Vitamin E is essential equine nutrient
May 01, 2004
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.
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).
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.