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PubMed2006

Seasonal variability of oxidative biomarkers, lysosomal parameters, metallothioneins and peroxisomal enzymes in the Mediterranean mussel Mytilus galloprovincialis from Adriatic Sea.

The Mediterranean mussel, Mytilus galloprovincialis, is a classical sentinel organism for monitoring the biological effects of contaminants through the use of molecular and cellular biomarkers. These biological responses can be modulated also by seasonal changes of both environmental and biological factors, potentially influencing responsiveness and sensitivity to pollutants. The aim of this study was to characterize in a reference mussel population from the Adriatic Sea, the natural fluctuations of several oxidative stress biomarkers widely used in ecotoxicological applications. Analyses of individual antioxidant defenses (catalase, glutathione S-transferases, glutathione reductase, glutathione peroxidases, levels of glutathione) were integrated with those of the total oxyradical scavenging capacity (TOSC-assay), which quantify the overall capability of a tissue to neutralize different forms of oxyradicals. Due to the close relationship between antioxidant efficiency and onset of various cellular alteration, the seasonal characterization was carried out also on lysosomal membrane stability, accumulation of malondialdehyde, neutral lipids and lipofuscin, levels of metallothioneins and activity of peroxisomal enzymes (acyl-CoA oxidase and d-aminoacid oxidase). Results indicated a significant seasonality for several biological responses; major variations occurred especially in spring and summer months suggesting the influence of natural factors, such as temperature, reproductive cycle and food availability. The observed seasonal oscillations revealed both similarities and differences with those reported for other Mediterranean mussel populations suggesting that opposite trends can occur when the same environmental prooxidant factors have a different regional influence.

Animals↗

PubMed2006

Biochemical responses of the marine mussel Mytilus galloprovincialis to petrochemical environmental contamination along the North-western coast of Portugal.

Following the development of urban and industrial centres petrochemical products have become a widespread class of contaminants. The aim of this study was to investigate the effects of petrochemical contamination in wild populations of mussels (Mytilus galloprovincialis) along the NW Atlantic coast of Portugal by applying antioxidant and energetic metabolism parameters as biomarkers. For that, mussels were collected at five sampling sites presenting different petrochemical contamination levels. To evaluate the mussels' antioxidant status, enzymatic activities of catalase, superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione S-transferases, as well as glutathione redox status were evaluated in gills and digestive glands of mussels collected from the selected sites. Lipid peroxidation was determined in the same tissues to quantify cellular oxidative damage. Furthermore, to investigate how energetic processes may respond to these contaminants, the activity of NADP(+)-dependent isocitrate dehydrogenase was determined in mussels' digestive glands, and octopine dehydrogenase was determined in mussels' posterior adductor muscle. Furthermore, the concentrations of aliphatic hydrocarbons, unresolved complex mixture and polycyclic aromatic hydrocarbons (PAHs) were quantified in mussels' tissue, and abiotic parameters were quantified in water samples collected at each site. Several biomarkers showed statistically significant differences among sampling sites. The redundancy analysis (RDA) used to perform the integrated analysis of the data showed a clear separation of the sampling sites in three different assemblages, which are in agreement with the PAHs levels found in mussels tissues. In addition, the RDA indicated that some of the selected biomarkers may be influenced by abiotic parameters (e.g. salinity, pH, nitrates and ammonia). The approach selected for this study seems to be suitable for monitoring petrochemical contamination.

Animals↗

PubMed2006

Prevention of cognitive impairments and neurodegeneration by Khamira Abresham Hakim Arshad Wala.

Khamira Abresham Hakim Arshad Wala (KAHAW) is an effective and potent cardiac tonic with well-known antioxidant properties. The extensive use of this preparation in Indian system of Unani medicine led us to hypothesize that the pretreatment of this drug to male Wistar rats would prevent cognitive and neurobehavioral impairments. The cognitive impairment was developed by giving single intracerebroventricular injection of 1.5 mg/kg body weight of streptozotocin (STZ) bilaterally. An increased latency and path length was observed in cognitive, i.e. STZ group as compared to sham group and these were restored significantly in STZ group pretreated with KAHAW (700 mg/kg body weight for 15 days). The activity of antioxidant enzymes, viz. glutathione reductase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase was decreased in STZ group as compared to sham group and pretreatment of STZ group with KAHAW has protected their activities significantly. Moreover, the significantly depleted content of reduced glutathione and significantly elevated level of thiobarbituric acid reactive substances (TBARS) in STZ group were protected significantly with KAHAW. The study concludes that the therapeutic intervention of KAHAW may be used to prevent or to decrease the deterioration of cognitive function and neurobehavioral activities, often associated with the generation of free radicals.

Animals↗

PubMed2005

Phytochelatin plays a role in UV-B tolerance in N2-fixing cyanobacterium Anabaena doliolum.

To study the role of Cd-induced phytochelatins in UV-B tolerance, lipid peroxidation, antioxidative enzymes (superoxide dismutase, catalase, ascorbate peroxidase and glutathione reductase), glutathione arid phytochelatin contents were measured in buthionine sulphoximine treated and untreated cells of Anabaena doliolum. Cd-pretreatment of the cyanobacterium reduced the lipid peroxidation as well as the antioxidative enzymes in comparison to UV-B treatment alone, whereas the phytochelatin content demonstrated an increase. In contrast to this, buthionine sulphoximine-induced inhibition of phytochelatin synthase, dramatically decreased the Cd-induced co-tolerance against UV-B, hence demonstrating that phytochelatin not only protects the cyanobacterium from heavy metal but participates in UV-B tolerance as well.

Adaptation, Physiological↗

PubMed2005

Altered antioxidant status in peripheral skeletal muscle of patients with COPD.

Despite the growing field of interest in the role of pulmonary oxidative stress in chronic obstructive pulmonary disease (COPD), barely any data are available with respect to antioxidant capacity in the peripheral musculature of these patients. The main objective of this study was to assess in detail the antioxidant status in skeletal muscle of patients with COPD. Biopsies from the vastus lateralis of 21 patients with COPD and 12 healthy age-matched controls were analysed. Total antioxidant capacity, vitamin E, glutathione, and uric acid levels were determined and the enzyme activities of superoxide dismutase, glutathione reductase, glutathione peroxidase, and glutathione-S-transferase were measured. Malondialdehyde was measured as an index of lipid peroxidation. The total antioxidant capacity and the uric acid levels were markedly higher in COPD patients than in healthy controls (25%, P = 0.006 and 24%, P = 0.029, respectively). Glutathione-S-transferase activity was also increased (35%; P = 0.044) in patients compared to healthy subjects. Vitamin E level was lower in patients than in controls (P < 0.05). The malondialdehyde level was not different between the two groups. It can be concluded that the muscle total antioxidant capacity is increased in patients with COPD. Together with the reduced vitamin E levels, the increased glutathione-S-transferase activity and normal levels of lipid peroxidation products, these findings suggest that the antioxidant system may be exposed to and subsequently triggered by elevated levels of reactive oxygen species.

Aged↗

PubMed1997

Glucose-6-phosphate dehydrogenase activity is higher in the olfactory bulb than in other brain areas.

The activity of antioxidant enzymes was measured in the olfactory bulb (OB) of rat and compared with cortex, hippocampus, striatum and septum. Glutathione reductase, glutathione peroxidase, catalase and superoxide dismutase were not significantly different in the five brain areas, while glucose-6-phosphate dehydrogenase (G6PD) and 6-phosphogluconate dehydrogenase activities were four times higher in the OB than in the other areas. This picture prompted us to explore the reasons of the marked increase of G6PD, since it is the enzyme that regulates the operation of the hexose monophosphate shunt. A first approach was to analyze the G6PD electrophoretic pattern. The analysis revealed that the high G6PD activity of the bulb was neither due to new isoenzymes nor to a modification of the equilibrium between the G6PD dimers. We secondly hypothesized an induction of G6PD activity in the OB by oxidant stress. The assay of markers of the oxidant stress, such as thiobarbituric acid reactive substances, oxidized and reduced glutathione, did not confirm this hypothesis. A third approach was the cytochemical analysis of cryostat sections of OB. By this method we identified a particular cell type which was very rich in G6PD and located at the border of the glomerular layer. Thus, we attributed the high G6PD activity of the OB to the consistent presence of periglomerular cells, that probably need a high G6PD activity for their regulatory function in the neurochemical transmission.

Animals↗

PubMed2001

Antioxidant defense status of red blood cells of patients with beta-thalassemia and Ebeta-thalassemia.

Anemia in beta-thalassemia is caused by a combination of ineffective erythropoiesis and premature hemolysis of RBC in the peripheral circulation. Excess of the alpha-globin chain present in beta-thalassemic RBC is mainly responsible for oxidative damage of erythrocyte membrane protein. The activities of glucose-6-phosphate dehydrogenase, glutathione reductase, glutathione peroxidase, and glutathione-S-transferase, and the catalytic activity of catalase and superoxide dismutase, and the concentrations of non-enzymic antioxidants such as reduced glutathione were measured to estimate the status of the antioxidant defense system in the erythrocytes for protection against oxidative stress. The extent of lipid peroxidation was also estimated in thalassemic erythrocytes. Significantly lower activities of reduced glutathione indicate the cell to be in a pro-oxidant state and decreased activity of catalase favors hydrogen peroxide-mediated lipid peroxidation in beta-thalassemic and Ebeta-thalassemic RBC.

Antioxidants↗

PubMed2001

Melatonin protects against renal oxidative stress after obstructive jaundice in rats.

The goals of this study were to analyze the renal oxidative status in experimental biliary obstruction and to evaluate the impact of melatonin on renal oxidative stress. Cholestasis was done by double ligature and section of the extra-hepatic biliary duct. Melatonin was injected i.p. (500 microg/kg/day). Malondialdehyde, reduced glutathione, catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione transferase were determined in the renal tissue. After biliary obstruction, an increase in malondialdehyde (P<0.0001) and a fall in reduced glutathione (P<0.0001) were seen. Moreover, the scavenger enzyme activity had significantly diminished. After melatonin administration, the malondialdehyde fell significantly (P<0.0001), whereas reduced glutathione showed an important increase (P<0.0001) compared with the ligated bile duct group. Experimental bile duct obstruction was associated to an increase of renal oxidative stress. Treatment with melatonin decreased the renal lipid peroxidation, and both the reduced glutathione as well as the scavenger enzyme activity recovered.

Animals↗

PubMed2002

Oxidative stress in the mussel Mytella guyanensis from polluted mangroves on Santa Catarina Island, Brazil.

Digestive glands of the mangrove mussel Mytella guyanensis, collected at one non-polluted site (site 1) and two polluted sites (sites 2 and 3), were analysed for different antioxidant defenses, lipid peroxidation and DNA damage. Thiobarbituric acid-reactive substance (TBARS) and 8-oxo-7,8-dihydro-2'-deoxyguanosine levels were enhanced at the polluted sites. With the exception of superoxide dismutase, the activities of catalase and glutathione peroxidase were also higher at the polluted sites. Greater increases were observed in glutathione reductase, glutathione S-transferase and etoxyresorufine-O-deethylase activities at the polluted sites. Conversely, reduced glutathione content was higher at the control site. Trace metal contents in mussels collected at polluted sites were increased compared to the control site, and there were strong positive correlations between TBARS and Cu and Pb contents. M. guyanensis is routinely exposed to an oxidative stress condition at both polluted sites, and considering xenobiotic bioaccumulation in bivalve molluscs, the mangrove mussel represents an excellent bioindicator for environmental monitoring studies.

Animals↗

PubMed2003

Early oxidative stress in the diabetic kidney: effect of DL-alpha-lipoic acid.

Oxidative stress is implicated in the pathogenesis of diabetic nephropathy. The attempts to identify early markers of diabetes-induced renal oxidative injury resulted in contradictory findings. We characterized early oxidative stress in renal cortex of diabetic rats, and evaluated whether it can be prevented by the potent antioxidant, DL-alpha-lipoic acid. The experiments were performed on control rats and streptozotocin-diabetic rats treated with/without DL-alpha-lipoic acid (100 mg/kg i.p., for 3 weeks from induction of diabetes). Malondialdehyde plus 4-hydroxyalkenal concentration was increased in diabetic rats vs. controls (p <.01) and this increase was partially prevented by DL-alpha-lipoic acid. F(2) isoprostane concentrations (measured by GCMS) expressed per either mg protein or arachidonic acid content were not different in control and diabetic rats but were decreased several-fold with DL-alpha-lipoic acid treatment. Both GSH and ascorbate (AA) levels were decreased and GSSG/GSH and dehydroascorbate/AA ratios increased in diabetic rats vs. controls (p <.01 for all comparisons), and these changes were completely or partially (AA) prevented by DL-alpha-lipoic acid. Superoxide dismutase, glutathione peroxidase, glutathione reductase, glutathione transferase, and NADH oxidase, but not catalase, were upregulated in diabetic rats vs. controls, and these activities, except glutathione peroxidase, were decreased by DL-alpha-lipoic acid. In conclusion, enhanced oxidative stress is present in rat renal cortex in early diabetes, and is prevented by DL-alpha-lipoic acid.

Albuminuria↗

PubMed1998

Role of intracellular second messengers and reactive oxygen species in the pathophysiology of V. cholera O139 treated rabbit ileum.

Vibrio cholerae O139 has pandemic potential and it produces copious amounts of fluid secretion. The levels of various second messengers (intracellular Ca2+, cAMP, IP3, PKC) were measured to determine the cause of fluid secretion produced by this strain of V. cholerae. There was a significant increase in the levels of these second messengers in V. cholerae O139 treated ileum as compared to control ileum (enterocytes). Levels of these second messengers were also assessed in V. cholerae 569B induced fluid secretion in rabbit ileum and it was found that the levels were raised more in V. cholerae O139 treated ileum than in V. cholerae 569B treated rabbit ileum. The intestinal damage was assessed by measuring changes in the extent of lipid peroxidation of the enterocytes. Intracellular second messengers are known to raise the extent of lipid peroxidation. In V. cholerae O139 treated loops calcium ionophore A23187 enhanced the extent of lipid peroxidation whereas l-verapamil could only marginally decrease the lipid peroxidation. Dantrolene and H7 significantly decreased the extent of lipid peroxidation of enterocytes in V. cholerae O139 treated rabbit ileum. However, PMA could not enhance further the extent of lipid peroxidation in V. cholerae O139 treated rabbit ileum. So intracellular calcium and protein kinase C appear to be involved in intestinal damage caused by V. cholerae O139. Reactive oxygen species are responsible for causing tissue damage and the extent of oxidative damage depends on the balance between the pro-oxidants and the anti-oxidants. So the changes in the enterocytes' antioxidant level during V. cholerae O139 mediated intestinal infection was estimated. There was a significant decrease in the enterocyte level of the antioxidant enzymes SOD, catalase, glutathione peroxidase, glutathione reductase, glutathione transferase and glucose-6-phosphate dehydrogenase in V. cholerae O139 mediated intestinal infection. So a significant decrease in the levels of antioxidant defenses and a significant increase in the levels of second messengers appear to be important in mediating V. cholerae O139 induced lipid peroxidation which contributes to the changes in membrane permeability and thus to fluid secretion.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1999

Influence of dietary fat and vitamin E on antioxidant status of muscles of turkey.

The aim of this study was to better understand the effects of more or less unsaturated fat source (tallow/soy oil/rapeseed oil) and/or vitamin E dietary supplementation (200 ppm) on the antioxidant status (at day 1 post-mortem) of turkey muscles [pectoralis major (Pm) and sartorius (S)]. More particularly, when turkeys were fed tallow, supplementation was sufficient to improve significantly the vitamin E status. Feeding rapeseed oil increased the antioxidant enzyme (AOE) activities (catalase, superoxide dismutase, glutathion reductase), glutathione concentration, and value from the benzoic acid test. Dietary soy oil increased glutathione peroxidase activity, compared to other dietary fat sources. With tallow, most of AOE activities were lower than with rapeseed or soy oil. Whatever the feeding mode, vitamin E supplementation did not affect the AOE activities, glutathione concentration, or values from the benzoic acid test. AOE activities were always higher in the oxidative S muscle than in the glycolytic Pm muscle. After feeding tallow, 9 days of storage increased TBA-RS and carbonyl contents, whereas the activity of many antioxidant enzymes and the total antioxidant activity (TEAC test and benzoic acid test) decreased.

Animals↗

PubMed2001

Role of glutathione-dependent peroxidase in regulation of lipoperoxide utilization in malignant tumors.

Glutathione content, the activity of glutathione-dependent enzymes (glutathione reductase, glutathione peroxidase, and glutathione S-transferase), and also SOD (superoxide dismutase) and catalase were studied in human malignant tumors (uterus, breast, and ovaries) and normal tissues. Glutathione level and the activity of glutathione-dependent enzymes were 2-3 times higher in the malignant tumors than in normal tissues. A negative correlation between the level of glutathione and glutathione-dependent enzymes (glutathione peroxidase and glutathione S-transferase) in tumors and the efficacy of postoperative chemotherapy may characterize the degree of tumor resistance to chemotherapy and therefore may have prognostic value. Low SOD and catalase activity and high activity of glutathione-dependent enzymes in tumors suggest that glutathione peroxidase and glutathione S-transferase play a major role in peroxide utilization in malignant tumors.

Catalase↗

PubMed2003

Dose-dependent protective effect of selenium in rat model of Parkinson's disease: neurobehavioral and neurochemical evidences.

Normal cellular metabolism produces oxidants that are neutralized within cells by antioxidant enzymes and other antioxidants. An imbalance between oxidant and antioxidant has been postulated to lead the degeneration of dopaminergic neurons in Parkinson's disease. In this study, we examined whether selenium, an antioxidant, can prevent or slowdown neuronal injury in a 6-hydroxydopamine (6-OHDA) model of Parkinsonism. Rats were pre-treated with sodium selenite (0.1, 0.2 and 0.3 mg/kg body weight) for 7 days. On day 8, 2 micro L 6-OHDA (12.5 micro g in 0.2% ascorbic acid in normal saline) was infused in the right striatum. Two weeks after 6-OHDA infusion, rats were tested for neurobehavioral activity, and were killed after 3 weeks of 6-OHDA infusion for the estimation of glutathione peroxidase, glutathione-S-transferase, glutathione reductase, glutathione content, lipid peroxidation, and dopamine and its metabolites. Selenium was found to be successful in upregulating the antioxidant status and lowering the dopamine loss, and functional recovery returned close to the baseline dose-dependently. This study revealed that selenium, which is an essential part of our diet, may be helpful in slowing down the progression of neurodegeneration in parkinsonism.

3,4-Dihydroxyphenylacetic Acid↗

PubMed1999

Effect of cis-unsaturated fatty acids on the activity of protein kinases and protein phosphorylation in macrophage tumor (AK-5) cells in vitro.

Cis-unsaturated fatty acids (c-UFAs) have been shown to be capable of decreasing the survival of macrophage tumor (AK-5) cells in vitro. This cytotoxic action of c-UFAs was found to be associated with an increase in free radical generation and lipid peroxidation process and a simultaneous decrease in cellular anti-oxidants such as superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase, glutathione and vitamin E. In the present study, it was observed that c-UFAs such as gamma linolenic acid (GLA), arachidonic acid (AA), eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) can activate phospholipase C (PLC) and enhance diacylglycerol formation; all the fatty acids except alpha linolenic acid (ALA) increased the binding of phorbol dibutyrate acetate (PDBu) suggesting translocation of protein kinase C (PKC) and at the same time these fatty acids (especially GLA, AA, EPA and DHA) also enhanced PKC activity. AA, EPA and DHA decreased the activity of protein kinase A (PKA) both in the cytosol and particulate fractions whereas ALA and GLA enhanced the PKA activity in the particulate fractions; all the fatty acids except ALA reduced cyclic AMP levels and an enhanced phosphorylation of about 13 proteins of the nuclear fraction and about eight proteins of the plasma membrane fraction was noted in c-UFA treated AK-5 cells in vitro. These results suggest that c-UFAs can alter the activities of second messenger systems such as diacylglycerol and protein kinases and can phosphorylate both plasma membrane and nuclear proteins which are likely to be components of NADPH oxidase. Based on these results, it is suggested that fatty acids may mediate their cytotoxic action in part by modulating the expression of PKC. Activated PKC may then intensify the pro-oxidant state by augmenting NADPH oxidase, so inducing superoxide anion generation which may ultimately lead to cytolysis.

Animals↗

PubMed1979

Conversion of glutathione to glutathione disulfide by cell membrane-bound oxidase activity.

An apparently specific glutathione oxidase activity is present in renal cortex, epididymal caput, jejunal villus tip cells, choroid plexus, and retina (but not in liver). The activity is membrane-bound and is localized on the luminal surface of the brush border membranes of the kidney and jejunum. The distribution and localization of the oxidase are similar to those of gamma-glutamyl transpeptidase, suggesting that there is a significant relationship among the translocation of intracellular glutathione, the extracellular oxidation of glutathione to glutathione disulfide, and the reactions of the gamma-glutamyl cycle. Thus, both glutathione present in the blood plasma and intracellular glutathione translocated to the cell surface are accessible to oxidation and transpeptidation. Acceptor substrates of the transpeptidase (e.g., L amino acids) promote transpeptidation and decrease oxidation of glutathione. Conversion of glutathione to glutathione disulfide is followed by utilization of the latter compound by gamma-glutamyl transpeptidase and dipeptidase. Although intracellular oxidation of glutathione to glutathione disulfide is readily reversed by the action of glutathione reductase, glutathione disulfide formed extracellularly cannot be reduced; instead, it undergoes hydrolytic and transpeptidation reactions leading to gamma-glutamyl amino acid and amino acid products which may be recovered by being transported into the cell.

Animals↗

PubMed1997

Modulation of radiation response of human tumour cells by the differentiation inducers, phenylacetate and phenylbutyrate.

The aromatic fatty acids phenylacetate (PA) and phenylbutyrate (PB) are novel antitumour agents currently under clinical evaluation. Their ability to induce tumour differentiation in laboratory models and their low clinical toxicity profile makes them promising candidates for combination with conventional therapies. In the present studies, we characterized the interactions between these aromatic fatty acids and radiation, using as a model cell lines derived from cancers of the prostate, breast, brain and colon. Analysis of the radiation response of the tumour lines using the linear-quadratic model, demonstrated that cellular exposure to pharmacological, non-toxic concentrations of either PA or PB resulted in time-dependent and contrasting changes in radiation response. While drug pretreatment for 24 h reduced radiation sensitivity (significant alterations in both alpha and beta parameters), pre treatment for 72 h significantly increased radiosensitivity (significant alterations in alpha and beta parameters). In replicating tumour cells, these changes were accompanied by a gradual G1-phase arrest. Cytostasis alone, however, could not explain radiosensitization, as similar alterations in radiation response were documented also in non-cycling cells. Modulation of tumour radiobiology by PA and PB was tightly correlated with early rise followed by decline in intracellular glutathione levels and the activity of antioxidant enzymes such as catalase, superoxide dismutase, glutathione reductase, glutathione peroxidase and glutathione S-transferase. Although in vitro findings identify the aromatic fatty acids PA and PB as a new class of non-toxic modulators of radiation response, the antagonistic effect of these compounds on radiation response needs further examination. Our data strongly suggest that for PA or PB to have a role in clinical radiotherapy, appropriate scheduling of combination therapies must take into account their time-dependent effects in order to achieve clinical radiosensitization.

Antimetabolites, Antineoplastic↗

PubMed2005

Momordin Ic and oleanolic acid from Kochiae Fructus reduce carbon tetrachloride-induced hepatotoxicity in rats.

Hepatoprotective effects of momordin Ic and oleanolic acid obtained from Kochiae Fructus (KF), the fruit of a traditional Oriental medicinal plant, were evaluated against carbon tetrachloride (CCl4)-induced liver damage in rats. Male Sprague-Dawley rats were divided into four groups: control, CCl4-treated, CCl4 plus momordin Ic-treated (MMDIc-CCl4), and CCl4 plus oleanolic acid-treated (OAA-CCl4). Momordin Ic (30 mg/kg of body weight) and oleanolic acid (30 mg/kg of body weight) were orally administered once a day for 14 days. A mixture of 0.2 mL/100 g of body weight of CCl4 in olive oil (1:1, vol/vol) was injected 30 minutes after the final administration of momordin Ic and oleanolic acid. The momordin Ic and oleanolic acid pretreatments resulted in significantly lower serum transaminase, lactic dehydrogenase, and gamma-glutamyltransferase levels in the CCl4-treated rats. The CCl4-treated rats had significantly lower activities of glutathione, glutathione reductase, glutathione S-transferase, superoxide dismutase, catalase, and glutathione peroxidase. However, pretreatment with momordin Ic and oleanolic acid reduced the effect of CCl4 and helped maintain levels of the enzymes. Pretreatment with momordin Ic and oleanolic acid resulted in significantly lower production of aminopyrine N-demethylase and aniline hydroxylase in the CCl4-treated rats. Pretreatment with momordin Ic resulted in lower catalase and aminopyrine N-demethylase activity induction by CCl4, towards normalization. Momordin Ic and oleanolic acid obtained from KF appear to contribute to alleviating the adverse effects of CCl4 treatment by enhancing the hepatic antioxidant defense system.

Administration, Oral↗