Protective effect of vitamin E on chromium (VI)-induced cytotoxicity and lipid peroxidation in primary cultures of rat Hepatocytes

1996 ◽  
Vol 71 (1-2) ◽  
pp. 20-24 ◽  
Author(s):  
N. Susa ◽  
Shunji Ueno ◽  
Yoshinori Furukawa ◽  
Masayasu Sugiyama
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Protective Effect ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Chromium Vi

S-Adenosylmethionine Exerts a Protective Effect against Thioacetamide-induced Injury in Primary Cultures of Rat Hepatocytes

2007 ◽  
Vol 35 (3) ◽  
pp. 363-371 ◽  
Author(s):  
Halka Lotková ◽  
Zuzana Čvervinková ◽  
Otto Kučera ◽  
Tomáš Roušar ◽  
Pavla Křiváková
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effect ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Glutathione Depletion ◽  
Dependent Manner ◽  
Simultaneous Treatment ◽  
Toxic Injury ◽  
Hepatocyte Injury

S-adenosylmethionine (SAMe) has been shown to protect hepatocytes from toxic injury, both experimentally-induced in animals and in isolated hepatocytes. The mechanisms by which SAMe protects hepatocytes from injury can result from the pathways of SAMe metabolism. Unfortunately, data documenting the protective effect of SAMe against mitochondrial damage from toxic injury are not widely available. Thioacetamide is frequently-used as a model hepatotoxin, which causes in vivo centrilobular necrosis. Even though thioacetamide-induced liver necrosis in rats was alleviated by SAMe, the mechanisms of this protective effect remain to be verified. The aim of our study was to determine the protective mechanisms of SAMe on thioacetamide-induced hepatocyte injury by using primary hepatocyte cultures. The release of lactate dehydrogenase (LDH) from cells incubated with thioacetamide for 24 hours, was lowered by simultaneous treatment with SAMe, in a dose-dependent manner. The inhibitory effect of SAMe on thioacetamide-induced lipid peroxidation paralleled the effect on cytotoxicity. A decrease in the mitochondrial membrane potential, as determined by Rhodamine 123 accumulation, was also prevented. The attenuation by SAMe of thioacetamide-induced glutathione depletion was determined after subsequent incubation periods of 48 and 72 hours. SAMe protects both cytoplasmic and mitochondrial membranes. This effect was more pronounced during the development of thioacetamide-induced hepatocyte injury that was mediated by lipid peroxidation. Continuation of the SAMe treatment then led to a reduction in glutathione depletion, as a potential consequence of an increase in glutathione production, for which SAMe is a precursor.

scholarly journals Asiatic Acid Derivatives Protect Primary Cultures of Rat Hepatocytes against Carbon Tetrachloride-Induced Injury via the Cellular Antioxidant System

2009 ◽  
Vol 4 (6) ◽  
pp. 1934578X0900400
Author(s):  
Mi Kyeong Lee ◽  
Seung Hyun Kim ◽  
Hyekyung Yang ◽  
Doo-Yeon Lim ◽  
Je-Ho Ryu ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Superoxide Dismutase ◽  
Antioxidant Enzymes ◽  
Carbon Tetrachloride ◽  
Primary Cultures ◽  
Rat Hepatocytes ◽  
Asiatic Acid ◽  
Antioxidative Defense ◽  
Protective Activity ◽  
Defense System

We attempted to elucidate the hepatoprotective mechanism of two asiatic acid (AS) derivatives, 3β,23-dihydroxyurs-2-oxo-12-ene-28-oic acid (AS-10) and 3β,23-dihydroxyurs-12-ene-28-oic acid (AS-14), which exhibited significant protective activity against carbon tetrachloride (CCl4)-induced hepatotoxicity in primary cultures of rat hepatocytes. Our findings showed that AS-10 and AS-14 preserved the level of glutathione and the activities of antioxidant enzymes such as glutathione reductase, glutathione peroxidase, superoxide dismutase and catalase. In addition, these compounds ameliorated lipid peroxidation, as demonstrated by a reduction in the production of malondialdehyde. Furthermore, AS-10 and AS-14 did not restore the reduced total GSH level by BSO, indicating that the hepatoprotective activities of these compounds may be involved, in part, by regulating GSH synthesis. From these results, we suggest that both AS-10 and AS-14 exerted their hepatoprotective activities against CCl4-induced injury by preserving the cellular antioxidative defense system.

scholarly journals Copper Toxicity and Lipid Peroxidation in Isolated Rat Hepatocytes: Effect of Vitamin E

1989 ◽  
Vol 25 (1) ◽  
pp. 55-62 ◽  
Author(s):  
Ronald J Sokol ◽  
Michael W Devereaux ◽  
Maret G Traber ◽  
Robert H Shikes
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Copper Toxicity ◽  
Rat Hepatocytes ◽  
Isolated Rat Hepatocytes ◽  
Isolated Rat

Sensitivity of ATPase-ADPase activities from synaptic plasma membranes of rat forebrain to lipid peroxidation in vitro and the protective effect of vitamin E

1996 ◽  
Vol 21 (3) ◽  
pp. 299-304 ◽  
Author(s):  
Marion Vietta ◽  
Silvana S. Frassetto ◽  
Ana M. O. Battastini ◽  
Adriane Bello-Klein ◽  
Cleci Moreira ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Vitamin E ◽  
Protective Effect ◽  
Plasma Membranes ◽  
Synaptic Plasma Membranes ◽  
Rat Forebrain
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