Effects of marginal dietary zinc deficiency and vitamin E supplementation on hepatic adenine dinucleotide phosphoribosyl transferase activity in female Sprague-Dawley rats

1991 ◽  
Vol 11 (4) ◽  
pp. 337-345 ◽  
Author(s):  
David S. Seres ◽  
Michael J. Bunk ◽  
Michael P. Osborne ◽  
Richard S. Rivlin ◽  
Raj K. Tiwari
Keyword(s):  
Vitamin E ◽  
Zinc Deficiency ◽  
Transferase Activity ◽  
Sprague Dawley ◽  
Dietary Zinc ◽  
Phosphoribosyl Transferase ◽  
Sprague Dawley Rats ◽  
Vitamin E Supplementation

scholarly journals Isoelectric focusing of glutathione S-transferases from rat liver and kidney

1978 ◽  
Vol 175 (3) ◽  
pp. 937-943 ◽  
Author(s):  
Barbara F. Hales ◽  
Valerie Jaeger ◽  
Allen H. Neims
Keyword(s):  
Substrate Specificity ◽  
Isoelectric Focusing ◽  
Transferase Activity ◽  
Sprague Dawley ◽  
Substrate Specificities ◽  
Liver Cytosol ◽  
Sprague Dawley Rats ◽  
Isoelectric Points ◽  
Liver And Kidney ◽  
Glutathione S Transferases

The glutathione S-transferases that were purified to homogeneity from liver cytosol have overlapping but distinct substrate specificities and different isoelectric points. This report explores the possibility of using preparative electrofocusing to compare the composition of the transferases in liver and kidney cytosol. Hepatic cytosol from adult male Sprague–Dawley rats was resolved by isoelectric focusing on Sephadex columns into five peaks of transferase activity, each with characteristic substrate specificity. The first four peaks of transferase activity (in order of decreasing basicity) are identified as transferases AA, B, A and C respectively, on the basis of substrate specificity, but the fifth peak (pI6.6) does not correspond to a previously described transferase. Isoelectric focusing of renal cytosol resolves only three major peaks of transferase activity, each with narrow substrate specificity. In the kidney, peak 1 (pI9.0) has most of the activity toward 1-chloro-2,4-dinitrobenzene, peak 2 (pI8.5) toward p-nitrobenzyl chloride, and peak 3 (pI7.0) toward trans-4-phenylbut-3-en-2-one. Renal transferase peak 1 (pI9.0) appears to correspond to transferase B on the basis of pI, substrate specificity and antigenicity. Kidney transferase peaks 2 (pI8.5) and 3 (pI7.0) do not correspond to previously described glutathione S-transferases, although kidney transferase peak 3 is similar to the transferase peak 5 from focused hepatic cytosol. Transferases A and C were not found in kidney cytosol, and transferase AA was detected in only one out of six replicates. Thus it is important to recognize the contribution of individual transferases to total transferase activity in that each transferase may be regulated independently.

Vitamin E Concentration in Rat Skeletal Muscle and Liver after Exercise

1998 ◽  
Vol 8 (2) ◽  
pp. 105-112 ◽  
Author(s):  
Jon N. Swift ◽  
James P. Kehrer ◽  
K. Stephen Seiler ◽  
Joseph W. Starnes
Keyword(s):  
Skeletal Muscle ◽  
Vitamin E ◽  
High Performance ◽  
Time Course ◽  
Vastus Lateralis ◽  
Sprague Dawley ◽  
Rat Skeletal Muscle ◽  
Sedentary Control ◽  
Sprague Dawley Rats ◽  
Response To Exercise

The purpose of this study was to determine whether submaximal exercise significantly changes the concentration of vitamin E (αToc) in rat liver and skeletal muscle and to establish a time course for the return to basal levels. Male Sprague-Dawley rats, age 8 to 10 weeks, were randomly divided into sedentary control (Con) (n = 7) and exercise n = 17) groups. Exercised animals ran 100 min on a motorized treadmill at approximately 70% VO2max for 3 consecutive days. They were then sacrificed immediately postexercise (0Post), 24 hr post (24Post), or 72 hr post (72Post). The gastrocnemius, red vastus lateralis (RV), white vastus lateralis (WV), and liver were excised and analyzed for αToc concentration by high-performance liquid chromolography utilizing electrochemical detection. We found that after 3 consecutive days of exercise, αToc was reduced in RV and WV at 0Post and 24Post but returned to control values by 72Post. Liver αToc content was not changed at OPost but was significantly reduced at 24 Post and 72 Post. No significant changes in αToc were observed in the gastrocnemius in response to exercise. The data indicate that following an exercise-related decrease, skeletal muscle vitamin E concentration requires more than 24 hr to return to the preexercise concentration, and that the replenishment process may involve redistribution of vitamin E from liver to muscle.

Dietary Zinc Deficiency Decreases Plasma Concentrations of Vitamin E

1989 ◽  
Vol 190 (4) ◽  
pp. 379-384 ◽  
Author(s):  
M. J. Bunk ◽  
A. M. Dnistrian ◽  
M. K. Schwartz ◽  
R. S. Rivlin
Keyword(s):  
Vitamin E ◽  
Zinc Deficiency ◽  
Plasma Concentrations ◽  
Dietary Zinc

Vitamin E reduces glomerulosclerosis, restores renal neuronal NOS, and suppresses oxidative stress in the 5/6 nephrectomized rat

2007 ◽  
Vol 292 (5) ◽  
pp. F1404-F1410 ◽  
Author(s):  
You-Lin Tain ◽  
Gary Freshour ◽  
Anna Dikalova ◽  
Kathy Griendling ◽  
Chris Baylis
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Vitamin E ◽  
Kidney Cortex ◽  
Antioxidant Vitamin ◽  
No Production ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Endothelial Nitric Oxide

Chronic kidney disease is accompanied by nitric oxide (NO) deficiency and oxidative stress, which contribute to progression. We investigated whether the antioxidant vitamin E could preserve renal function and NO bioavailability and reduce oxidative stress in the 5/6th nephrectomy (NX) rat model. We studied the following three groups of male Sprague-Dawley rats: sham ( n = 6), 5/6 NX control ( n = 6), and 5/6 NX treated with vitamin E (5,000 IU/kg chow; n = 5). The 5/6 NX group showed increased severity of glomerulosclerosis vs. sham, and this was ameliorated by vitamin E therapy. Both 5/6 NX groups showed similar elevations in plasma creatinine and proteinuria and decreased 24-h creatinine clearance compared with sham. There was increased NADPH-dependent superoxide production in 5/6 NX rats vs. sham that was prevented by vitamin E. Total NO production was similarly reduced in both 5/6 NX groups. There was unchanged abundance of endothelial nitric oxide synthesis (NOS) in renal cortex and medulla and neuronal (n) NOS in medulla. However, in kidney cortex, 5/6 NX rats had lower nNOS abundance than sham, which was restored by vitamin E. An increased plasma asymmetric dimethylarginine occurred with 5/6 NX associated with decreased renal dimethylarginine dimethylaminohydrolase activity and increased type 1 protein arginine methyltransferase expression.

Yes-Associated Protein Promotes Impaired Proliferation of Hippocampal Neural Stem Cells in Zinc-Deficient Sprague-Dawley Rats

2020 ◽  
Vol 12 (3) ◽  
pp. 383-391
Author(s):  
Xiaodong Zhao ◽  
Dandan Bai ◽  
Ming Xu ◽  
Lei Song ◽  
Haiying Li ◽  
...  
Keyword(s):  
Stem Cells ◽  
Stem Cell ◽  
Cyclin D1 ◽  
Zinc Deficiency ◽  
Molecular Mechanisms ◽  
Sprague Dawley ◽  
Sd Rats ◽  
Sprague Dawley Rats ◽  
Abnormal Brain ◽  
Hippocampal Neural Stem Cells

Zinc deficiency results in abnormal brain development and dysfunction, although the precise molecular mechanisms underlying these observations remain unclear. In this study, we aimed to investigate the mechanisms underlying impaired hippocampal neural stem cell (NSC) proliferation observed in zinc-deficient Sprague-Dawley (SD) rats. Zinc-deficiency was associated with reduced expression of co-localizing Yes-associated protein (YAP) and cyclin D1 in NSCs in hippocampal tissue. Moreover, we observed a significant reduction in the ratio of proliferating hippocampal NSCs in rats maintained on zinc-deficient diets. Reduced proliferation was also observed in immortalized C17.2 NSCs exposed to N, N, N′, N′ -Tetrakis (2-pyridylmethyl) ethylenediamine (TPEN); these findings were associated with diminished expression of both YAP and cyclin D1. Overexpression of YAP rescued the C17.2 cells from zinc-deficiency-induced reductions in cyclin D1 expression as well as impaired proliferation. Taken together, these results demonstrate that downregulation of YAP contributes to impaired proliferation of NSCs observed in response to zinc-deficient.

Effects of Dietary Carnosine and Vitamin E on Antioxidant and Oxidative Status of Rats

2008 ◽  
Vol 78 (45) ◽  
pp. 230-237 ◽  
Author(s):  
Wissam Ibrahim ◽  
Vickie Tatumi ◽  
Che-Chung Yeh ◽  
Chuen Bin Hong ◽  
Ching Kuang Chow
Keyword(s):  
Vitamin E ◽  
Antioxidant Status ◽  
Conjugated Dienes ◽  
Oxidative Status ◽  
Tocopheryl Acetate ◽  
Protein Carbonyls ◽  
Dietary Vitamin ◽  
Sprague Dawley ◽  
Deficient Diet ◽  
Sprague Dawley Rats

The purpose of this study was to determine if moderate levels of carnosine supplement, alone or in combination with vitamin E, enhance antioxidant status and/or provide protection against oxidative stress. Fiftyfour one-month-old male Sprague-Dawley rats were fed a basal vitamin E-deficient diet supplemented with either 0, 200, or 1000 mg L-carnosine, and either 0, 10, or 100 IU vitamin E (as all rec-α-tocopheryl acetate) per kg diet for 15 weeks. The antioxidant and oxidative status were assessed in the skeletal muscle, liver, and blood. Dietary vitamin E, but not carnosine, increased levels of vitamin E, decreased tissue peroxidizability, prevented incidence of myodegeneration, and reduced erythrocyte hemolytic stress. The levels of conjugated dienes, protein carbonyls, ascorbic acid, and nonprotein sulfhydryls, and activities of catalase, glutathione (GSH) peroxidase, and aldehyde dehydrogenase were not significantly altered by dietary carnosine or vitamin E. The results obtained suggest that supplementation of carnosine at levels of up to 1000 mg/kg diet does not significantly affect the antioxidant and oxidative status of rats.

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