Prevention is better than cure, as the old adage goes, and the body has taken this to heart. Recall that transition metals like iron and copper are capable of donating or accepting free electrons during intracellular reactions - and are thus able to generate free radicals. To obviate this, the most obvious option is to simply eliminate these transition metals altogether, but the problem with this idea is that these substances are absolutely vital to the formation of several crucial substances (like haemoglobin!). Instead, the body chooses the more moderate and sensible option or keeping the metals bound in an inactive state to proteins until the exact time when they are needed. For instance, iron is transported around the blood complexed with transferrin and when it is stored it is first bound up with ferritin.
Antioxidants are another of the body's tricks to ameliorate the potentially pernicious effects of free radicals. An antioxidant is any substance that prevents the formation of free radicals, or inactivates them once they are formed. The more important ones are vitamin A, vitamin C, vitamin E and glutathione. For instance, vitamin E is often found embedded in the cell membrane, and it is perfectly suited in this position to prevent the lipid peroxidation chain reaction that we mentioned in this post.
The last set of defences against free radicals are a set of enzymes that act as free radical scavengers. The prominent examples of these are:
- Superoxide dismutases, which convert superoxide to H2O2.
- Catalases, which decompose H2O2 to form oxygen and water.
- Glutathione peroxidase, the most important peroxidase, also catalyses the 'detoxification' of H2O2.
Actually, there are several catalases and perioxidases, and the general scheme looks something like this:
The above constitute the body's innate antioxidant mechanisms. An increase in free radicals, or a decrease in antioxidant functioning, creates an imbalance of the two forces in the free radicals' favour, a condition known as oxidative stress.
Main source: Robbins Pathologic Basis of Disease; 6th edn., Cotran, Kumar, Collins