As the human body converts food to energy, oxygen is used to make water. Some of these oxygen molecules, however, bond with other elements to form toxic compounds. These molecules are called reactive oxygen species (ROS) and include superoxide, hydrogen peroxide, and free radicals.
ROS can damage iron-containing proteins, leading to the release of iron. Because this iron is not bound to a protein, it can freely penetrate other cells. These cells could as a result stop growing or die, a process called ferroptosis.
Certain amounts of ROS in the body are necessary for major functions like hormone synthesis and immune responses. Excess iron, however, can convert the beneficial ROS into a form that is very toxic to other cells in the body, such as those that mature into red blood cells.
When ROS accumulation damages red blood cell production in the bone marrow, red blood cells already in the circulatory system aren’t being replaced. Because red blood cells carry iron via hemoglobin, less iron is being transported throughout the body. This process could make conditions like hemolytic anemia worse (even though excess iron is what may have contributed to oxidative stress – ironic!).
Hemolytic anemia is most often seen in patients with sickle cell disease or thalassemia but can also be seen in patients who are marathon runners, infantry soldiers, or who have mechanical heart valves. Decreasing oxidative stress through antioxidants could be good therapy for hemolytic anemia. Antioxidants capture and stabilize free radicals before they can react with other cells and cause serious damage.
Dietary phenols, chemical compounds found in plants, have antioxidant effects and are found in foods like berries, apples, kale, broccoli, and ginger. Nutritionists have been researching how phenols like curcumin (an ingredient of turmeric) and quercetin (a plant pigment) prevent cancer and inflammation in the brain.
To learn more about research on antioxidants and how they impact iron disorders, visit healtheiron.com.
Posted on Sat, July 30, 2016
by Kayla Wiles