Vitamin E is an essential nutrient for horses beneficial in combating the multitude of effects of free radical production
that can damage membranes and components of cells.
As such, vitamin E is beneficial to young, rapidly growing foals, pregnant mares, stallions, and, especially, equine athletes
with no access to lush pasture.
Free radicals may harm cells
Free radicals are unstable atoms with unpaired numbers of electrons that are formed when oxygen interacts with other molecules
in all cells.
Once formed, these reactive radicals can initiate chain reactions resulting in a cascading negative effect on many other molecules
within cells and cell walls resulting in oxidative stress within the animal. Free radicals are commonly produced as part of
normal cell metabolism, but also can become excessive following injury or disease. Uncontrolled, free radicals can cause considerable
irreparable damage to cells. They can alter the structure of cell membranes, and create havoc to polyunsaturated fatty acids
(PUFA), and proteins and DNA within cells.
Molecular structure of Vitamin E
The more active the cell, the greater the potential risk of cellular damage. Excessive free radical production or oxidative
stress results when the formation of free radicals overwhelms the body's ability to break the chain reactions that occur when
an imbalance between production and removal of free radicals occurs. Uncontrolled oxidative stress can overpower the horse's
ability to fight back and may result in tissue damage, thus possibly impairing its life.
In several species, including humans, this damage has recently been linked to degenerative diseases such as rheumatoid arthritis,
cancer, cardiovascular disease, inflammatory bowel disease, renal disease, Parkinson's disease, cataracts and may have a deleterious
affect on the immune system (NRC Dietary Reference Intakes for Vitamin C, Vitamin E, Selenium and Carotenoids, 2000).
Help prevent cell damage
Antioxidants are the horse's major defense system against the scourge of free radicals and oxidative stress keeping their
damage to a minimum. Enzymatic antioxidants are synthesized in the body to neutralize free radical production. Key enzymatic
antioxidants include superoxide dismutase, glutathione peroxidase, and catalase. Other major sources of antioxidants available
to the horse are non-enzymatic or nutritional antioxidants. Non-enzymatic antioxidants, like vitamin E, carotenoids and vitamin
C, scavenge and convert free radicals to relatively stable compounds and stop the chain-reaction of free radical damage. Therefore,
all antioxidants are critically important to protect horses from tissue damage, disease, and may during these processes, enhance
immunity. For the horse, the critical phases of reproduction in mares and stallions, growth of foals, and exercise of equine
athletes, are all especially important. Thus, for the horse, vitamin E appears to be the most important dietary fat-soluble
non-enzymatic antioxidant to assist in combating free radical production and propagation in the horse. Since the horse can
synthesize vitamin C, vitamin E and possibly carotenoids, appear to be the only major antioxidant vitamins needed from dietary
Figure 1: Seasonal variation in vitamin e status of horses in western canada
Vitamin E is unique among vitamins in that it is not required for a specific metabolic function. As alpha-tocopherol, vitamin
E's major function appears to be the body's major fat-soluble antioxidant. Thus, vitamin E is notably essential for the proper
function of the reproductive, muscular, nervous, circulatory and immune systems.
Determining vitamin E needs
Since selenium is in glutathione peroxidase, an enzymatic antioxidant, it is often difficult to distinguish between the signs
of vitamin E and selenium deficiencies. Signs representing possible deficiencies of both nutrients have been described in
the foal and in adult horses (NRC, 1989, Schougaard et al., 1972; Wilson et al., 1976). Myodegeneration was common, with pale
diffuse or linear areas in skeletal and cardiac muscle. Histological examination revealed hyaline and granular degeneration,
as well as swelling and fragmentation of muscle fibers from several sites, including the tongue. The latter defect may interfere
with normal nursing. Subcutaneous and intramuscular edema, pulmonary congestion and occasionally, steatitis were also observed.
Liu et al. (1983) reported a degenerative myelopathy in six Przewalski horses up to 14 years of age. They had been fed commercially
prepared horse pellets, timothy hay, and fresh grass in the summer. The horse pellets contained 22 IU of vitamin E and 0.3
mg of selenium/kg. Plasma alpha-tocopherol concentrations were low and ranged from less than 0.3 to 0.8 µg/ml. Ataxia was
evident in all, including uncoordinated movement of the hind limbs, and an abnormally wide-based gait and stance. No gross
lesions were observed in the brain, vertebrae, or spinal cord, but histologic examination revealed degeneration of the neural
processes in the ventral and lateral funiculi. Myelin sheaths were dilated and vacuolated, and a number of axons were swollen,
fragmented or lysed. Neuronal degeneration, phagocytosis, and accumulation of periodic acid-Schiff-positive, xylol-insoluble
lipopigment occurred in the affected neurons of the dorsal root ganglia.