Alteration of Kupffer Cell Function and Morphology by Low Melt Point Paraffin Wax in Female Fischer-344 but Not Sprague–Dawley Rats

1998 ◽  
Vol 46 (1) ◽  
pp. 176-184
Author(s):  
N Hoglen
Keyword(s):  
Kupffer Cell ◽  
Cell Function ◽  
Paraffin Wax ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats

scholarly journals Alteration of Kupffer Cell Function and Morphology by Low Melt Point Paraffin Wax in Female Fischer-344 but Not Sprague-Dawley Rats

1998 ◽  
Vol 46 (1) ◽  
pp. 176-184 ◽  
Author(s):  
N. C. Hoglen ◽  
S. P. Regan ◽  
J. L. Hensel ◽  
H. S. Younis ◽  
J-M. Sauer ◽  
...  
Keyword(s):  
Kupffer Cell ◽  
Cell Function ◽  
Paraffin Wax ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats

Comparative 90-day dietary study of paraffin wax in Fischer-344 and Sprague–Dawley rats

2010 ◽  
Vol 48 (1) ◽  
pp. 363-372 ◽  
Author(s):  
L.C. Griffis ◽  
L.E. Twerdok ◽  
S. Francke-Carroll ◽  
R.W. Biles ◽  
R.E. Schroeder ◽  
...  
Keyword(s):  
Paraffin Wax ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats ◽  
Dietary Study

Activated Kupffer cells cause a hypermetabolic state after gentle in situ manipulation of liver in rats

2001 ◽  
Vol 280 (6) ◽  
pp. G1076-G1082 ◽  
Author(s):  
Peter Schemmer ◽  
Nobuyuki Enomoto ◽  
Blair U. Bradford ◽  
Hartwig Bunzendahl ◽  
James A. Raleigh ◽  
...  
Keyword(s):  
Liver Transplantation ◽  
Kupffer Cells ◽  
Cell Function ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hypermetabolic State ◽  
Hypoxia Marker ◽  
Factor Α ◽  
Necrosis Factor

Harvesting trauma to the graft dramatically decreases survival after liver transplantation. Since activated Kupffer cells play a role in primary nonfunction, the purpose of this study was to test the hypothesis that organ manipulation activates Kupffer cells. To mimic what occurs with donor hepatectomy, livers from Sprague-Dawley rats underwent dissection with or without gentle organ manipulation in a standardized manner in situ. Perfused livers exhibited normal values for O2 uptake (105 ± 5 μmol · g−1 · h−1) measured polarigraphically; however, 2 h after organ manipulation, values increased significantly to 160 ± 8 μmol · g−1 · h−1 and binding of pimonidazole, a hypoxia marker, increased about threefold ( P < 0.05). Moreover, Kupffer cells from manipulated livers produced three- to fourfold more tumor necrosis factor-α and PGE2, whereas intracellular calcium concentration increased twofold after lipopolysaccharide compared with unmanipulated controls ( P < 0.05). Gadolinium chloride and glycine prevented both activation of Kupffer cells and effects of organ manipulation. Furthermore, indomethacin given 1 h before manipulation prevented the hypermetabolic state, hypoxia, depletion of glycogen, and release of PGE2 from Kupffer cells. These data indicate that gentle organ manipulation during surgery activates Kupffer cells, leading to metabolic changes dependent on PGE2 from Kupffer cells, which most likely impairs liver function. Thus modulation of Kupffer cell function before organ harvest could be beneficial in human liver transplantation and surgery.

Measurement of Cell Proliferation in the Kidneys of Fischer 344 and Sprague-Dawley Rats after Gavage Administration of Hydroquinone

1994 ◽  
Vol 23 (3) ◽  
pp. 397-406 ◽  
Author(s):  
J. C. ENGLISH ◽  
LOUISE G. PERRY ◽  
MILAN VLAOVIC ◽  
CAROLYN MOYER ◽  
JOHN L. O'DONOGHUE
Keyword(s):  
Cell Proliferation ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats

Glucose-induced insulin secretion by perfused pancreas of 2- and 12-mo-old Fischer 344 rats

1984 ◽  
Vol 247 (3) ◽  
pp. E385-E388
Author(s):  
D. L. Curry ◽  
G. Reaven ◽  
E. Reaven
Keyword(s):  
Insulin Secretion ◽  
Islet Cell ◽  
Cell Mass ◽  
Fischer 344 Rats ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats ◽  
Glucose Challenge ◽  
Species Specific ◽  
Beta Cell Response

Previous studies have shown that cells from older Sprague-Dawley rats secrete insulin less efficiently in response to a maximal glucose challenge than do beta-cells from young animals. In the current study we have asked whether this change in beta-cell response occurs in another strain of rat, and, if so, whether the secretory defect occurs at submaximal as well as maximal glucose stimulatory levels. Pancreas perfusions were carried out on 2- and 12-mo-old Fischer 344 rats at perfusate glucose concentrations of 150 and 300 mg/dl. The secretory data for each pancreas was subsequently corrected for differences in islet cell mass and expressed as insulin secretion per unit islet cell. The results show that 12-mo-old Fischer rats release more insulin per total pancreas than do 2-mo-old animals at both glucose concentrations. However when corrected for islet cell mass, the amount of insulin secretion per islet cell is actually reduced in the older Fischer rat. These data are comparable to those seen previously in the 12-mo-old Sprague-Dawley rat and indicate that the insulin secretory defect seen as rats grow older is not species specific.

1,2-Dichlorobenzene-Mediated Hepatocellular Oxidative Stress in Fischer-344 and Sprague–Dawley Rats

2000 ◽  
Vol 163 (2) ◽  
pp. 141-148 ◽  
Author(s):  
H.S. Younis ◽  
N.C. Hoglen ◽  
R.K. Kuester ◽  
L. Gunawardhana ◽  
I.G. Sipes
Keyword(s):  
Oxidative Stress ◽  
Sprague Dawley ◽  
Fischer 344 ◽  
Sprague Dawley Rats

Modulation of in vivo 3-deoxyglucosone levels

2003 ◽  
Vol 31 (6) ◽  
pp. 1433-1437 ◽  
Author(s):  
T.R. Brown ◽  
B. Su ◽  
K.A. Brown ◽  
M.A. Schwartz ◽  
A.M. Tobia ◽  
...  
Keyword(s):  
Fold Increase ◽  
Rat Plasma ◽  
Diabetic Rat ◽  
Kidney Tubules ◽  
Sprague Dawley ◽  
Birth Rates ◽  
Fischer 344 ◽  
Sprague Dawley Rats ◽  
Eker Rat

Fructoselysine 3-phosphate is synthesized in vivo by the recently discovered fructoseamine-3-kinase (F3K) from fructoselysine and ATP and decomposes to lysine, Pi and 3-deoxyglucosone (3DG). This pathway appears to dominate 3DG production in vivo, making it possible to modulate 3DG levels by stimulating or inhibiting the reaction. Present inhibitors are non-reacting substrate analogues with relatively high Ki values and can inhibit F3K sufficiently in vivo to reduce 3DG in diabetic rat plasma by approx. 50%. Stimulation of the F3K pathway by feeding glycated casein causes an increase of 10–20-fold in plasma levels of 3DG and 3-fold in kidney tubules. Consequences of this increase were studied in two systems: the Eker rat, a model of susceptible kidney tubules; and birth rates in two rat strains. In both cases substantial pathological effects were observed. In the Eker rats, an approx. 3-fold increase in kidney lesions was observed (P<0.00001). In both Fischer 344 and Sprague–Dawley rats, birth rates were reduced by 56% (P<0.0001) and 12% (P<0.015) respectively. These results suggest that inhibition of F3K is a promising new therapeutic target for diabetic complications, as well as other 3DG-dependent pathologies.

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