Effect of ascorbic acid and alpha-tocopherol supplementation on plasma corticosterone and production performance of commercial broilers

2021 ◽  
Vol 38 (1) ◽  
pp. 100-104
Author(s):  
Amir Amin Sheikh ◽  
Aditya Mishra ◽  
Anand Kumar Jain ◽  
R.P.S. Baghel
2003 ◽  
Vol 82 (8) ◽  
pp. 1343-1351 ◽  
Author(s):  
JF Young ◽  
J Stagsted ◽  
SK Jensen ◽  
AH Karlsson ◽  
P Henckel

Redox Report ◽  
2013 ◽  
Vol 18 (1) ◽  
pp. 36-46 ◽  
Author(s):  
P Prathibha ◽  
S Rejitha ◽  
R Harikrishnan ◽  
S Syam Das ◽  
P A Abhilash ◽  
...  

Author(s):  
Marija Bursać-Mitrović ◽  
Dragan R. Milovanović ◽  
Radoslav Mitić ◽  
Danijela Jovanović ◽  
Miroslav Sovrlić ◽  
...  

1998 ◽  
Vol 156 (3) ◽  
pp. 551-561 ◽  
Author(s):  
JF Mutaku ◽  
MC Many ◽  
I Colin ◽  
JF Denef ◽  
MF van den Hove

The effects of the vitamins dl-alpha-tocopherol, ascorbic acid and beta-carotene, free radical scavengers and lipid peroxidation inhibitors, were analyzed in male Wistar rats made goitrous by feeding a low iodine diet (< 20 micrograms iodine/kg) and perchlorate (1% in drinking water) for 4, 8, 16, and 32 days. Groups of control or goitrous rats received for at least 16 days before killing a diet containing 0.6% vitamin E (as dl-alpha-tocopherol acetate), 1.2% vitamin C (ascorbic acid) and 0.48% beta-carotene, either simultaneously (vitamin cocktail) or separately. This treatment led to a 5-fold increase of vitamin E in the thyroid gland, a 24-fold increase in the liver and a 3-fold increase in the plasma. In control rats, vitamin cocktail administration increased slightly the thyroid weight with little changes in thyroid function parameters. During iodine deficiency, administration of the vitamin cocktail or vitamin E alone reduced significantly the rate of increase in thyroid weight, and DNA and protein contents, as well as the proportion of [3H]thymidine labeled thyroid follicular cells, but not that of labeled endothelial cells. Plasma tri-iodothyronine, thyroxine, TSH levels, thyroid iodine content and concentration as well as relative volumes of glandular compartments were not modified. The proportion of necrotic cells rose from 0.5% in normal animals to about 2% after 16 days of goiter development. No significant protective effect of the vitamins was observed. These results suggest that these vitamins, particularly vitamin E, modulate one of the regulatory cascades involved in the control of thyroid follicular cell growth, without interfering with the proliferation of endothelial cells.


2010 ◽  
Vol 28 (No. 5) ◽  
pp. 385-391 ◽  
Author(s):  
H. Wang ◽  
M.W. Martin ◽  
S. Yin

Isoflavone daidzein brings potential health benefits. Its antioxidant properties are considered to be responsible in part for its protective effects. We investigated the antioxidant effects of daidzein and its interactive effects with<br />&alpha;-tocopherol or ascorbic acid on Fe<sup>2+/</sup>ascorbate-induced oxidation of rat liver microsomes and copper-induced human low-density lipoprotein (LDL) oxidation. Although the inhibitory effect of daidzein on lipid peroxidation in microsome was weak, it effectively prevented LDL against oxidative modification by prolonging the lag time, decreasing the propagating rate, and suppressing malonaldehyde (MDA) and carbonyls formation. When daidzein was combined with &alpha;-tocopherol in microsomes oxidation and with ascorbic acid in LDL oxidation, the protection was significantly greater than the calculated additive effect of the two individual actions. Thus, daidzein can protect LDL from oxidative modification, and its combination with nutrients may be superior to the action of it alone. These results can help to get a better understanding of the interactions of different antioxidants in vivo.


1963 ◽  
Vol 205 (6) ◽  
pp. 1083-1088 ◽  
Author(s):  
J. J. Van Goch ◽  
D. De Wied ◽  
E. Schönbaum

Several indices of adrenocorticotropic (ACTH) activity were compared in order to establish the index most suitable for assay purposes, particularly of ACTH in blood. In hypophysectomized rats, the effects of ACTH on adrenal ascorbic acid, cholesterol, and steroid formation in vitro were studied. In intact rats, the effects of formalin on these variables as well as on the adrenal and plasma corticosterone levels and hypophyseal and blood ACTH activity were measured. Adrenal corticosterone as well as steroid formation in vitro increased very rapidly after stimulation by ACTH. In hypophysectomized rats, after intravenous ACTH, significant increases were observed after 5 min. In normal rats, 3 min after the injection of formalin, significant increases of steroid formation in vitro and ACTH activity were observed. The in vitro technique is suitable for the study of changes in ACTH activity. ACTH increases the fraction of corticosterone found in the total amount of corticoid secreted by rat adrenals in vitro.


1994 ◽  
Vol 303 (1) ◽  
pp. 295-301 ◽  
Author(s):  
A Van der Vliet ◽  
D Smith ◽  
C A O'Neill ◽  
H Kaur ◽  
V Darley-Usmar ◽  
...  

Endothelial cells and activated phagocytes produce both nitric oxide (.NO) and superoxide (O2.-), which react to form peroxynitrite. Peroxynitrite has been suggested to be directly cytotoxic and also to decompose into other toxic species. In order to understand the consequences of peroxynitrite generation in vivo, we examined its reaction with human blood plasma. Peroxynitrite decreased the total peroxyl-trapping capacity of plasma. In terms of specific antioxidants, addition of peroxynitrite to plasma leads to rapid oxidation of ascorbic acid, uric acid and plasma SH groups. The oxidation of plasma SH groups was enhanced in dialysed plasma and returned to control levels by the addition of physiological levels of bicarbonate. Evidence was found for formation of nitro-adducts to aromatic side chains in plasma proteins by peroxynitrite. Peroxynitrite also leads to depletion of ubiquinol and formation of traces of lipid hydroperoxides in plasma, although alpha-tocopherol levels were only slightly decreased. Peroxynitrite formation in human body fluids is likely to cause antioxidant depletion and oxidative damage.


1995 ◽  
Vol 38 (15) ◽  
pp. 2880-2886 ◽  
Author(s):  
J. Martin Grisar ◽  
Gilbert Marciniak ◽  
Frank N. Bolkenius ◽  
Joelle Verne-Mismer ◽  
Eugene R. Wagner

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