We have often discussed the importance of recognizing the problem of oxidation. This is true for the feed itself, but also for the animals that consume the feed. Oxidative stress is a physiological process affected in periods of high stress, wherein animals consuming oxidized feeds possess less of a defense against internal oxidation. Thus, there is need to protect feeds and animals by incorporating feed antioxidants, often of synthetic origins, and animal antioxidants, mostly of biological origin.
Despite ample literature that demonstrates the impact of oxidation on animal productivity and the true nature of the problem both in vivo and in vitro, there is still resistance in adopting antioxidant nutrition in every day formulation practices. There are two reasons for this understandable resistance. First, we cannot measure oxidative stress in animals with any degree of accuracy, not unless we revert to clinical assays used in human medicine; in other words, we lack a rapid commercial kit to test oxidative stress under practical conditions. Second, we are not exactly aware of what happens when feed and animals are faced with oxidation and what happens between oxidation and reduced animal health, and most importantly, performance. We shall examine this second aspect in some more detail below.
Oxidized feed
It is a common observation that animals, and especially young ones, refuse to eat feed that is oxidized. In fact, the more oxidized the feed is, the less desirable it becomes. Oxidized feed is usually rich in lipids (fats and oils) that have become oxidized through an interactive process that involves oxygen from the air, humidity and catalysts (aiding factors), like certain minerals — all in ample quantities in commercial feeds for animals. The end result of oxidation is the formation of long-lived free radicals, which eventually degrade into ketones and aldehydes.
I am confident we have all consumed some of these products without being able to really attribute the abnormal flavor to anything in specific.
Such compounds impart an unpleasant flavor to the feed. This is why animals refuse to eat oxidized feeds. In addition, and this is perhaps even more important, what little feed is consumed contributes to the storage of these compounds into animal tissues, imparting an even more unpleasant flavor to animal products like meat, eggs and milk. I am confident we have all consumed some of these products without being able to really attribute the abnormal flavor to anything in specific.
Oxidative stress
Oxidation is a normal process within the animal organism. As such, there are neutralizing counter processes that ensure free radicals do not cause damage. However, oxidative stress — a condition where normal antioxidant mechanisms are overwhelmed — occurs under two situations. First, when animals consume free radicals, that is oxidized feed. The second is when conditions such as disease, crowding, weaning stress, overhandling, cold and heat stress, etc., cause the animals to deviate from their normal metabolism.
Learn more: How to control oxidation in finished feeds
Again, there is some capacity for internal handling of oxidative stress, but it is seldom sufficient for animals raised under intensive production systems. It is theorized that the high genetic capacity for production of modern animals has not been followed by a concomitant increase in oxidative capacity. High productivity itself is considered by some nutritionists and veterinarians as a basal level oxidative stress that needs to be addressed.
Clinical effects
Oxidation primarily destroys natural antioxidants, such as pigments, vitamin A and vitamin E. It further diminishes the capacity of organs and systems that depend on these antioxidants, such as kidneys and the immune system. Let us examine these in some further detail.
Pigments. Natural (and synthetic) pigments are antioxidant compounds that are only too readily available to become oxidized instead of lipids. Although this sounds as a good proposition — as natural antioxidants do not become unstable free radicals — pigmentation of animal products may suffer. Such is the case with egg yolk color and broiler skin pigmentation. To this end, under periods of high stress (summer heat under high humidity conditions) it is advisable to increase the level of pigments where such compounds are needed.
Vitamin A. This most-essential vitamin is often taken for granted, but it can be oxidized easily and thus becomes unavailable to the animal. Deficiency ensues and causes damage to lungs and kidneys in growing animals, followed by long-term damage to mouth and eye tissues in breeding animals. Not only do these organs cease to function properly — supporting maximal productivity — but they also become prone to infections. This is often not easily diagnosed as being the cause of vitamin deficiency, but it contributes to overall health decline.
Vitamin E. This is a natural antioxidant, and it is used as such, but when it is already oxidized or not in sufficient quantities, then serious problems follow. One of the first symptoms is neural degeneration, such as encephalomalacia in broilers, a condition that leads to high levels of mortality if left untreated. Less severe symptoms include what is called transudative diathesis, or in other words, leakage of fluids from peripheral vessels into surrounding tissues. This is seen as accumulation of a green-yellow fluid throughout the carcasses’ external areas. And, finally, vitamin E deficiency causes the well-known condition of muscular dystrophy, a condition causing weakness and eventual loss of muscular tissue — the opposite of what is required in modern animal production.
In general, animals that receive oxidized feed or are exposed to conditions conducive to oxidative stress respond by reduced feed intake, a worse feed efficiency rate, impaired growth rates and diminished health. Excessive oxidation leads to increased mortality through deficiencies in vitamins A and E, where secondary infections can appear to be the primary cause.
