Ethanol-induced Oxidative Damage Research Articles

Protective Effect of Selenium-enriched Peptide from Cardamine violifolia on Ethanol-induced L-02 Hepatocyte Injury.

In this study, we investigated the protective effect of selenium (Se)-enriched peptide isolated from Cardamine violifolia (SPE) against ethanol-induced liver injury. Cell proliferation assays show that different concentrations of SPE protect human embryonic liver L-02 cells against ethanol-induced injury in a dose-dependent manner. Treatment with 12 μmol/L Se increases the cell survival rate (82.44%) and reduces the release of alanine aminotransferase, aspartate transaminase, lactate dehydrogenase, and apoptosis rate. SPE treatment with 12 μmol/L Se effectively reduces the concentration of intracellular reactive oxygen species and increases the contents of intracellular superoxide dismutase (51.64 U/mg), catalase (4.41 U/mg), glutathione peroxidase (1205.28 nmol/g), and glutathione (66.67 μmol/g), thereby inhibiting the effect of ethanol-induced oxidative damage. The results of the transcriptomic analysis show that the glutathione metabolism and apoptotic pathway play significant roles in the protection of L-02 hepatocytes by SPE. Real-time qPCR analysis shows that SPE increases the mRNA expression of GPX1 and NGFR. The results of this study highlight the protective effects of SPE against ethanol-induced liver injury.

Effect of Purple Sweet Potato Using Different Cooking Methods on Cytoprotection against Ethanol-Induced Oxidative Damage through Nrf2 Activation in HepG2 Cells.

The aim of this study was to investigate the effects of different cooking methods on the hepatoprotective effects of purple sweet potatoes against alcohol-induced damage in HepG2 cells. Purple sweet potatoes (Ipomeoea batatas L. Danjami) were subjected to different cooking methods, including steaming, roasting, and microwaving. Steaming resulted in a higher cytoprotective effect against alcohol damage than the other cooking methods. Additionally, the highest inhibition of glutathione depletion and production of reactive oxygen species against alcohol-induced stress were observed in raw and/or steamed purple sweet potatoes. Compared to roasted and/or microwaved samples, steamed samples significantly increased the expression of NADPH quinone oxidoreductase 1, heme oxygenase 1, and gamma glutamate-cysteine ligase in alcohol-stimulated HepG2 cells via the activation of nuclear factor erythroid 2-related factor 2. Moreover, ten anthocyanins were detected in the raw samples, whereas five, two, and two anthocyanins were found in the steamed, roasted, and microwaved samples, respectively. Taken together, steaming purple sweet potatoes could be an effective cooking method to protect hepatocytes against alcohol consumption. These results provide useful information for improving the bioactive properties of purple sweet potatoes using different cooking methods.

Protective Effect of Sargassum fusiforme Fucoidan against Ethanol-Induced Oxidative Damage in In Vitro and In Vivo Models.

Our previous studies have evaluated the bioactivities of a fucoidan isolated from Sargassum fusiforme (SF-F). To further investigate the health benefit of SF-F, in the present study, the protective effect of SF-F against ethanol (EtOH)-induced oxidative damage has been evaluated in in vitro and in vivo models. SF-F effectively improved the viability of EtOH-treated Chang liver cells by suppressing apoptosis. In addition, the in vivo test results indicate that SF-F significantly and dose-dependently increased the survival rate of zebrafish treated with EtOH. Further research results show that this action works through decreasing cell death via reduced lipid peroxidation by scavenging intracellular reactive oxygen species in EtOH-stimulated zebrafish. These results indicate that SF-F effectively protected Chang liver cells and zebrafish against EtOH-induced oxidative damage and suggest the potential of SF-F to be used as an ingredient in the functional food industry.

Nephroprotective Effects of Hesperidin and Myricetin Against High-Fat Diet Plus Ethanol-Induced Renal Oxidative Damage in Mice

Nephroprotective Effects of Hesperidin and Myricetin Against High-Fat Diet Plus Ethanol-Induced Renal Oxidative Damage in Mice

Influence of lipopolysaccharide on the development of oxidative-nitrosative stress in the liver of rats under conditions of chronic alcohol intoxication

Alcohol abuse is a common phenomenon among the countries of the European continent. One of the first organs suffering from alcohol-induced damage is the liver. Activation of Kupffer cells, as part of the mononuclear phagocyte system, plays a significant role in the development of oxidative-nitrosative damage of the liver. Systemic inflammatory response affects the polarization of macrophages throughout the body and may affect the development of alcohol damage of hepatocytes. The aim of this work is to study the effect of in vivo stimulation by S. typhi bacterial lipopolysaccharide on the development of oxidative-nitrosative stress in rat liver under conditions of chronic alcohol intoxication. Male Wistar rats were randomly divided into 4 groups: I - control; II - rats received 0.4 μg/kg of bacterial lipopolysaccharide of S. typhi; III - rats with induced alcoholic hepatitis, and IV - rats with chronic alcohol intoxication and injected bacterial lipopolysaccharide. The experiment lasted 63 days. We studied pro-oxidants antioxidant enzymes, the concentration of sulfide anion, nitric oxide production and malonic dialdehyde concentration in liver tissues. In vivo administration of bacterial lipopolysaccharide enhances ethanol-induced oxidative liver damage via increased production of superoxide anion despite the adaptive increase in the activity of antioxidant enzymes. Nitric oxide, the production of which increases in the liver during prolonged stimulation of the rat body with bacterial lipopolysaccharide, chronic alcohol intoxication and their combination, mainly metabolizes to peroxynitrite

Zinc Prevents Ethanol-Induced Oxidative Damage in Lingual Tissues of Rats.

The current study was designed to investigate the effects of zinc sulfate on cell proliferation, metallothionein (MT) immunoreactivity and antioxidant system against acute ethanol-induced oxidative damage in tongue tissues of rats. Wistar albino male rats, 2.5 to 3.0 months, were divided into four groups: Group I (n = 8), intact control rats; group II (n = 8), control animals given only zinc sulfate (100 mg/kg/day, for 3 consecutive days); group III (n = 14), animals given 1 mL absolute ethanol; group IV (n = 11), animals given zinc sulfate and absolute ethanol at the same dose and time. Animals were sacrificed under anesthesia 2 h after ethanol administration or 4 h after the last zinc sulfate treatment. Ethanol administration caused a marked decrease in the number of MT immunopositive cells and the proliferating cells in the lingual epithelium. A statistically significant decline in reduced glutathione levels, catalase activity and superoxide dismutase activities was also observed, whereas a significant elevation of lipid peroxidation levels and lactate dehydrogenase activities was detected in the ethanol group. In contrast, these changes were reversed by administration of zinc sulfate to ethanol-treated rats. In conclusion, it shows that zinc sulfate has therapeutic effects on acute ethanol-induced oxidative damage in the tongue tissues of rats.

Reparative Effects of Ethanol-Induced Intestinal Barrier Injury by Flavonoid Luteolin via MAPK/NF-κB/MLCK and Nrf2 Signaling Pathways.

Luteolin, a dietary flavonoid, has gained increasing interest as an intestinal protectant. This study aimed to evaluate the reparative effect of luteolin against ethanol-induced intestinal barrier damage in a Caco-2 cell monolayer model and the potential mechanisms. Luteolin attenuated ethanol-induced intestinal barrier injury, by increasing transepithelial monolayer resistance (TEER, 27.75 ± 14.75% of the ethanol group, p < 0.01), reducing Lucifer yellow flux (13.21 ± 1.23% of ethanol group, p < 0.01), and upregulating the expression of tight junction (TJ) proteins zonulin occludin-1 (ZO-1), occludin, and claudin-1 (37.963 ± 8.62%, 17.69 ± 7.35%, and 29.40 ± 8.08% of the ethanol group, respectively, p < 0.01). Further mechanistic studies showed that luteolin suppressed myosin light chain 2 (MLC) phosphorylation, myosin light chain kinase (MLCK) activation, nuclear factor kappa-B (NF-κB) nuclear translocation, and mitogen-activated-protein-kinase (MAPK) phosphorylation. Moreover, luteolin also acted as antioxidants indirectly by upregulating antioxidant-responsive-element (ARE) and nuclear factor (erythroid-derived 2)-like 2 (Nrf2) nuclear translocation to relieve ethanol-induced oxidative damage and TJ dysfunction. The results of the study indicate that luteolin may play an effective role in relieving intestinal barrier damage, and this effect is at least partially due to its indirect antioxidant capacity.

Aqueous extract of Polygonatum sibiricum ameliorates ethanol-induced mice liver injury via regulation of the Nrf2/ARE pathway.

This study investigates the hepatoprotective effect of the aqueous extract of Polygonatum sibiricum (AEPS) against ethanol-induced oxidative stress and explores underlying mechanisms. AEPS was administered by gavage to ICR mice for 30days. The experimental mice were fed a 5% (v/v) ethanol on last 10days and followed by a single megadose of ethanol (5g/kg) to induce ethanol-induced liver injury. Pretreatment with AEPS significantly suppressed the ethanol-induced elevation of aminotransferase activities, total bilirubin (TBIL) level, triglyceride level, and alleviated liver histopathological lesions. Meanwhile, AEPS reduced the level of oxidative stress in the liver and significantly suppressed the mRNA levels of NOX1, p67phox, gp91phox, and CYP2E1. Additionally, AEPS significantly increased the mRNA and protein levels of Nrf2 and its downstream antioxidant genes and promoted the nuclear translocation of Nrf2 in mice liver. Therefore, AEPS can effectively reduce ethanol-induced liver injury via regulation of the Nrf2/ARE pathway. PRACTICAL APPLICATIONS: Alcohol abuse and alcoholism have become a serious public health problem worldwide. Since liver is the major organ of alcohol metabolism, the most impactful damage of alcohol occurs in the liver. Polygonatum sibiricum is a traditional Chinese galenical and it also can be used as food ingredients. Most studies have reported that polysaccharide, flavonoids and saponins are the main bioactive compounds in Polygonatum sibiricum which play important roles in anti-oxidation. AEPS is the aqueous extract of Polygonatum sibiricum and AEPS can protect the mice liver against ethanol-induced oxidative damage. Thus it can be potential antioxidants to product hepatoprotective food and the study also provides a theoretical basis for the development and application of food about Polygonatum sibiricum.

Curcumin and Baicalin ameliorate ethanol-induced liver oxidative damage via the Nrf2/HO-1 pathway.

One of the key mechanisms of alcoholic liver disease is oxidative stress. Both Curcumin and Baicalin exert antioxidant effects, but the mechanism of their combined effects of ethanol-induced liver injury is still unclear. This study was conducted to evaluate the dual antioxidant activity of Curcumin combined with Baicalin against ethanol-induced liver injury in rats. Rats were divided into five groups, a control, ethanol, ethanol+Curcumin (50mg/kg), ethanol+Baicalin (50mg/kg), and ethanol+Curcumin +Baicalin group with ten rats per group. The effects of ethanol on liver enzymes, oxidative stress indicators and the levels of Nrf2/HO-1 pathway related proteins and mRNA were observed along with liver histopathology in rats. Our results found that the serum ALT and AKP levels were increased in ethanol-treated rats, which also showed a rising trend of 8-OHdG and LPO levels while hydroxyl radical scavenging ability, T-AOC, and the activities of SOD and GSH-Px were decreased in liver. The mRNA levels of Nrf2 and HO-1, the ratio of p-Nrf2/Nrf2, the protein level of HO-1 were decreased while NQO1 mRNA level, Nrf2, p-Nrf2, and NQO1 protein levels were increased in ethanol-treated rats. Combination treatment of Curcumin and Baicalin significantly reversed the ethanol-induced liver oxidative damage and further activate the Nrf2/HO-1 pathway, which was more effective than each drug alone. In conclusion, evidence has shown for the first time in this study that Curcumin combined with Baicalin ameliorated ethanol-induced liver oxidative damage in rats and revealed liver-protection. PRACTICAL APPLICATIONS: Many drugs for treating alcoholic liver disease are available commercially, but some adverse effects they have may cause secondary damage to the liver. At present, the combined treatment of different natural phytochemicals has attracted special attention in modern medicine. Curcumin, a kind of phytochemicals, is extracted from turmeric rhizome. Baicalin is one of the major active components of Scutellaria Baicalensis. The current research is to explore the antioxidant effect of Curcumin and Baicalin in ethanol-induced liver injury in rats. Our research proves that Curcumin combined with Baicalin on ethanol-induced liver oxidative damage is superior to single drug treatment. Therefore, the combination of Curcumin and Baicalin may provide a more prospective natural remedy to combat ethanol-induced liver injury.

Effect of melatonin on antioxidation in the PC12 cell line after exposure to ethanol

Excessive ethanol consumption may increase the production of reactive oxygen species (ROS), which results in the oxidative damage of tissues. The purpose of this study was to evaluate the effects of melatonin on the antioxidative status in the PC12 cell line after exposure to ethanol. In this study, the PC12 cells were treated with the different concentrations of melatonin for 24 hr. Subsequently, the cells were incubated with a fresh medium containing 150 mM of ethanol for 4 hr. To observe the oxidative damage and evaluate the antioxidative status after acute exposure to ethanol, cell viability, percentage of lactate dehydrogenase released (% LDH released), glutathione (GSH) level, activities of superoxide dismutase (SOD) and glutathione reductase (GRx), and concentrations of the protein carbonyls were assayed. The results showed that cell viability and GSH were increased, whereas the ethanol-induced cytotoxicity and protein carbonyl concentration decreased when the PC12 cells were treated with 10, 100 and 1000 μM melatonin. In contrary, there was no significant difference in the activity of SOD in the ethanol-treated group. In addition, there were no significant differences in the activity of GRx in the groups with the treatment of 10 and 100 μM melatonin; however, GRx activity decreased in the cells treated with 1000 μM melatonin. In conclusion, melatonin of moderate concentration may be a protective agent to alleviate acute ethanol-induced oxidative damage by the generation of GSH in the PC12 cell line.

The Protective Action of Carnosine and Organic Lithium Salts against Ethanol-Induced Oxidative Damage of Blood Plasma Proteins and Lipids of Healthy Persons and Alcoholic Patients

Organic lithium salts containing anionic components (succinate, fumarate, pyruvate) and antiox-idant ascorbate were tested for protection of blood plasma proteins and lipids against ethanol-induced oxidation in vitro. The normothymic agent lithium carbonate and well-known antioxidant dipeptide carnosine (β-alanyl-L-histidine) were used as the reference drugs. The oxidized proteins and lipids were determined by the level of carbonylated proteins (CP) and TBA-reactive substances (TBARS), respectively. In alcoholic patients the level of oxidized proteins and lipids was higher than in healthy persons. Incubation of blood with ethanol resulted in an increase in oxidized proteins and lipids in plasma of healthy persons but had no impact on the level of CP and TBARS in plasma of alcoholic patients. Lithium carbonate, lithium ascorbate, and lithium succinate exhibited protective action against ethanol-induced oxidation of biomolecules of blood plasma of healthy people. These effects were comparable with the carnosine action. The studied compounds had no effect on the level of CP and TBARS in plasma of alcoholic patients.

Protective action of carnosine and organic lithium salts in case of ethanol-induced oxidative damage of proteins and lipids of blood plasma in healthy persons and alcoholic patients

Organic lithium salts containing anionic components (succinate, fumarate, pyruvate and antioxidant ascorbate) were tested for protection of blood plasma proteins and lipids against ethanol-induced oxidation in vitro. We used normothymic lithium carbonate and well-known antioxidant dipeptide carnosine (b-alanyl-L-histidine) as the reference drugs. The oxidized proteins and lipids were determined by the level of carbonylated proteins (CP) and TBA-reactive products (TBA-RP), respectively. In alcoholic patients the level of oxidized proteins and lipids was higher than in healthy persons. Incubation of blood with ethanol resulted in an increase in oxidized proteins and lipids in blood plasma of healthy persons but had no influence on the level of CP and TBA-RP in blood plasma of alcoholic patients. Lithium carbonate, lithium ascorbate, and lithium succinate exhibited protective action against ethanol-induced oxidation of biomolecules of blood plasma of healthy people. These effects were comparable with carnosine action. The studied compounds had no effect on the level of CP and TBA-RP of blood plasma of alcoholic patients.

Modulatory effects of Viola odorata flower and leaf extracts upon oxidative stress-related damage in an experimental model of ethanol-induced hepatotoxicity.

Ethanol is the most widely abused drug in the world and its long-term use induces oxidative stress in the liver tissue. The aim of this study was to evaluate protective effect of Viola odorata against ethanol-induced hepatotoxicity in Wistar rat. Animals were divided into 9 groups as follows: control (normal saline), ethanol (10 mg/kg, intraperitoneally), ethanol with 3 doses (125, 250, and 500 mg/kg) of ethyl acetate flower and leaf extracts, and positive control (vitamin E 80 mg/kg). Animals were gavaged 30 min before ethanol injection for 28 days. Then, animals were killed and the livers were separated. Oxidative stress parameters, including reactive oxygen species, lipid peroxidation, and protein carbonyl as well as glutathione content, were evaluated. Also, histopathological examination was performed and assessment of blood alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and total antioxidant capacity were evaluated. Ethanol significantly increased oxidative stress markers in liver. Interestingly, administration of both extracts significantly decreased oxidative stress markers in liver tissue and biochemical parameters in the plasma. In addition, abnormal pathological features were improved after treatment with flower and leaf extracts. These results suggested that V. odorata can be considered a candidate for improving conditions due to ethanol-induced tissue oxidative damage because of its antioxidant activity.

Alpha-Tocopherol Supplementation Restricts Aluminium- and Ethanol-Induced Oxidative Damage in Rat Brain but Fails to Protect Against Neurobehavioral Damage

ABSTRACTThe concurrent presence of oxidative stress (OS) and aluminium exposure is an inducer of neurodegenerative changes. Aluminium can augment OS in a pro-oxidant dominant condition. Antioxidative property of α-tocopherol may be useful in restricting these degenerative changes in the brain. OS parameters are tested in frontal cortex (FC), hippocampus (HC), and cerebellum (CL) of α-tocopherol-supplemented (5 IU/day) male Wistar rats exposed to aluminium (10 mg Al/Kg/day; “Al”), ethanol (0.6 g ethanol/Kg/day; “Et”), and both (“Al-Et”) and vehicle-treated control (“C”) for 4 weeks. The α-tocopherol supplementation restricted regional alterations of reduced glutathione, superoxide dismutase, catalase, and glutathione peroxidase. Accordingly, the regional superoxide and peroxide handling capacities (SPHC) also remain unaltered. Al-Et group demonstrated significant elevation in the lipid peroxidation level in FC and CL regions compared to the group C; similar elevations in lipid peroxidation were noted in all the tested brain regions of Al group. Likewise, declines in glutathione reductase activity were noted in HC (versus Et group) and CL (versus Al and Et groups) of Al-Et group. Interestingly, changes in behavioral patterns of all the treatment groups are comparable while differing from that of the control group. Significant difference with group C is observed during first through fourth weeks, third to fourth weeks, and second to third weeks in terms of spontaneous motor activity, Rota Rod performance, and Hebb-Williams maze performance, respectively. Hence, the current dose and duration of α-tocopherol supplementation failed to provide full protection against the aluminium-induced neurodegeneration; nevertheless, it could provide only partial protection toward aluminium-induced augmentation of OS in specific brain regions.

A Blend of Extracts from Houttuynia cordata, Nelumbo nucifera, and Camellia sinensis Protects Against Ethanol-Induced Liver Damage in C57BL/6 Mice.

The protective activity of a mixture of aqueous and ethanolic extracts from Houttuynia cordata Thunb, Nelumbo nucifera G. leaves, and Camellia sinensis seed (HNC) was evaluated in C57BL/6 mice. Pretreatment with HNC prevented the elevation of serum aspartate aminotransferase and alanine aminotransferase caused by ethanol-induced hepatic damage. The HNC-treated mice showed significantly lower triglyceride levels, reduced CYP2E1 activity, and increased antioxidant enzyme activities and lipogenic mRNA levels. These results suggest that HNC might be a candidate agent for liver protection against ethanol-induced oxidative damage, through enhancement of antioxidant and antilipogenic activity.

Hepatoprotective Effects of Aqueous Extract of Watermelon (Citrullus lanatus) Seeds on Ethanol-Induced Oxidative Damage in Wister Rats

Background: Watermelon (Citrullus lanatus) is a roundish or ovoid fruit rich in antioxidant supplements that prevent oxidative stress in hepatic tissues due to generation of reactive oxygen species following exposure to alcohol. The present study aimed to investigate the protective effects of watermelon seed on ethanol-induced oxidative damage in liver of Wister rats. Methods: Twenty-five adult Wister rats of both sexes were randomly divided into five groups of five rats each. Rats in group I were administered distilled water for 8 days. Group II were administered distilled water for 7 days followed by 20 mL/kg body weight of 40% ethanol per body weight on day 8. Groups III and IV were administered 200 and 400 mg/kg, respectively, of the extract for 7 days followed by 20 mL/kg of 40% ethanol on day 8. Group V received 100 mg/kg body weight of silymarin for 7 days followed by 20 mg/kg of 40% ethanol on day 8. Animals were sacrificed on day 8. Liver was excised and then processed for histopathological examination. Biochemical assay for the following hepatic marker enzymes was carried out: alanine amino-transferase (ALT), aspartate amino-transferase (AST), alkaline phosphates (ALP), and protein concentration. Results: The results showed that watermelon treatment leads to increase in body weight. Furthermore, pretreatment with watermelon seed extract lead to significant decrease (P < 0.05) in plasma AST, ALT, ALP, and protein concentration, compared to ethanol treatment group. Conclusion: Watermelon seed extract demonstrates hepatoprotective effect in ethanol-induced oxidation in the liver of Wister rats, which might be linked to various antioxidant phytochemical content present in the extract.

In vitro and In vivo hepatoprotective studies on methanolic extract of aerial parts of Ludwigia hyssopifolia G. Don Exell

Background: Ludwigia hyssopifolia of family Onagraceae is traditionally used in the treatment of jaundice. There were no reports on the plant for both in vivo and in vitro hepatoprotective studies. Objective: The current study was aimed to evaluate the methanolic extract of aerial parts of L. hyssopifolia (LHME) for its in vitro and in vivo hepatoprotective activity against ethanol-induced oxidative damage in HepG2 cell lines and Wistar rats, respectively, and in vivo hepatoprotective activity against paracetamol and antihepatotoxic activity against D-galactosamine in rats. Materials and Methods: The antioxidant potential of the extract was investigated by employing different in vitro methods. The in vitro hepatoprotective activity of the extract was assessed by estimating cell supernatant for aspartate aminotransferase (AST), Alanine aminotransferase (ALT), and lactate dehydrogenase (LDH) while the in vivo hepatoprotective activity of the extract was assessed on the basis of improvement in the altered level of various serum biochemical parameters and in the changes occurred in the histology of liver of the rats. Results: Among the three test doses of LHME, 100 μg/kg and 200 mg/kg were found to be the effective doses in in vitro and in vivo hepatoprotective methods, respectively. Conclusion: The extract, LHME, exhibited significant (P < 0.01) hepatoprotective activity in both in vitro and in vivo models, which may be attributed to its antioxidant property revealed in both in vitro and in vivo studies. Abbreviation used: DPPH: 1,1 Diphenyl-1-picryl hydrazyl; ALT: Alanine transaminase; ALB: Albumin; ALP: Alkaline phosphatase; AST: Aspartate transaminase; CHOL: Cholesterol; DB: Direct bilirubin; FBS: Fetal bovine serum; GAE: Gallic acid equivalents; GGT: Gamma glutamyl transferase; GLU: Glucose; LDH: Lactate dehydrogenase; MEM: Modified Eagle's Medium; NBT: Nitro blue tetrazolium; PMS: Phenazine methosulphate; RE: Rutin equivalents; LHME: The methanolic extract of Ludwigia hyssopifolia; TBA: Thiobarbituric acid; TB: Total bilirubin; TP: Total protein; TCA: Trichloro acetic acid.

Hepatoprotective effect of 10% ethanolic extract from Curdrania tricuspidata leaves against ethanol-induced oxidative stress through suppression of CYP2E1

The hepatoprotective effect of 10% ethanolic extract of Curdrania tricuspidata (CTE) was investigated in HepG2/2E1 cells and C57BL/6 J mice. When compared ethanol-only treated HepG2/2E1 cells, pretreatment of CTE prevented increased intra-cellular reactive oxygen species levels and decreased antioxidant activities by ethanol-induced oxidative stress. In C57BL/6 J mice, CTE at a dose of 250 mg/kg/day was administered for 10 days, with ethanol (5 g/kg/day) administered for the final 3 days. Pretreatment with CTE prevented the elevated activities of serum aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase caused by ethanol-induced hepatic damage. CTE-treated mice displayed a reduced level of malondialdehyde and increased antioxidant activities of catalase, glutathione S-transferase, glutathione peroxidase, and superoxide dismutase, as well as a reduced level of glutathione as compared with ethanol-only-treated mice. CTE-treated mice exhibited significant inhibition of CYP2E1 activities and expression. These results suggest that CTE could be a useful agent for the prevention of ethanol-induced oxidative damage in the liver, elevating antioxidative potentials and alleviating oxidative stress by suppressing CYP2El.

Beneficial effects of rosmarinic acid against alcohol-induced hepatotoxicity in rats.

Alcohol is a severe hepatotoxicant that causes a variety of liver disorders. Rosmarinic acid (RA), a natural phenol, shows some biological activities, including antioxidant and anti-inflammatory effects. We investigated the effects of RA (10 mg/kg) against ethanol-induced oxidative damage and hepatotoxicity in rats. Animals received ethanol (4 g/kg, i.g.) and (or) RA (10 mg/kg, i.g.) daily for 4 weeks. At the end of the treatment period, rats were weighed and use for biochemical, molecular, and histopathological examinations. Ethanol increased hepatic lipid peroxidation (P < 0.001) and decreased hepatic levels of reduced glutathione (P < 0.01), catalase (P < 0.05), and superoxide dismutase (P < 0.001) compared with control group. RA prevented the prooxidant and antioxidant imbalance induced by ethanol in liver. Furthermore, RA ameliorated the increased liver mass, serum levels of ALT, AST, LDH, TNF-α, and IL-6 in ethanol group. Necrosis and infiltration of inflammatory cells in liver parenchyma were attenuated by RA treatment. Our findings showed that RA prevents ethanol-induced oxidant/antioxidant imbalance and liver injury in an experimental model of ethanol-induced hepatotoxicity. Therefore, RA may be a good candidate to protect against ethanol-induced hepatotoxicity; this deserves consideration and further examination.

Protection of proteins and lipids of blood plasma by different lithium salts under ethanol-induced oxidative damage

IntroductionThe creation of new lithium compounds with antioxidant activity is relevant problem for psychiatry. The aim of this work was study of the protective effect of lithium salts against ethanol-induced oxidative damage to proteins and lipids of human blood plasma in vitro.MethodsWe used lithium ascorbate and lithium carbonate 0.6 mmol/L which correspond to the therapeutic dose (in terms of lithium ions). Antioxidant carnosine (β-Ala-L-His) was used as comparison drug. We used the blood of 12 healthy donors. The heparinized blood samples were incubated in presence of tested preparations for one hour at 37 °C. The final ethanol concentration in samples was 0.5%. Oxidative modification of proteins was determined as the level of carbonylated proteins with 2.4–dinitrophenilhydrazine, lipid peroxidation products–as the level of TBA-reactive products by spectrometry. Statistical analysis was performed with “Statistika 10” program.ResultsThe addition of ethanol in the blood led to a significant increase in carbonylated proteins and TBA-reactive products in the plasma (carbonylated proteins: without ethanol 0.26 ± 0.01 nmol/mg of protein; with ethanol 0.33 ± 0.02 nmol/mg; TBA-reactive products: without–3.2 ± 0.1 nmol/mL; with–4.0 ± 0.2 nmol/mL, P &lt; 0.05). In the presence of carnosine such increase of oxidized products of biomolecules is not observed, i.e. carnosine had a protective effect against ethanol-induced oxidative damage. Lithium ascorbate showed a protective effect like carnosine. Lithium carbonate revealed no detectable influence on biomolecules in the conditions of our experiment.ConclusionLithium ascorbate has a protective effect on blood plasma proteins and lipids under ethanol-induced oxidative damage of biomolecules.Disclosure of interestThe authors have not supplied their declaration of competing interest.