 number of free radicals in the body. They do so by being free radicals themselves or by adding energy that provokes electrons 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
Oxidative stress refers to an imbalance in any cell, tissue, or organ between the number 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, atherosclerosis (hardening of arteries), arthritis, diabetes, kidney disease, Alzheimer’s 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, specifically, the mitochondria lose their efficiency, which leads to increases in free radical production, oxidative stress, and inflammation thus influencing the stress response of tissues as they age.
Contributors
The Pennsylvania State University Nutritional Sciences Program: Alison Borkowska, Ph.D
The University of Hawai’i at Mānoa Food Science and Human Nutrition Program: Allison Calabrese, Cheryl Gibby, Billy Meinke, Marie Kainoa Fialkowski Revilla, and Alan Titchenal
