Effects of chronic administration of Thioacetamide (TAA) on the structure of bile canaliculi and tight junctions in the rat liver as revealed by freeze-fracturing

1980 ◽  
Vol 32 (1) ◽  
pp. 57-67 ◽  
Author(s):  
Horst Robenek ◽  
Hermann Themann
Keyword(s):  
Tight Junctions ◽  
Rat Liver ◽  
Chronic Administration ◽  
Bile Canaliculi ◽  
Freeze Fracturing

scholarly journals In vivo induction of tight junction proliferation in rat liver.

1976 ◽  
Vol 68 (3) ◽  
pp. 793-798 ◽  
Author(s):  
R Montesano ◽  
G Gabbiani ◽  
A Perrelet ◽  
L Orci
Keyword(s):  
Cell Membrane ◽  
Tight Junction ◽  
Tight Junctions ◽  
Rat Liver ◽  
Chronic Administration ◽  
Rat Hepatocytes ◽  
Bile Canaliculi ◽  
Parallel Orientation ◽  
In Vivo Induction

The chronic administration of phalloidin induces an extensive development of tight junctions between rat hepatocytes. The junctional strands lose their predominantly parallel orientation with respect to the canalicular lumen and extend abluminally in irregular patterns which cover large membrane areas at considerable distance from the bile canaliculi. These changes indicate both proliferation and provide further evidence that these junctions are not permanent differentiations of the cell membrane.

Glucocorticoid effects on respiration and metabolism by rat liver homogenates

1962 ◽  
Vol 202 (2) ◽  
pp. 343-346 ◽  
Author(s):  
Dennis D. Goetsch ◽  
L. E. McDonald
Keyword(s):  
Lactic Acid ◽  
Oxygen Uptake ◽  
Rat Liver ◽  
Inorganic Phosphate ◽  
Chronic Administration ◽  
Glucocorticoid Treatment ◽  
Carbohydrate Utilization ◽  
Protein Levels ◽  
Liver Homogenates ◽  
And Control

The effects of glucocorticoid administration on oxygen uptake, glucose and glycogen disappearance, lactic acid formation, and inorganic phosphate and protein levels in rat liver homogenates have been studied. A single injection of hydrocortisone, prednisolone, or 9 α-fluoroprednisolone 5 hr before sacrifice resulted in a highly significant increase in oxygen uptake by rat liver homogenates, whereas chronic administration of prednisolone daily for 7 days caused a marked inhibition in homogenate respiration. Glycolytic rate did not appear to be affected by single injections since endogenous carbohydrate utilization was similar in liver homogenates prepared from control and treated animals. Incubation of liver homogenates under aerobic conditions disclosed that inorganic phosphate levels were decreased in homogenates from corticoid-treated rats, whereas these levels were similar in treated and control liver homogenates incubated under nitrogen. Under anaerobic conditions, liver homogenates from treated rats accumulated lactic acid more rapidly than untreated liver homogenates. Glucocorticoid treatment did not appear to affect protein disappearance since no differences between protein levels in treated and untreated rat liver homogenates were detected following incubation.

scholarly journals In vivo assembly of tight junctions in fetal rat liver.

1975 ◽  
Vol 67 (2) ◽  
pp. 310-319 ◽  
Author(s):  
R Montesano ◽  
D S Friend ◽  
A Perrelet ◽  
L Orci
Keyword(s):  
Tight Junctions ◽  
De Novo ◽  
Early Stage ◽  
Fetal Life ◽  
Bile Canaliculi ◽  
Linear Arrays ◽  
Fetal Rat ◽  
Particle Aggregates ◽  
Fetal Rat Liver

Examination of glutaraldehyde-fixed, freeze-fractured livers from 14-15-day rat fetuses provided the basis for the following observations. Membrane particles align in otherwise poorly particulated areas of the presumptive pericanalicular plasma membrane (A face), frequently forming a discontinuous "honey-comb" network joining small particle islands. Even at this early stage, contiguous B-fracture faces contain furrows, rather than rows of pits, distinguishing the linear particle aggregates on the A face as developing tight junctions rather than gap junctions. Short segments of these linear arrays merge with smooth ridges clearly identifiable as segments of discontinuous tight junctions. With the continuing confluence of particulate and smooth ridge segments, mature tight junctions become fully appreciable. We conclude that tight junctions form de novo by the alignment and fusion of separate particles into beaded ridges which, in turn, become confluent and are transformed into continuous smooth ones. At 21 days of fetal life, most of the images of assembly have disappeared, and the liver reveals well-formed bile canaliculi sealed by mature tight junctions.

Induction of rat liver DNA alterations by chronic administration of peroxisome proliferators as detected by 32P-postlabeling

1991 ◽  
Vol 247 (1) ◽  
pp. 65-76 ◽  
Author(s):  
Erika Randerath ◽  
Kurt Randerath ◽  
Ranjani Reddy ◽  
Tracy F. Danna ◽  
M. Sambasiva Rao ◽  
...  
Keyword(s):  
Rat Liver ◽  
Chronic Administration ◽  
Peroxisome Proliferators ◽  
Dna Alterations

Effects of vasopressor hormones and modulators of protein kinase C on glutathione efflux from perfused rat liver

1991 ◽  
Vol 261 (4) ◽  
pp. G578-G584 ◽  
Author(s):  
D. S. Raiford ◽  
A. M. Sciuto ◽  
M. C. Mitchell
Keyword(s):  
Protein Kinase C ◽  
Angiotensin Ii ◽  
Protein Kinase ◽  
Tight Junctions ◽  
Rat Liver ◽  
Perfused Rat Liver ◽  
Oxidized Glutathione ◽  
Glutathione Disulfide ◽  
Mediated Effects ◽  
Kinase C

Vasopressor hormones alter efflux of glutathione (GSH) and increase permeability of tight junctions in perfused rat liver. Infusions of 10 nM angiotensin II, 10 microM phenylephrine, and 10 nM vasopressin significantly increased efflux of GSH into perfusate by 32-41% and decreased biliary efflux by 31-57%. Direct modulation of protein kinase C (PKC) activity by 600 nM phorbol 12,13-dibutyrate (PDB), 5 microM 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H-7), 5 microM sphingosine, or 10 nM staurosporine altered the pattern of efflux of GSH but not biliary oxidized glutathione disulfide (GSSG)-GSH ratios. Phorbol dibutyrate mimicked the vasopressor-mediated effects, increasing perfusate efflux by 31% and decreasing biliary efflux by 45%. Inhibitors of PKC caused qualitatively opposite responses, changing perfusate GSH by -37 to 18% and increasing biliary efflux by 22-161%. Whereas vasopressin increased penetration of [14C]sucrose into bile, modulation of PKC activity by PDB and H-7 did not affect the permeability of tight junctions to [14C]sucrose. Although pretreatment with H-7 blocked vasopressin-mediated changes in efflux of GSH, it did not prevent the increase in [14C]sucrose penetrance. We conclude that alterations in sinusoidal and biliary efflux of GSH can occur independent of changes in permeability of hepatocellular tight junctions. These findings suggest a role for protein kinase C in modulating the hepatic efflux of GSH.

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