Increased chemiluminescence and superoxide production in the liver of chronically ethanol-treated rats

Boveris, Alberto; Fraga, César G.; Varsavsky, Alicia I.; Koch, Osvaldo R.

doi:10.1016/0003-9861(83)90482-4

Cited by 204 publications

(91 citation statements)

References 23 publications

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“…The present results agree with previously reported data (JAYAKUMAR; RAMESH; GERALDINE, 2006;SRINIVASAN et al, 2005;SINGAB et al, 2005;CHIDAMBARA MURTHY;ZHU et al, 1999). Since free radicals play an important role in CCl 4 -induced hepatotoxicity, it seems logical that compounds that neutralize such radicals may have a hepatoprotective effect.…”

Section: Discussionsupporting

confidence: 94%

“…SOD was determined by measuring the inhibition of the adrenochrome formation rate (MISRA; FRIDOVICH, 1972) in the reaction medium containing 1mM-adrenaline (epinephrine) and 50 mM-glycine/NAOH, pH 9.6 (BOVERIS et al, 1983). The treatment with CCl 4 induced the autoxidation of epinephrine; therefore, the inhibition of autoxidation had a reduction of 34% compared with the control group.…”

Section: Influence Of a Crassiflora Seed And Peel Extracts On Hepatimentioning

confidence: 99%

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Effect of extracts from araticum (Annona crassiflora) on CCl4-induced liver damage in rats

Roesler¹

2011

Ciênc. Tecnol. Aliment.

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Section: Discussionsupporting

confidence: 94%

Section: Influence Of a Crassiflora Seed And Peel Extracts On Hepatimentioning

confidence: 99%

Effect of extracts from araticum (Annona crassiflora) on CCl4-induced liver damage in rats

Roesler¹

2011

Ciênc. Tecnol. Aliment.

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“…Microsomes isolated from the livers of rats treated chronically with ethanol have been shown to generate 02-. and H202 at elevated rates compared to pair-fed controls (Lieber and DeCarli, 1970;Thurman, 1973;Boveris et al, 1983;Ekstrom and Ingelman-Sundberg, 1989;Rashba-Step et al, 1993). In the presence of iron, microsomes from the ethanol-treated rats were more reactive in generating OH and catalysing lipid peroxidation (Klein et al, 1983;Dicker and Cederbaum, 1987;Ekstrom and Ingelman-Sundberg, 1989;Cederbaum, 1986, Puntarulo andCederbaum, 1988a;Ekstrom et al, 1986).…”

Section: Introductionmentioning

confidence: 97%

DNA strand cleavage as a sensitive assay for the production of hydroxyl radicals by microsomes: role of cytochrome P4502E1 in the increased activity after ethanol treatment

Kukielka

Cederbaum

1994

Biochemical Journal

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There is increasing interest in the role of reactive oxygen radicals in the hepatotoxicity associated with ethanol consumption. Reactive oxygen intermediates interact with DNA and can cause single-strand breaks of supercoiled DNA. Experiments were carried out to evaluate the utility of this system as a sensitive assay for the detection of potent oxidants generated by rat liver microsomes isolated from pair-fed control rats and rats treated chronically-uwith ethanol. DNA strand cleavage was assayed by monitoring the migration of the supercoiled and open circular forms in agarose. Microsomes catalysed DNA strand breakage with either NADPH or NADH as cofactors; iron was required to catalyse the reaction and various ferric complexes were effective in promoting the reaction. DNA strand cleavage was prevented by catalase, superoxide dismutase, GSH and hydroxyl-radicalscavenging agents, suggesting that a hydroxyl-radical-like species was the oxidant responsible for the breakage. This assay system proved to be much more sensitive in detecting hydroxyl radicals than are other methods, such as e.s.r. spectroscopy or oxidation of chemical scavenging agents with respect to the amount of microsomal protein and the nature and concentration of the iron catalyst required. Microsomes from ethanol-treated rats were more reactive than control microsomes in catalysing the DNA strand cleavage with either NADPH or NADH; increased catalytic activity was observed with various ferric complexes and was sensitive to the above antioxidants. Compared with preimmune IgG, anti-(cytochrome P4502E1) IgG had no effect on DNA strand cleavage by the control microsomes, but completely prevented the NADPH-and the NADH-dependent increased activity found with microsomes from the ethanol-treated rats. Inhibitors of cytochrome P4502E1, such as diethyl dithiocarbamate and tryptamine, also lowered the extent of increase of DNA strand cleavage produced by microsomes from the ethanoltreated rats. These results indicate that DNA strand cleavage is a very sensitive assay for detecting the production of hydroxyl radicals by microsomes and to demonstrate increased activity by microsomes after chronic ethanol treatment. This increased activity with NADPH and NADH is due, at least in part, to induction of cytochrome P4502E1.

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“…Then acetaldehyde is decomposed to acetic acid by acetaldehyde dehydrogenase (ALDH) in mitochondria. Several studies have provided evidences for reactive oxygen species (ROS) generation during ethanol metabolism, including superoxide radical [1] , hydrogen peroxide [2] , hydroxyl radical [3] , and 1-hydroxyethyl radical [4] . Numerous studies have indicated that excessive ethanol intake induces the mass production of free radicals in the body, which are considered to be associated with alcoholic liver disease [5] .…”

Section: Introductionmentioning

confidence: 99%

Effects of ethanol on antioxidant capacity in isolated rat hepatocytes

Yang

Huang

Chen³

et al. 2005

WJG

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AIM:To investigate dose-response and time-course of the effects of ethanol on the cell viability and antioxidant capacity in isolated rat hepatocytes. METHODS:Hepatocytes were isolated from male adult Wistar rats and seeded into 100-mm dishes. Hepatocytes were treated with ethanol at concentrations between 0 (C), 10 (E10), 50 (E50), and 100 (E100) mmol/L (dose response) for 12, 24, and 36 h (time course). Then, lactate dehydrogenase (LDH) leakage, malondialdehyde (MDA) concentration, glutathione (GSH) level, and activities of glutathione peroxidase (GPX), glutathione reductase (GRD), superoxide dismutase (SOD), and catalase (CAT) were measured. RESULTS:Our data revealed that LDH leakage was significantly increased by about 30% in group E100 over those in groups C and E10 at 24 and 36 h, The MDA concentration in groups C, E10 and E50 were significantly lower than that in group E100 at 36 h. Furthermore, the concentration of MDA in group E100 at 36 h was significantly higher by 4.5-and 1.7-fold, respectively, than that at 12 and 24 h. On the other hand, the GSH level in group E100 at 24 and 36 h was significantly decreased, by 32% and 28%, respectively, compared to that at 12 h. The activities of GRD and CAT in group E100 at 36 h were significantly less than those in groups C and E10. However, The GPX and SOD activities showed no significant change in each group. CONCLUSION:These results suggest that longtime incubation with higher concentration of ethanol (100 mmol/L) decreased the cell viability by means of reducing GRD and CAT activities and increasing lipid peroxidation.

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Increased chemiluminescence and superoxide production in the liver of chronically ethanol-treated rats

Cited by 204 publications

References 23 publications

Effect of extracts from araticum (Annona crassiflora) on CCl4-induced liver damage in rats

Effect of extracts from araticum (Annona crassiflora) on CCl4-induced liver damage in rats

DNA strand cleavage as a sensitive assay for the production of hydroxyl radicals by microsomes: role of cytochrome P4502E1 in the increased activity after ethanol treatment

Effects of ethanol on antioxidant capacity in isolated rat hepatocytes

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