Protective effect of 16,16-dimethyl prostaglandin E2 on isolated rat hepatocytes against complement-mediated immune attack

1992 ◽  
Vol 37 (5) ◽  
pp. 645-649
Author(s):  
Yoichi Kurebayashi ◽  
Takuya Ikeda ◽  
Yuko Honda
Keyword(s):  
Protective Effect ◽  
Prostaglandin E2 ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Immune Attack ◽  
Isolated Rat

scholarly journals Protective effect of metallothionein on cadmium toxicity in isolated rat hepatocytes

1985 ◽  
Vol 230 (2) ◽  
pp. 395-402 ◽  
Author(s):  
W S Din ◽  
J M Frazier
Keyword(s):  
Protective Effect ◽  
Cadmium Toxicity ◽  
Membrane Damage ◽  
Rat Hepatocytes ◽  
Protective Effects ◽  
Isolated Rat Hepatocytes ◽  
Detoxification Mechanism ◽  
Isolated Rat

An isolated rat hepatocyte preparation was used to study the cellular toxicity of cadmium and the protective effects of metallothionein on cadmium-induced toxicity. Exposure of primary suspension cultures of isolated rat hepatocytes to Cd2+ (0-35.7 microM) for 15 min resulted in a dose-dependent reduction in the synthesis of cellular proteins during a subsequent 6 h incubation. Such inhibition could not be correlated with cellular lethality or gross membrane damage. Pre-induction of metallothionein in hepatocytes by zinc treatment in vivo of donor rats protected hepatocytes in vitro from cadmium-induced inhibition of protein synthesis. The protective effects in zinc-pre-induced hepatocytes are not due to alterations in the level of total cellular cadmium, but could be accounted for by the redistribution of intracellular cadmium in the presence of high levels of zinc-metallothionein. The data suggest that metallothionein exerts its protective effect by a kinetic detoxification mechanism, i.e. a decrease in reactive intracellular cadmium.

Protective Effect of Green Tea Extract and Tea Polyphenols against the Cytotoxicity of 1,4-Naphthoquinone in Isolated Rat Hepatocytes

1997 ◽  
Vol 61 (11) ◽  
pp. 1901-1905 ◽  
Author(s):  
Chika Miyagawa ◽  
Chen Wu ◽  
David Opare Kennedy ◽  
Teruyo Nakatani ◽  
Kimiko Ohtani ◽  
...  
Keyword(s):  
Protective Effect ◽  
Green Tea ◽  
Rat Hepatocytes ◽  
Green Tea Extract ◽  
Tea Polyphenols ◽  
Isolated Rat Hepatocytes ◽  
Tea Extract ◽  
Isolated Rat

Protective effect of nitric oxide on isolated rat hepatocytes submitted to an oxidative stress

Metabolism ◽  
2002 ◽  
Vol 51 (2) ◽  
pp. 175-179 ◽  
Author(s):  
Aur[eacute]lie-Anne Chausse ◽  
Val[eacute]rie Nivet-Antoine ◽  
Chantal Martin ◽  
Jean-Pierre Clot ◽  
Fran[ccedil]ois-Xavier Galen
Keyword(s):  
Oxidative Stress ◽  
Nitric Oxide ◽  
Protective Effect ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

Exogenous fructose 1,6-bisphosphate reduces K+ permeability in isolated rat hepatocytes

1997 ◽  
Vol 273 (2) ◽  
pp. C473-C478 ◽  
Author(s):  
T. Roig ◽  
R. Bartrons ◽  
J. Bermudez
Keyword(s):  
Protective Effect ◽  
Cell Injury ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Channel Arrest ◽  
Metabolic Fluxes ◽  
Fructose 1,6 Bisphosphate ◽  
The Relationship ◽  
K Permeability ◽  
Isolated Rat

The relationship between the protective effect of fructose 1,6-bisphosphate (F-1,6-P2) against cell injury and the modifications produced in the metabolic fluxes and in the membrane permeability to K+ was studied in isolated rat hepatocytes. Incubation of these cells in the presence of F-1,6-P2 reduced metabolic activity without affecting the ATP content, which suggests a downregulation of the ATP turnover. Using 86Rb+ as a tracer, we analyzed the relationship between these metabolic changes and alterations in K+ fluxes. In the presence of F-1,6-P2 the passive and the active K+ fluxes in hepatocytes decreased. However, the Na(+)-K+ pump from semipurified membranes was not directly affected by F-1,6-P2, which suggests a secondarily induced reduction of Na(+)-K+ pump activity. Moreover, galactosamine-treated cells showed a marked increase in permeability to K+ that was abolished by the presence of F-1,6-P2. This protective effect may be related to the prevention of K+ efflux. The results reported here strongly suggest the induction of channel arrest, and the associated metabolic downregulation, as the primary protective effect of F-1,6-P2, as has been shown in the prevention of galactosamine-induced hepatotoxicity.

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