The influence of selenium deficiency on chosen biochemical parameters and histopathological changes in muscles of goat kids.

The research was conducted on 40 young alpine goats (kids) divided into two groups. First group consisted of 20 kids demonstrating clinical signs of muscular dystrophy. Second group was a control and consisted of 20 animals that received intramuscular injection (2ml per animal) of vitamin E and selenium preparation containing in 1ml 50 mg of tocopherol acetate, 0.5mg of sodium selenite and solvent on 2nd day of life. The kids were clinically examined and blood for laboratory analyses was sampled three times from day 5 of their life in 10 day intervals. In addition, six 24 days old kids demonstrating clinical signs of muscular dystrophy and six control kids were subjected to biceps femoris biopsy. Serum total protein, glucose, triglycerides, cholesterol as well as AST, CK and LDH were determined in all the animals. In addition, the activity of glutathione peroxidase (GSH-Px) was determined in whole blood and serum concentrations of selenium and vitamin E were deter-mined in 6 kids from each group. Total lactate dehydrogenase activity and its separation into isoenzymatic fractions were determined in the collected biopsy material. The muscle samples collected were additionally subjected to histopathological examination consisting of HE staining and HBFP staining to detect necrotic muscle fibers. Symptoms of muscular dystrophy began to appear in the first group between 17 and 23 days of age and included tremors of the limbs, poor posture, stilt gait and increased time of laying. The control animals did not show any symptoms of the disease during the experiment. Hypo-proteinemia, hypoglycemia, cholesterol reduction and elevated triglycerides level associated with lipolysis of adipose tissue have been found in the sick kids. A significant decrease in selenium, vitamin E and activity of glutathione peroxidase levels was observed in the kids with symptoms of muscular dystrophy. The activity of AST, CK and LDH was significantly higher in the animals with symptoms of the disease as well. Five isoenzymes were obtained in the electrophoretic separation of lactate dehydrogenase into isoenzymatic fractions in the muscle tissue. LDH4and LDH5 isoenzymes were dominating, and a significant increase in LDH5 fraction of the sick animals was also observed. Histopathological examination of muscle samples from sick animals revealed changes characteristic for the presence of Zenker necrosis.

Congenital nutritional myodegeneration (white muscle disease) in a red deer (Cervus elaphus) calf.

CASE HISTORY: A 5-day-old red deer calf was submitted with tachypnoea and dyspnoea, and was reluctant to move. CLINICAL FINDINGS: Muscular damage was established via elevated creatinine phosphokinase (CPK) activities (5,000 U/L), while concentrations of Se in whole blood were low (24.8 nmol/L). The animal died despite treatment with penicillin and streptomycin and 0.1 mg/kg Se/vitamin E administered by S/C injection. DIAGNOSIS: Necropsy and histological examination of cardiac and skeletal muscle confirmed the presumptive diagnosis of congenital white muscle disease (WMD). Prophylactic administration of a Se/vitamin E commercial preparation (as above) to another calf born in the same herd one month later was associated with good health and apparently normal growth and development. CLINICAL RELEVANCE: Congenital WMD due to Se deficiency can be fatal in red deer calves. However, prophylactic administration of Se and vitamin E to neonatal calves may be beneficial for neonatal red deer calves.

Serum selenium, vitamin E, and sialic acids concentrations in lambs with white muscle disease.

The aim of this study was to determine the serum concentrations of selenium, vitamin E, and total- and lipid-bound sialic acid (LBSA) in lambs with white muscle disease (WMD) before and after treatment with a commercial preparation containing selenite and vitamin E. Fifteen lambs with WMD and ten control animals were used as research materials. Blood samples were collected from both groups before- and 1 month after treatment for Se analysis by fluorimetry, whereas vitamin E and sialic acid were measured by HPLC and spectrophotometry, respectively. Compared to controls, in the diseased animals, there was a significant increase of serum total sialic acid (TSA) and LBSA, together with significant decreases of serum Se and vitamin E concentrations (p < 0.001). One month after treatment, a reversal of trend was observed with decreases of TSA and LBSA and increases of Se and vitamin E concentrations. The TSA and LBSA levels, however, remained significantly higher than those of the controls, p < 0.05 and 0.001, respectively. The Se and vitamin E concentrations of the treated animals were the same as those of controls. This is the first study on total and LBSA concentrations in lambs with WMD, showing that these markers can be used in the prognosis of the disease.

[Congenital white muscle disease in a Belgian blue calf]. / Congenitale white muscle disease bij een Belgisch witblauw kalf.

In this case report about white muscle disease (WMD) in a Belgian Blue herd, the disease is described both as an individual and as a herd problem. Aetiology, diagnosis, and therapy of WMD are discussed. WMD is a disease of animals with muscle damage due to the presence of free radicals. Unsaturated fatty acids in the cell membrane are transformed into a radical form in a chain reaction: a fatty acid next to the fatty acid radical can be transformed into another free radical. In healthy animal the chain reaction is stopped by anti-oxidants such as vitamin E and glutathione peroxidase. WMD can occur when more free radicals are produced than the available anti-oxidants can deal with. The disease occurs in calves, lambs, and foals.

Rationale for clinical trials of selenium as an antioxidant for the treatment of the cardiomyopathy of Friedreich's ataxia.

A pure selenium deficiency is harmful to the heart and causes a fatal dilated congestive cardiomyopathy in animals (white muscle disease) and in man (Keshan disease). Both of these syndromes are selenium-responsive. A deficiency of the micronutrient has also been reported in patients with Friedreich's ataxia and there are histological similarities between Friedreich's cardiomyopathy and Keshan disease. A low selenium status results in reduced selenium-dependent glutathione peroxidase activity. This essential antioxidant enzyme protects membrances from oxidative deterioration, a function it shares in common with vitamin E. As iron-induced mitochondrial lipid peroxidation is central to the pathology of Friedreich's ataxia, the administration of selenium supplements should normalize the antioxidant activity of myocardial glutathione peroxidase and slow the progression of the life-shortening cardiomyopathy associated with this illness.

Calcium uptake and ATPase activity of sarcoplasmic reticulum vesicles isolated from control and selenium deficient lambs.

The calcium uptake and ATPase activity were studied using fragmented sarcoplasmic reticulum (FSR) vesicles from normal and selenium (vitamin E)--deficient lambs. The latter group was suffering from white muscle disease (WMD). The calcium uptake of FSR vesicles from muscle of WMD lambs was reduced 10-fold as compared to those from normal lambs. An inverse relationship was found with the calcium uptake ability of the FSR vesicles and the severity of WMD. ATPase activity was nonsignificantly lower in vesicles from WMD lambs. The most active FSR vesicles from both normal and WMD lambs banded at 27% when purified on linear sucrose density gradients. The number of protein bands appearing in acrylamide gels of the purified vesicles appeared to be directly proportional to the severity of WMD. The 75Se cosedimented with the calcium uptake and ATPase activity when FSR vesicles from a lamb injected with 75Se-selenite were subjected to linear sucrose density gradient centrifugation, suggesting that selenium is incorporated into these vesicles. Injection of selenium into WMD lambs resulted in significantly greater calcium uptake activity in vesicles 18 and 38 days later as compared with untreated WMD lambs. Injection of selenium in WMD lambs resulted in a marked decrease in plasma CPK activity and a significant increase of glutathione peroxidase activity in the blood.

Effect of disulfiram in experimentally induced vitamin E deficiency myopathy in lambs.

Vitamin E deficiency myopathy (white muscle disease) was induced in 14 suckling lambs (2 experiments; 7 lambs/experiment) by addition of cod liver oil to the diet. Disulfiram, an antioxidant, was administered orally once each day to 8 of the 14 lambs at 2 different doses. Serum creatine kinase (CK) activity was measured weekly for 5 weeks. Increased CK activity was evident in some lambs beginning at week 3. By week 4, serum CK was abnormally increased in 5 of the 6 nontreated lambs (ie, disulfiram not given) and in 4 of the 8 treated lambs. The combined disulfiram groups had significantly lower serum CK values during the study (P less than 0.05). Serum alpha-tocopherol, measured on samples from week 5 for lambs of experiment 1, was significantly higher in treated lambs (P less than 0.01). Microscopic examination of the vastus lateralis muscle indicated that the most severe lesions, consistent with nutritional myopathy, were seen in nontreated lambs. Therefore, disulfiram may have an antioxidant effect in lambs with vitamin E deficiency.

The effects of dietary selenium and vitamin E on avian white muscle disease as measured by both chemical and physical parameters.

Commercial chicken broilers were fed a semipurified diet deficient in vitamin E and selenium from day 1 to day 13 ex ova and subsequently fed varying levels of dietary selenium and vitamin E. All birds were sacrificed on the 28th day, stored for 36 hr at 2 C to allow the onset and resolution of rigor, and frozen at -32 C until needed. Total cathepsin content of the Pectoralis major depended upon dietary vitamin E for birds receiving 0 to 12 IU/kg, whereas selenium administered at .05 to .16 ppm in the diet showed no statistically significant effect. Similarly, total protein content of P. major increased with increasing level of dietary vitamin E, but the level of dietary selenium had no effect. Muscle break strength was significantly affected by dietary selenium and vitamin E (P = .0092) interacting together. Catheptic activity and muscle protein explained 6.36% and 3.58% of the viriability in muscle break strength. Birds with more advanced avian white muscle disease showed higher break strength values. Ultrastructural deterioration of the myipathic muscle included disintegration of blood vessel walls, transverse tubules, and mitochondrial membranes as well as the obvious disruption of the myofibrillar components. Myelin figures were present in diseased, but not in normal, muscle. Accumulation of adipocytes both extracellularly and intracellularly occurred in selenium and vitamin E-deficient birds.