Free radicals occur in the body due to a wide variety of metabolic processes and are usually quickly and effectively neutralised.  Free radicals also arise as a result of physical exertion, stress or the influence of environmental factors such as cigarette smoke, environmental toxins or UV radiation. Immune cells also produce free radicals as part of targeted infection responses. 

When these situations are resolved, the free radicals are eliminated.   If too many free radicals are formed, or persist for too long, or if there are problems neutralising them, they can attack and damage cells and  tissues. This is referred to as oxidative stress.

Over the long term, this can lead to premature aging, or to a wide variety of illnesses and chronic inflammation [1]. Ultimately, there is hardly any disease which doesn’t involve oxidative stress and damage from Reactive Oxygen Species (ROS) [2-4].

Certain metals, iron in particular, play a central role in the formation of free radicals.  Free iron offers a potential opportunity for the increased formation of free radicals, particularly in cell walls [5]. 

This reaction sequence is the iron-catalysed Haber-Weiss reaction.  The relatively harmless oxygen products, superoxide and hydrogen peroxide, are converted into the highly reactive hydroxyl radical. Lactoferrin has the ability to counteract the Haber-Weiss reaction [6]. 

Lactoferrin has the potential to act as an antioxidant at many levels.

In what’s known as the Fenton reaction, the 2nd stage of the Haber-Weiss reaction, divalent iron is converted into trivalent iron. This produces large amounts of free radicals that can trigger programmed cell death (apoptosis). The presence of an iron chelator, an iron-binding substance, can down-regulate this process.

By binding catalytic iron in body fluids and inflamed areas, lactoferrin counteracts iron-induced oxidative stress, thus protecting the cells from damage or cell death. (You can read more in our article on the role of lactoferrin & disorders of iron metabolism).

Lactoferrin can also act indirectly by binding bacterial cell components and toxins.  This reduces the need for the antibacterial activity of immune cells (macrophages), which is also a significant source of free radicals. 

In a smaller study by Mulder et al. from 2008, the effects of oral lactoferrin administration on immunological and antioxidant parameters were investigated [7]. Eight healthy male subjects were first given a placebo over a period of three weeks.  This was then followed by lactoferrin at two different doses (1 week: 100mg, 1 week: 200 mg).  With reference to the antioxidant capacity, there was a significant improvement after the two weeks. The oxygen radical absorbance capacity in the blood served as the measurement parameter here.

Given the low number of participants, the results of this study would require confirmation in larger, randomised trials.  The authors conclude that in illnesses where the aetiology features oxidative stress and inflammation, oral administration of lactoferrin could play a supporting role.