There are three functional forms of vitamin A: retinol (the alcohol), retinal (the aldehyde) and retinoic acid (the acid). The ‘all-trans’ (all the double bonds are in the trans configuration) form of retinol is the major active form of the vitamin.
Vitamin A, in its pre-formed state, can only be found in animal tissues. Fish oils and offal, especially liver, are good sources. Provitamin A, which can be converted to vitamin A in herbivores, can be found in green pasture or plants. The provitamin in plants are called carotenoids. The more green the food, the greater the content of carotenoids. The most important form of the provitamins is beta-carotene. Vitamin A may also be produced synthetically for animal supplements.
Most species can convert beta-carotene to vitamin A but a differing efficiencies. In theory, two molecules of vitamin A are produced from one molecule of beta-carotene. Cats, foxes, and minks cannot convert beta-carotene because they lack the enzyme needed to do this. Thus, they must get their vitamin A pre-formed from the diet.
Metabolism and Storage
When food is digested, retinyl esters from animals and carotenoids from plants are absorbed by the intestinal mucosal cells. Here, the retinyl esters are converted to retinol and the beta-caretnoids are converted to retinal which is then converted to retinol. The retinol from the intestinal mucosal cells are then converted to retinyl palmitate and travel in chylomicrons in the lymph to the liver where it is stored.
Vitamin A has several important functions including:
- Vision: it is responsible for the formation of rhodopsin
- Maintenance of epithelial cell differentiation and mucous production.
- Growth: especially bone
- Immune response and healing (it is a scavenger of free radicals).
Vitamin A Deficiency
As a result, deficiencies in Vitamin A will lead to the following clinical signs:
- Opthalmic disease, particularly night-blindness and xerophthalmia (dry eyes).
- Skin disease
- Bone lesions due to the excessive deposition of bone
- Increased CSF pressure
- Reproductive failure: teratogenesis, failure of spermatogenesis and the abortion of foetuses
- Failure of growth
Vitamin A Toxicity
Vitamin A toxicity may result if excess amounts of vitamin A are included in an animal’s diet. Signs of toxicity include:
- Changes in the skin and mucous membranes:
o Skin thickening
o Scaly dermatitis
o Swelling/crusting of eyelids
o Sloughing of skin
o Hair loss
o Excess mucous production.
- Anorexia and weight loss
- Decreased bone strength
- Malformed young
There are many forms of vitamin D but not all occur naturally. The most important forms are D2 (ergocalciferol – found in plants) and D3 (Cholecalciferol – found in animal tissues).
Ergosterol is the provitamin of D2 and 7-dehydrocholesterol (7-DHC) is the provitamin of D3. UV radiation is required to convert the provitamin to the vitamin and this process occurs in the skin.
Pre-formed vitamin D3 is not abundant in foods. This is not usually an issue because vitamin D3 is produced by the skin in excess of what is required by mammals. Dietary supplements are only required when animals have little exposure to sunlight. Fish liver oils have high vitamin D content. Egg yolk, margarine, lard, shrimp and sardines have a medium amount of vitamin D. Foods that have a low amount of vitamin D include grain, vegetable oils, meat, butter, milk, cream and cheese.
Cats are unable to synthesis vitamin D3 even if their skin comes into contact with sunlight. This is because they lack the enzymes required for the conversion of the provitamin to the vitamin. Thus, they need to obtain their vitamin D preformed in the diet. Lactating cows may also need a higher level of vitamin D in their diet.
Metabolism and Storage
Vitamin D3 enters the plasma through absorption of pre-formed vitamin D in the small intestine or alternatively through the conversion of 7-DHC in the skin in the presence of sunlight. Once in the plasma it travels to the liver and then the kidneys where it is converted to calcitriol. This substance has a regulative activity on calcium use and absorption.
Calcitriol stimulates the absorption of Calcium in the intestines as well as bone calcium resorption. These effects cause an increase in plasma calcium levels and unsurprisingly is most active when these levels are low.
Vitamin D Deficiency
A deficiency in vitamin D results in impaired absorption of calcium and phosphorus. Thus, clinical signs include abnormal skeletal development and inadequate calcification of bone.
Vitamin D Toxicity
Vitamin D is also toxic in excess and this involves the mineralisation of soft tissues such as the liver.
There are eight vitamers of vitamin E which belong to two groups: tocopherols and tocotrienes. “Natural vitamin E” is actually called d-α-tocopherol and is the most common form. Synthetic vitamin E refers to dl-α-tocopherol acetate. The stability of vitamin E is reduced by heat as well as exposure to sunlight and peroxidising lipids.
Exercise, growth and the amount of polyunsaturated fatty acids in the diet all increase vitamin E requirements. Thus, growing as well as lactating animals require more vitamin E than other animals. Poly-unsaturated fatty acids (PUFAs) increase the requirement of Vitamin E because they are susceptible to peroxidation and the vitamin acts as an antioxidant.
The main job of vitamin E is as an antioxidant to protect the body from damaging reactions (known as peroxidation) that are produced by many normal metabolic processes and exogenous toxins. The vitamin works as a free radical scavenger, it also protects membranes from damage and helps prolong the lifespan of red blood cells. It also is important for the function of the immune system.
The presence of either vitamin C, beta-carotene or selenium enhances the antioxidant effects of vitamin E. Vitamin E also reduces the use of the liver’s Vitamin A stores.
Good sources of vitamin E include vegetable oils, cold-pressed seed oils and wheat germ. Other sources of this vitamin include nuts, seeds, whole grains and leafy green vegetables. Although vegetable oils are a good source, this is normally not a large part of most livestock’s diet.
Metabolism and Storage
Vitamin E absorbed mainly from the jejunum where it is repackaged as chylomicrons to travel in the lymph. It is stored in fatty tissue, liver and muscle but not to the same extent as Vitamin A and so it is important to that Vitamin E is received from the diet regularly.
The presence of either vitamin C, beta-carotene or selenium enhances the antioxidant effects of vitamin E. Vitamin E also reduces the use of the liver’s Vitamin A stores. The presence of iron in the diet will reduce the availability of vitamin E to the body.
Vitamin E Deficiency
Signs of Vitamin E deficiency include:
- Reproductive Failure
o Embryos degenerate
o Sterility and testicular atrophy
o Ovarian failure
- Derangement of Cell Permeability
o This affects the liver, brain, kidneys and capillaries
o It may be present as encephalomalacia and exudative diathesis.
- Nutritional Muscular Dystrophy
o This includes White Muscle Disease which affects the skeletal muscle of sheep, and Mulberry Heart Disease which effects the cardiac muscle of pigs.
- Pansteatitis (also known as Yellow Fat Disease).
o This is when fat becomes inflamed and starts to go necrotic.
Vitamin E Toxicity
There are few reports of Vitamin E toxicity as it has little or no toxicity in metabolism. Vitamin E is also expensive which means that it is not likely to be given to animals in excess.
Vitamin K has several different forms but what they all have in common is a menadione ring. Plants and bacteria can synthesise this ring but animals can’t. Vitamin K1 is also known as phylloquinone and is found in plants. Vitamin K2 is also called menaquinone and is made by bacteria, while K3 are the menadione compounds that are produced synthetically.
Vitamin K is involved in blood clotting as it is needed for the synthesis of prothrombin by the liver which is the inactive precursor of thrombin. Thrombin converts fibrinogen in the blood to fibrin which holds the blood clot together. Before prothrombin can be activated it must be bound to calcium. Vitamin K deficiency results in low levels of the amino acid responsible for this binding.
Good sources of vitamin K in the diet include fresh leafy plants; animal based feeds such as egg yolk, liver and fishmeal; as well as bacteria in the gut. It generally quite stable but may be rapidly destroyed by light.
Normally, the bacteria that live in the animal’s digestive tract produce vitamin K needed. However, animals that are being treated with antibiotics that may reduce the amount of vitamin-K producing bacteria may need vitamin K supplements. This is also true for birds that are housed on wire mesh and aren’t able to perform coprophagy. This is because faeces is a source of Vitamin K that has been produced by the bacteria in the gut. In birds, the vitamin K that is synthesised by bacteria may not be able to be absorbed because the site of production is too distal for adequate absorption.
Supplements are also required for animals that may be consuming vitamin K antagonists. An example of this is dicoumarol which is produced by fungi found in weather-damaged legume hay or silage.
Vitamin K Deficiency
Symptoms of vitamin K deficiency are not reported in ruminants, horses and pigs because of the bacteria in their gut which produces adequate amounts of this vitamin.
In birds, signs of deficiency include anaemia and delayed blood clotting.
Vitamin K Toxicity
There is little risk of vitamin K poisoning except when high levels are given by injection.
That's all for this post, see you next time :)