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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pentane, which evolves from the reaction involving omega-6 fatty acids, is a good index of lipid peroxidation. We describe a method for measuring breath pentane excretion in adult humans. After a 4-minute washout period, expired air was analyzed by gas chromatography. Breath was passed through a cooled loop of alumina to adsorb, concentrate, and release, on heating, pentane. Pentane was analyzed by a Porasil-D column with a derived calibration curve. The mean excretion of pentane in 10 normal adults was 6.34 +/- 0.96 pmol X kg-1 X min-1 (mean +/- SEM) and was significantly higher in five patients with plasma vitamin E deficiency (15.39 +/- 1.84 pmol X kg-1 X min-1). There was a significant negative correlation between pentane output and plasma vitamin E levels (r = -0.66, p less than 0.01). Moreover, breath pentane excretion was significantly decreased after a 10-d supplementation with vitamin E in five normal subjects. We conclude that breath pentane output is a sensitive, noninvasive, functional test for assessing vitamin E status.
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PMID:Breath pentane analysis as an index of lipid peroxidation: a functional test of vitamin E status. 311 28

Unmyelinated axons of normal and regenerated sciatic nerve were counted in controls and vitamin E-deficient rats. No significant change in the number of unmyelinated axons of uninjured nerve was found in the vitamin E deficiency in comparison to controls (12961 +/- 1591 and 12450 +/- 1290, respectively, mean +/- SEM). In regenerated nerve of control rats the number of unmyelinated axons was higher than in uninjured nerve (16971 +/- 1854 and 20786 +/- 1574 at 1 and 2 months after crush, respectively). In vitamin E-deficient rats the increase in number of unmyelinated axons was greater than in corresponding controls (21880 +/- 662) at 1 month after lesion, but the number returned to value found in uninjured nerve at 2 months after lesion (12536 +/- 659). These results suggest that sprouting at lesion may be enhanced but some regenerated axons does not survive at long term in vitamin E-deficiency.
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PMID:Regeneration of unmyelinated peripheral axons in vitamin E-deficient rats. 774 6

Plasma concentrations of alpha-tocopherol (vitamin E) and other analytes in Asian elephants (Elephas maximus) in Nepal were determined during typical work camp management of the elephants. Elephants foraged for food for 4-6 hr each day under the control of mahouts and were also provided daily with cut forage and supplements of unhusked rice, cane molasses, and salt. Blood samples were taken monthly for 1 yr without chemical restraint from 26 female elephants in four camps. Elephants were 6-60+ yr of age. Mean (+/-SEM) alpha-tocopherol concentration was 0.77+/-0.047 microg/ml, with a range of 0.23-1.57 microg/ml. Subadults had lower concentrations than did older elephants, and there were significant differences in mean concentrations from different camps and in mean monthly concentrations. Plasma alpha-tocopherol concentration appears to vary widely between individuals, and a single value of <0.3 microg/ml is not sufficient to diagnose incipient vitamin E deficiency. Mean (+/-SEM) plasma retinol (vitamin A) concentration was 0.063+/-0.003 microg/ml with a range of 0.01-0.12 microg/ml. Subadults had higher concentrations than did older elephants, and mean retinal values differed significantly among camps. Beta-carotene was not found in plasma. Twenty-five other analytes determined or derived were generally similar to those reported in other Asian and African (Loxodonta africana) elephants. Estimates of nutrient intake, based upon diet composition, suggested that dietary concentrations of zinc and sodium may have been marginal, but the absence of signs of any nutrient deficiencies indicates that dietary husbandry in these elephant camps was generally satisfactory.
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PMID:Plasma vitamin E and other analyte levels in Nepalese camp elephants (Elephas maximus). 980 97

Vitamin E content of cardiac tissue has been proposed to play a major role in the damage caused by myocardial ischemia-reperfusion (I-R). Previous studies using in vitro models have examined vitamin E deficiency and I-R-induced myocardial damage with equivocal results. The purpose of this study was to use an in vivo model of myocardial I-R to determine the effects of vitamin E deficiency on myocardial I-R-induced damage. Female Sprague-Dawley rats (4-mo old) were assigned to either: 1) control diet (CON), or 2) vitamin E deficient diet (VE-DEF). The CON diet was prepared to meet AIN-93M standards, which contains 75 IU vitamin E/kg diet. The VE-DEF diet was the AIN-93M diet prepared with tocopherol stripped corn oil and no vitamin E. Following a 14-week feeding period, significant differences (p < 0.05) existed in mean myocardial VE levels between groups (mean values +/- SEM: CON = 48.2 +/- 3.5; VE-DEF = 12.4 +/- 1.4 micrograms VE/g wet weight). Animals from both experimental groups were subjected to an in vivo I-R protocol consisting of 25 minutes of left coronary artery occlusion followed by 10 minutes of reperfusion. No group differences (p > 0.05) existed in cardiac performance (peak arterial pressure or ventricular work) or the incidence of ventricular arrhythmias during the I-R protocol. VE-DEF animals had significantly higher (p < 0.05) levels of myocardial lipid peroxidation and lower (p < 0.05) protein thiols following I-R compared to the CON animals. These data suggest that although vitamin E deficiency increases oxidative damage resulting from myocardial I-R, it does not affect cardiac performance during the insult.
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PMID:Vitamin E deficiency fails to affect myocardial performance during in vivo ischemia-reperfusion. 1121 54