It is known that certain toxic elements and infections in the environment lead to diseases and even death. At the cellular level, these harmful agents may not only cause cell death but also modify the normal functioning of the cells. This review determines the common mechanisms by which harmful environmental toxins affect cellular destruction, degeneration, and also death. It is found that iron metabolism by the body and its reaction at the cellular level may be the cause for many diseases. The author also explores the use of agents called chelators that can bind and render iron harmless, and antioxidants to fight oxidative stress.
Minerals form a part of the human diet and the environment. It is known that toxins and chemicals can lead to disease and death. At the cellular level, studies have been conducted to assess the level of damage and destruction that is caused by these chemicals. Iron is an abundant mineral in the environment and is essential for the human body to form components of blood, several enzymes, and compounds important for normal human functioning. Iron can exist in more than one chemical form in the body. Each of the iron molecules can further bind to six different molecules called ligands at once. Iron has the potential to cause oxidative damage by means of several reactions in the body. However, studies have shown that “iron can also have a dark side.” When iron is in the ferrous chemical form and not bound to any of the ligands it can react with chemicals like hydrogen peroxide and lead to serious oxidative damage. This review assessed the mechanisms by which iron can cause cellular damage in humans.
This review included studies that assessed the damage caused by iron at cellular levels leading to various diseases like stroke, Parkinson’s disease, and Alzheimer’s disease. This review excluded those studies that assessed the effects of overdosage or excess iron burden situations, which were caused by certain diseases. The studies reported until 14 June 2010 were included for the assessment of cellular damage caused by iron in humans in this review.
* The results from the review showed that iron in its free form where it is not bound to ligands and in its ferrous chemical form through interaction with hydroxyl radicals may lead to oxidative stress, which results in cell death.
* The results from reviews also showed that most of the degenerative diseases of the nervous system like Huntington’s disease, Alzheimer’s disease, Parkinsonism, Friedreich’s ataxia, amyotrophic lateral sclerosis, multiple sclerosis, and age-related macular degeneration were linked to the disruption of normal iron metabolism.
* Agents that can bind and inactivate iron (known as iron chelators) and some antioxidants that can fight iron-mediated oxidative stress may be useful in the prevention of these diseases.
Further studies are needed to understand therapies that can prevent iron-mediated damage. Some of these may act by binding with free and harmful iron, while some may work against oxidative stress. These studies could help in the development of nutritional and drug therapies against many of the central nervous system diseases. This speculation requires further research work for better understanding of the mechanism involved in cell death pathways.
This extensive review of previous studies shows that iron and its impaired metabolism are both linked to several chemical cellular level damages. Notable among these damages is oxidative damage. This study reveals that there are numerous chemical reactions that lead to cellular damage, destruction, degeneration, and death due to iron and other toxins. These chemical reactions are all related and interconnected. The main cause of this damage is the unbound ferrous form of iron. According to the studies, the chemical reactions at the micro level are responsible for numerous nerve and brain diseases. A deeper understanding of this as well as of the agents that can bind and inactivate iron and fight against its oxidative potential could aid in the prevention of diseases like Parkinsonism, Alzheimer’s disease, Huntington’s disease, Friedreich’s ataxia, amyotrophic lateral sclerosis, multiple sclerosis, and age-related macular degeneration and in the development of suitable treatments for these diseases.
For More Information:
Towards a Unifying, Systems Biology Understanding of Large-scale Cellular Death and Destruction Caused by Poorly Liganded Iron
Publication Journal: Archives of Toxicology, August 2010
By Douglas B. Kell; University of Manchester, England