Nutritional Myopathy in Ducklings: a Growth Rate-Dependent Symptom of ‘Tissue Peroxidosis’ due to a Net Nutritional Shortage of Vitamin E plus Selenium in Skeletal Muscle

1981 ◽  
Vol 25 (5) ◽  
pp. 299-306 ◽  
Author(s):  
J. Vos ◽  
C.E. Hulstaert ◽  
I. Molenaar
2011 ◽  
Vol 115 (3) ◽  
pp. 296-301 ◽  
Author(s):  
Michael K. Watters ◽  
Michael Boersma ◽  
Melodie Johnson ◽  
Ciara Reyes ◽  
Evan Westrick ◽  
...  

2007 ◽  
Vol 113 (12) ◽  
pp. 459-466 ◽  
Author(s):  
José Magalhães ◽  
Rita Ferreira ◽  
Maria J. Neuparth ◽  
Paulo J. Oliveira ◽  
Franklim Marques ◽  
...  

In the present study, the effect of vitamin E (α-tocopherol) on mice skeletal muscle mitochondrial dysfunction and oxidative damage induced by an in vivo acute and severe hypobaric hypoxic insult (48 h at a barometric pressure equivalent to 8500 m) has been investigated. Male mice (n=24) were randomly divided into the following four groups (n=6): control (C), hypoxia (H), vitamin E (VE; 60 mg/kg of body weight intraperitoneally, three times/week for 3 weeks) and hypoxia+VE (HVE). A significant increase in mitochondrial protein CGs (carbonyl groups) was found in the H group compared with the C group. Confirming previous observations from our group, hypoxia induced mitochondrial dysfunction, as identified by altered respiratory parameters. Hypoxia exposure increased Bax content and decreased the Bcl-2/Bax ratio, whereas Bcl-2 remained unchanged. Inner and outer mitochondrial membrane integrity were significantly affected by hypoxia exposure; however, vitamin E treatment attenuated the effect of hypoxia on mitochondrial oxidative phosphorylation and on the levels of CGs. Vitamin E supplementation also prevented the Bax and Bcl-2/Bax ratio impairments caused by hypoxia, as well as the decrease in inner and outer mitochondrial membrane integrity. In conclusion, the results suggest that vitamin E prevents the loss of mitochondrial integrity and function, as well as the increase in Bax content, which suggests that mitochondria are involved in increased cell death induced by severe hypobaric hypoxia in mice skeletal muscle.


1959 ◽  
Vol 197 (2) ◽  
pp. 491-493 ◽  
Author(s):  
A. D. Bender ◽  
D. D. Schottelius ◽  
B. A. Schottelius

Myoglobin concentration was determined in gastrocnemius and masseter muscles of guinea pigs maintained up to 15 days on vitamin E-deficient and vitamin E-supplemented diets. A statistically significant increase in myoglobin was noted in muscles of animals on the deficient diet for 15 days. That the increase was real and not apparent was attested by studies of total nitrogen, noncollagen nitrogen, percentage of solids and muscle wet weight, all of which were the same in control and experimental muscles. Histological sections and creatine excretion studies confirmed the impression of mild, incipient nutritional dystrophy.


Nature ◽  
1984 ◽  
Vol 312 (5989) ◽  
pp. 75-77 ◽  
Author(s):  
G. Nilsson ◽  
J. G. Belasco ◽  
S. N. Cohen ◽  
A. von Gabain

Blood ◽  
1978 ◽  
Vol 52 (1) ◽  
pp. 187-195 ◽  
Author(s):  
AC Chou ◽  
GO Jr Broun ◽  
CD Fitch

Abstract Rabbits fed a vitamin E-deficient diet developed severe muscular dystrophy in 3–4 wk, but they did not become anemic. Nevertheless, reticulocyte counts increased in deficient rabbits (3.2%) compared to control rabbits (0.9%), and erythroid hyperplasia was evident in the bone marrow. Comparing deficient rabbits to controls, the plasma iron concentration was lower (134.4 versus 206.6 microgram/dl); the TIBC was higher (335.9 versus 228.3 microgram/dl); the whole blood protoporphyrin concentration was higher (131.6 versus 81.7 microgram/dl); and the total iron content was lower in spleen (71 versus 153 microgram), higher in skeletal muscle (4956 versus 3054 microgram), and unchanged in bone marrow, liver, and heart. Studies of iron absorption and excretion using 59Fe showed no abnormalities in deficient rabbits. There were abnormalities of ferrokinetics, however. The half-time of disappearance of 59Fe was shorter (100.6 versus 169.4 min), the plasma iron turnover was greater (1.25 versus 0.95 mg/dl blood/day), and the reappearance of 59Fe in circulating erythrocytes at day 9 was greater (77.2% versus 57.2%) in deficient rabbits. Anemia induced by phlebotomy accentuated the abnormal iron metabolism of deficient rabbits, and the animals were unable to correct the anemia. These findings show that vitamin E deficiency in rabbits causes abnormal erythropoiesis associated with abnormal iron metabolism and sequestration of iron in skeletal muscle.


1984 ◽  
Vol 18 (10) ◽  
pp. 1012-1016 ◽  
Author(s):  
Jen-Yih Chu ◽  
Phitsamai Kanjananggulpan ◽  
Albert C Chou ◽  
Daphne E De Mello ◽  
Coy D Fitch
Keyword(s):  

2000 ◽  
Vol 182 (2) ◽  
pp. 536-539 ◽  
Author(s):  
Justina Voulgaris ◽  
Dmitry Pokholok ◽  
W. Mike Holmes ◽  
Craig Squires ◽  
Catherine L. Squires

ABSTRACT Growth rate-independent rrn P1 promoter mutants were tested for their ability to respond to changes in rrn gene dosage. Most were found to be normal for the feedback response. In addition, cellular levels of the initiating nucleoside triphosphates remained unchanged when the rrn gene dosage was altered. These results suggest that the feedback response cannot be the mechanism for growth rate-dependent control of rRNA synthesis and that the relationship between these two processes may be more complicated than is currently understood.


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