Exacerbating effect of dietary 12-keto oleic acid on vitamin E deficiency in the rat.

12-Keto oleic acid, possibly one of the oxidation products of long-chain, unsaturated fatty acids, was added to the feed of weanling male rats at the 1% level. Their growth curves, tissue weights, plasma alkaline phosphatase, GOT, and GPT activities, and plasma and liver lipid (cholesterol, triglyceride and phospholipid) levels were investigated and compared with those of weanlings fed a vitamin E deficient diet. Both the diet containing 12-keto oleic acid and the diet deficient in vitamin E decreased the growth rate of body weight and tissue weight, and increased the liver triglyceride and cholesterol levels. Parallel with these, increased hemolysis and stimulation of lipid peroxidation and fluorescent production in the liver homogenate were observed. Elevated plasma alkaline phosphatase and GOT activities which may be considered to be due to a functional disorder of the liver were also observed.     

The effect of dietary vitamin E deficiency on plasma zinc and copper concentrations

Vitamin E and zinc have a number of functions in common, including membrane stabilisation, antioxidant function and modulation of prostaglandin metabolism. Previous studies have shown vitamin E malabsorption during zinc depletion and it appears that there is an interaction between the two nutrients. In this study we have investigated whether vitamin E deficiency affects zinc and copper concentrations in experimental animals. Male Wistar rats were maintained on a vitamin E deficient diet for either 6 or 10 months. At the end of the experimental period all animals had undetectable plasma vitamin E levels and increased red cell fragility. Plasma zinc concentrations were significantly reduced in all vitamin E deficient animals compared to control rats (p<0.002) and copper levels were reciprocally elevated (p<0.002). It appears likely that decreased zinc levels may represent redistribution of circulating zinc to tissues and cells as a secondary antioxidant, or for membrane stabilisation or prostaglandin synthesis.     

Influence of dietary vitamin E on the red cells of ozone-exposed rats

The effect of dietary vitamin E on the susceptibility of red blood cells to ozone exposure was studied in rats. One- and two-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet with or without 45 ppm vitamin E for 4 and 3 months, respectively, and were exposed to 0 or 0.8 ppm ozone continuously for 7 days. Ozone exposure resulted in a significant increase in the activities of glutathione (GSH) peroxidase, pyruvate kinase, and lactate dehydrogenase, and a decrease in GSH level in the red cells of vitamin E-deficient rats, but not in those of the supplemented group. The activities of glucose-6-phosphate dehydrogenase, catalase, and superoxide dismutase and levels of thiobarbituric acid reactants, methemoglobin, hemoglobin, and reticulocytes were not significantly altered by ozone exposure or by the nutritional status of vitamin E. The results suggest that depletion of dietary vitamin E renders animals more susceptible to ozone exposure.     

Influence of dietary vitamin E on nutritional pancreatic atrophy in selenium-deficient chicks

Studies were conducted to determine the relationship between dietary vitamin E (VE) and the development of nutritional pancreatic atrophy (NPA) in selenium (Se)-deficient chicks. Selenium- and VE-depleted chicks reared on a low Se, amino acid-based diet containing 100 IU VE (as all-rac-alpha-tocopheryl acetate) per kilogram were found to have exceedingly low pancreatic activities of Se-dependent glutathione peroxidase (SeGSHpx) at 8 d of age. Supplementation of the purified diet with 500 or 1,000 IU VE/kg prevented both NPA and the associated growth depression. Use of graded dietary VE levels showed that addition of at least 300 IU/kg was required to overcome the growth depression associated with severe Se deficiency. Although tissue alpha-tocopherol concentrations increased linearly with increasing dietary levels of VE, the response in pancreas was less than (about one-half of) those in liver and heart and, unlike the response in heart, was not affected by dietary Se level. That protection against NPA involved the antioxidant action of VE was suggested by results showing that NPA is promoted by high dietary levels of linoleic acid, that high VE levels correct membrane unsaturated fatty acid losses due to Se deficiency and that NPA is prevented by high levels of other antioxidants. It is suggested that the normally low activities of SeGSHpx and concentrations of alpha-tocopherol in the pancreas may predispose that organ to lesions due to oxidative stress under conditions of severe nutritional Se deficiency that results in further depletion of SeGSHpx. This situation may be overcome by feeding VE at 15-20-fold excesses over the levels normally regarded as nutritionally required.     

Relationship of dietary vitamin E to prostanoid production in rat lung

To study the relationship between dietary vitamin E and pulmonary prostaglandin (PG) production, weanling rats were fed either a vitamin E-deficient (-Vit E) or a supplemented diet (+Vit E) containing 200 mg all-rac-α-tocopheryl acetate/kg diet. Four rats from each group were killed after 9, 12, and 15 wk. Serum tocopherol in the deficient animals was 0.28 ± 0.17 μg/ml, compared to 13.81 ± 0.61 μg/ml in the supplemented group. Peroxidation in lung tissue, as measured by malondialdehyde levels, was significantly higher (p<0.001) in -Vit E than in +Vit E (0.210 ± 0.043 and 0.037 ±0.010 μmoles/g tissue, respectively). Excized, minced lung was incubated in Krebs-Ringer bicarbonate buffer at 37°C with shaking in an atmosphere of 95% O₂, 5% CO₂ for 10 min. Production of PGE, PGF_2α, thromboxane B₂ (TXB₂), and the prostacyclin metabolite, 6-keto-PGF_1α, in lung tissue was measured by radioimmunoassay. No significant differences in prostanoid levels were found between the -Vit E and +Vit E groups.     

Osteoporotic vertebral fracture with spinal cord compression

Osteoporotic vertebral fractures with neurologic complications are rarely reported in the literature. We report a case of a 66-year-old woman who developed an osteoporotic fracture of T6 followed one month later by spinal cord compression without aseptic vertebral osteonecrosis. Diagnosis is based on magnetic resonance imaging and examination of vertebral biopsy specimens. After reviewing the literature, we stress some features: the osteoporotic vertebral fractures does not have any particularity compared to the uncomplicated form; the neurological complication occurs progressively and belatedly; the usual mechanism is the recoil of one of posterior vertebral corners.     

康复健康教育对脊髓损伤患者康复疗效的影响

目的：探讨康复健康教育对脊髓损伤患者康复疗效的影响。方法：57例脊髓损伤患者在人院后、康复全过程中、出院前进行康复健康教育指导;进行入院时、出院前疾病康复知识、预防并发症知识、ADL各项目评分比较。结果：患者出院前疾病康复知识、预防并发症知识均高于人院时;ADL各项目评分比较均高于人院时,差异均有统计学意义（P〈0．01）。结论：康复健康教育对提高脊髓损伤患者康复疗效有较大影响;对促进脊髓损伤患者的康复起着至关重要的作用。     

Modification of sympathetic nervous system activity in rat tissues by dietary vitamin E

Noradrenaline content and turnover rate were measured in sympathetically innervated tissues of adult male rats that were fed diets varying in alpha-tocopherol for 10 to 11 weeks. At the end of the feeding period, increasing amounts of vitamin E increased the levels of noradrenaline in liver and white adipose tissue but no differences were observed in heart and interscapular brown adipose tissue. By contrast, increased amounts of dietary vitamin E decreased both the rate constant for the decline of specific activity of noradrenaline with time and the noradrenaline turnover rate in heart and brown adipose tissue. No significant differences were observed in these parameters in liver and white adipose tissue. These results indicate that vitamin E in the diet may affect activity of the sympathetic nervous system.