Hepatic antioxidant enzymes and lipid peroxidation in carbon tetrachloride-induced liver cirrhosis in rats

Nadkarni, G.D.; D’Souza, Nympha B.

doi:10.1016/0885-4505(88)90102-8

Cited by 23 publications

(16 citation statements)

References 10 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…CCI 4 -induced toxic liver injury which is a well characterized model for hepatic fibrosis has been extensively performed [6,7]. In our study, CCI 4 increased the levels of AST and ALT, reflecting hepatic necrosis, as well as, enhanced infiltration of the inflammatory cells, necrosis, fibrosis and expression of α-SMA.…”

Section: Discussionmentioning

confidence: 52%

“…CCI 4 damages hepatocellular membrane via lipid peroxidation, and this is followed by the release of inflammatory mediators from the activated inflammatory cells which are thought to potentiate CCl 4 -induced hepatic injury [5,7,17]. TNF-α is a pleiotropic proinflammatory cytokine produced rapidly by macrophages in response to tissue injury [18].…”

Section: Discussionmentioning

confidence: 99%

“…The chronic liver injury was induced by CCI 4 as previously described [6][7][8]. The rats were randomized into three equal groups (n=9 in each group).…”

Section: Experimental Animalsmentioning

confidence: 99%

“…Subsequently, this process is resulted in fragmentation of the lipid peroxide radicals, lipid hydroperoxides and other products, each acting like an active oxidizing agent [5][6][7]. Consequently, the structure of the cell membrane and intracellular organelles are completely deteriorated, and the structural damage expands [6].…”

Section: Introductionmentioning

confidence: 99%

“…These processes are immediately followed by the infiltration of inflammatory cells and release of various cytokines and growth factors [6]. As a result, lipid peroxidation has a vital role on the CCI 4 -induced liver injury [7,8]. Moreover, level of TNF-α consistently rises during the ongoing CCI 4 -induced liver toxicity [9].…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

et al. 2008

View full text Add to dashboard Cite

To assess the effect of infliximab, an anti-tumor necrosis factor (TNF)-alpha agent, on the carbon tetrachloride (CCl(4))-induced hepatic fibrosis in rats. Rats were randomized into three groups (n=9). The control group received only intraperitoneal (i.p.) olive oil. Hepatic fibrosis was induced by repeated i.p. injections of 1.5 ml/kg CCl(4) (1:3 mixture with olive oil) for 5 weeks in the remaining two groups which were also injected subcutaneous saline or 2 mg/kg infliximab. Infliximab reduced the levels of aspartate aminotransferase and alanine aminotransferase (p<0.05 for both). The scores of hepatic necrosis, inflammation and fibrosis, and expression of alpha-smooth muscle actin were lower in the infliximab-treated group than the CCI(4)-treated group (p<0.01, p<0.001, p<0.01, p<0.001, respectively). However, there was no significant difference in terms of liver tissue and plasma malondialdehyde, and serum TNF-alpha levels, while infliximab relatively reduced the level of transforming growth factor-beta(1) (373.0+/-153.1 vs. 280.8+/-127.1 pg/ml). Treatment with infliximab attenuated the necro-inflammation and fibrogenesis in the CCI(4)-induced hepatic fibrosis, and thus it might be effective as a therapeutic anti-fibrotic agent.

show abstract

Section: Discussionmentioning

confidence: 52%

Section: Discussionmentioning

confidence: 99%

“…The chronic liver injury was induced by CCI 4 as previously described [6][7][8]. The rats were randomized into three equal groups (n=9 in each group).…”

Section: Experimental Animalsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

et al. 2008

View full text Add to dashboard Cite

show abstract

The mallory body: Theories on development and pathological significance (part 2 of a literature survey)

Jensen

Gluud

1994

Hepatology

View full text Add to dashboard Cite

Drawing on data from a previously published literature survey on the clinical and experimental epidemiology of the Mallory body, we discuss current theories on its development in a pro et contra manner. Conclusions have been largely left open to the interpretations of the reader because many are still speculative. The main results of this study characterize Mallory bodies as stereotypical histological byproducts to diverse hepatic injuries (mostly alcohol associated) of questionable pathogenic importance. The temporal characteristics of Mallory bodies cast doubt on their role in hepatic neoplasia both as a disease marker and a causative agent, and prognosis studies suggest that they may be considered preterminal markers in some nonalcoholic liver diseases but remain prognostically unimportant in most studies on alcoholic patients. By similar line of inquiry, no consistent relationships may be found with disease severity or duration in alcoholic liver diseases. The roles of vitamin A deficiency and protein-calorie malnutrition are circumstantial. Drugs known to have calcium-antagonist properties and the physiological characteristics of the stress-response protein ubiquitin support the concept of defective protein systems in Mallory body pathogenesis. Disproportionate hepatic copper accumulation seems both epidemiologically and topographically associated with Mallory bodies, but these connections are largely unsupported by exposure studies. Many arguments still downplay the importance of uncoordinated changes in hepatic oxygen delivery and consumption, but ischemia-reperfusion studies suggest a role of oxygen-derived free radicals in the liver injuries under scrutiny. Finally, the role of Mallory bodies in the control system of hepatocyte function is addressed, and indirect evidence lends credence to a cybernetic approach in future study designs. It is reasonable to assume that different elements of a multifactorial setting operate with varying intensity over time as this may account for some of the controversies that exist. In conclusion, the biological significance of Mallory bodies is still mystery. It is not known whether Mallory bodies represent an epiphenomenon or play a role themselves in the initiation and continuation of liver damage.

show abstract

Balance between oxidative damage and proliferative potential in an experimental rat model of CCl4-induced cirrhosis: Protective role of adenosine administration

et al. 1997

View full text Add to dashboard Cite

Oxidative stress and its consequent lipid peroxidation (LP) exert harmful effects, which have been currently involved in the generation of carbon tetrachloride-induced cirrhosis. However, the recent report that "physiological" LP can be associated with liver regeneration (LR) makes it necessary to discriminate between oxidative stress-induced and LR-associated LP. In rats rendered cirrhotic by continuous CCl4 administration for 4 weeks, moderate cell necrosis and fine fatty infiltration were found. The histological abnormalities were accompanied by increased LP, mainly accounted for by the microsomal and cytosolic fractions and evidence of oxidative stress (decreased hepatic glutathione content and changes in xanthine oxidase and pentose phosphate pathway activities). After 8 weeks, a micronodular cirrhosis developed, but oxidative stress was greatly attenuated, only persisting in the enhanced LP confined to microsomes. Simultaneous administration of adenosine, a reliable hepatoprotector that readily prevents the onset of liver fibrosis, was able to block the oxidative stress induced by the long-term CCl4 treatment but elicited a selective subcellular distribution of increased LP, similar to that found during LR. The adenosine-induced changes in liver LP (mainly in the nuclear fraction) correlated with an increased activity of thymidine kinase. Therefore, data suggest that adenosine-mediated preservation of energy availability and mitochondrial function could participate in preventing the onset of oxidative stress in cirrhotic rats. The latter could induce a successful liver recovery, curtailing the sequence of events leading to fibrogenesis.

show abstract

Hepatic antioxidant enzymes and lipid peroxidation in carbon tetrachloride-induced liver cirrhosis in rats

Cited by 23 publications

References 10 publications

Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

Hepatoprotective Effect of Infliximab, an Anti-TNF-α Agent, on Carbon Tetrachloride-Induced Hepatic Fibrosis

The mallory body: Theories on development and pathological significance (part 2 of a literature survey)

Balance between oxidative damage and proliferative potential in an experimental rat model of CCl4-induced cirrhosis: Protective role of adenosine administration

Contact Info

Product

Resources

About