White Muscle Disease
Uterine prolapse in 2 dromedary camels. (1/6)
Two cases of uterine prolapse in dromedary camels in a herd with concomitant cases of white muscle disease are described. Serum selenium and glutathione peroxidase in whole blood were investigated in both patients and showed statistical difference compared with a control group. Results suggest that selenium deficiency could promote uterine prolapse in dromedary camels. (+info)Evaluation of copper concentration in subclinical cases of white muscle disease and its relationship with cardiac troponin I. (2/6)
(+info)The two faces of selenium-deficiency and toxicity--are similar in animals and man. (3/6)
The purpose of this review article is to demonstrate the close parallelism of daily requirements, biological activity and minimum and maximum tolerable levels of selenium for animals and man. In addition, the carcinogenic/anticarcinogenic properties of selenium are discussed and a postulate of how these dichotomous effects may occur in accordance with selenium-induced immunomodulation is presented. A review of pertinent literature pertaining to the biological action of selenium in animals and man, including deficiency, toxicity, carcinogenicity and effects on immunity, is included to support these concepts. The predominant biochemical action of selenium in both animals and man is to serve as an antioxidant via the selenium-dependent enzyme, glutathione peroxidase, and thus protect cellular membranes and organelles from peroxidative damage. The signs and symptoms of selenium deficiency closely simulate each other for animals and man. Severe deficiency is characterized by cardiomyopathy while moderate deficiency results in less severe, myodegenerative syndromes such as muscular weakness and pain as well as a variety of other selenium-associated diseases. Clinical manifestations of many of these disorders require contributory factors, such as stress, to precipitate symptoms which are documented for animals and implicated for humans. Current evidence suggests that a daily selenium consumption for man of approximately 30 micrograms is necessary to prevent the selenium-deficient syndrome, Keshan disease, while approximately 90 micrograms/day/adult should be the minimum daily requirement for optimum biological performance. Recognizing that humans in several countries do not meet the proposed minimum daily requirement of 90 micrograms, several compelling reasons are presented in deriving this minimal daily nutritional intake. Selenosis can occur in laboratory animals, livestock, and humans following long-term exposure to selenium concentrations as low as 5 mg selenium/kg of diet (5 ppm). The selenium-induced lesions for all species are similar, which once again illustrates a positive corollary for selenium effects in both animals and man. From compilation of available data, the maximum tolerable level for selenium in man could be considered in the range of 1000 to 1500 micrograms/day. This is in contrast to the currently recommended maximum human tolerable level of 500 micrograms/day. The amount of selenium that can be tolerated, however, is dependent upon individual biological variation, nutritional status and general state of health.(ABSTRACT TRUNCATED AT 400 WORDS) (+info)Effects of selenium and vitamin E deficiencies in lambs on hepatic microsomal hemoproteins and mitochondrial respiration. (4/6)
Microsomal hemoprotein levels and delta-amino levulinic acid dehydrase activity were determined in livers and rate of oxygen uptake, ADP:O ratios, and respiration control index were determined on mitochondria from muscle, liver, and heart of normal and white muscle diseased (WMD) lambs. WMD lambs were produced by feeding their dams either low selenium purified or alfalfa hay diets. Vitamin E and/or selenium was injected in a 2 x 2 factorial treatment in the ewes fed purified diets. Hepatic microsomal cytochrome P 450 levels and total heme content were significantly lower in WMD lambs. Cytochrome b5 content was significantly lower in lambs on the -E-Se or -E + Se treatments than those on the +E--Se treatment, but the cytochrome b5 content was not different between WMD and normal lambs from ewes fed the hay diet. No differences were found in hepatic delta-amino levulinic acid dehydrase activity, or in the rate of oxygen uptake, ADP:O ratios or respiratory control index between mitochondria from normal and WMD lamb tissue on any of the treatments. (+info)Effects of selenium and vitamin E deficiencies on reproduction, growth, blood components, and tissue lesions in sheep fed purified diets. (5/6)
Three 2 X 2 factorial experiments were conducted with sheep fed purified diets to determine the effects of selenium and vitamin E on the incidence of white muscle disease (WMD) and blood components. All lambs reaching 6 weeks of age in the group receiving no vitamin E or selenium developed WMD lesions, whereas only a few lambs in either the +E - Se or -E + Se treatment groups developed these lesions. Plasma activities of creatine phosphokinase, lactic dehydrogenase and glutamic oxaloacetic transaminase were significantly elevated in lambs receiving no vitamin E or selenium, whereas these enzyme activities in those receiving only selenium were non-significantly elevated. The enzyme activities in plasma of those on the +E - Se or +E + Se treatments were maintained at low levels, suggesting vitamin E alone is more effective in preventing WMD than selenium alone. The metabolic interactions of these essentials are discussed. (+info)Effects of selenium and vitamin E on blood selenium levels, tissue glutathione peroxidase activities and white muscle disease in sheep fed purified or hay diets. (6/6)
The effects of selenium and vitamin E on blood selenium levels and tissue glutathione peroxidase activities were determined in sheep fed purified and hay diets. A significant increase of blood levels of this element and tissue glutathione peroxidase activities was found in sheep given selenium as compared to those not receiving this element. Of the tissues examined, the highest glutathione peroxidase activity was found in the heart. Vitamin E had no influence on either the blood selenium levels or upon the tissue glutathione peroxidase activity. With hydrogen peroxide as the substrate, tissue glutathione peroxidase activity was not correlated with the incidence of white muscle disease. Evidence is presented to suggest that 0.1 ppm dietary selenium is not sufficient under some conditions to meet the physiological requirements for this element. (+info)White muscle disease is not a formal medical term, but it is a condition commonly referred to in veterinary medicine, particularly in the context of livestock and wildlife. It's also known as nutritional muscular dystrophy or enzootic muscular dystrophy.
The term "white muscle disease" refers to a group of conditions characterized by degeneration and necrosis (death) of skeletal and cardiac muscle tissue, primarily caused by deficiencies in certain nutrients, particularly selenium and vitamin E. These nutrients play crucial roles in the antioxidant defense system within the body, protecting cells from oxidative damage.
In affected animals, the lack of these essential nutrients leads to muscle damage, which can result in various clinical signs, such as:
1. Weakness
2. Stiffness
3. Reluctance to move
4. Difficulty swallowing or breathing (in severe cases)
5. Sudden death (often due to heart failure)
White muscle disease is most commonly observed in ruminants like cattle, sheep, and goats, as well as certain species of swine, poultry, and wild animals. It can be prevented through dietary supplementation with selenium and vitamin E or by providing these nutrients through mineral-rich soil and forage. In some cases, treatment may involve administering selenium and vitamin E injections to help support muscle recovery and prevent further damage.
Muscular diseases, also known as myopathies, refer to a group of conditions that affect the functionality and health of muscle tissue. These diseases can be inherited or acquired and may result from inflammation, infection, injury, or degenerative processes. They can cause symptoms such as weakness, stiffness, cramping, spasms, wasting, and loss of muscle function.
Examples of muscular diseases include:
1. Duchenne Muscular Dystrophy (DMD): A genetic disorder that results in progressive muscle weakness and degeneration due to a lack of dystrophin protein.
2. Myasthenia Gravis: An autoimmune disease that causes muscle weakness and fatigue, typically affecting the eyes and face, throat, and limbs.
3. Inclusion Body Myositis (IBM): A progressive muscle disorder characterized by muscle inflammation and wasting, typically affecting older adults.
4. Polymyositis: An inflammatory myopathy that causes muscle weakness and inflammation throughout the body.
5. Metabolic Myopathies: A group of inherited disorders that affect muscle metabolism, leading to exercise intolerance, muscle weakness, and other symptoms.
6. Muscular Dystonias: Involuntary muscle contractions and spasms that can cause abnormal postures or movements.
It is important to note that muscular diseases can have a significant impact on an individual's quality of life, mobility, and overall health. Proper diagnosis and treatment are crucial for managing symptoms and improving outcomes.
