ubiquinone and Liver-Diseases

As mitochondrial oxidative damage contributes to a wide range of human diseases, antioxidants designed to be accumulated by mitochondria in vivo have been developed. The most extensively studied of these mitochondria-targeted antioxidants is MitoQ, which contains the antioxidant quinone moiety covalently attached to a lipophilic triphenylphosphonium cation. MitoQ has now been used in a range of in vivo studies in rats and mice and in two phase II human trials. Here, we review what has been learned from these animal and human studies with MitoQ.

Topics: Administration, Oral; Animals; Antioxidants; Cations; Clinical Trials, Phase II as Topic; Disease Models, Animal; Fatty Liver; Humans; Liver Diseases; Mice; Mitochondria; Organophosphorus Compounds; Oxidative Stress; Rats; Treatment Outcome; Ubiquinone

Topics: Alzheimer Disease; Animals; Antioxidants; Benzoquinones; Cerebrovascular Disorders; Friedreich Ataxia; Humans; Liver Diseases; Ubiquinone

Evidence for in vivo antioxidative activity of reduced CoQ homologs has been presented. This came from studies with experimental endotoxemia in mice, reoxygenation of rat liver following ischemia, and reoxygenation of canine heart following 24-hour cold preservation. In radical-induced injury of hepatocytes, it has been first shown that reduced CoQ9 acts as a potential antioxidant regardless of its cellular concentration, whereas reduced CoQ10 acts in cells containing CoQ10 as the predominant homolog. The antioxidant activity of reduced CoQ homologs appears to be independent of that of alpha-tocopherol under the conditions employed.

Topics: Animals; Antioxidants; Chemical and Drug Induced Liver Injury; Free Radicals; Humans; Liver Diseases; Oxidation-Reduction; Ubiquinone; Vitamin E

Liver injury induced by burn plus delayed resuscitation (B + DR) is life threatening in clinical settings. Mitochondrial damage and oxidative stress may account for the liver injury. MitoQ is a mitochondria-targeted antioxidant. We aimed to evaluate whether MitoQ protects against B + DR-induced liver injury.. Rats were randomly divided into three groups: (1) the sham group; (2) the B + DR group, which was characterized by third-degree burn of 30% of the total body surface area plus delayed resuscitation, and (3) the treatment group, in which rats from the B + DR model received the target treatment. MitoQ was injected intraperitoneally (i.p) at 15 min before resuscitation and shortly after resuscitation. In the vitro experiments, Kupffer cells (KCs) were subjected to hypoxia/reoxygenation (H/R) injury to simulate the B + DR model. Mitochondrial characteristics, oxidative stress, liver function, KCs apoptosis and activation of the NLRP3 inflammasome in KCs were measured.. B + DR caused liver injury and oxidative stress. Excessive ROS lead to liver injury by damaging mitochondrial integrity and activating the mitochondrial DNA (mtDNA)-NLRP3 axis in KCs. The oxidized mtDNA, which was released into the cytosol during KCs apoptosis, directly bound and activated the NLRP3 inflammasome. MitoQ protected against liver injury by scavenging intracellular and mitochondrial ROS, preserving mitochondrial integrity and function, reducing KCs apoptosis, inhibiting the release of mtDNA, and suppressing the mtDNA-NLRP3 axis in KCs.. MitoQ protected against B + DR-induced liver injury by suppressing the mtDNA-NLRP3 axis.

Topics: Animals; Apoptosis; Burns; Cell Hypoxia; Cytokines; Delayed Emergence from Anesthesia; DNA, Mitochondrial; Kupffer Cells; Liver; Liver Diseases; Membrane Potential, Mitochondrial; Mice; Mitochondria; NLR Family, Pyrin Domain-Containing 3 Protein; Organophosphorus Compounds; Protective Agents; Rats, Sprague-Dawley; RAW 264.7 Cells; Reactive Oxygen Species; Resuscitation; Ubiquinone

Sepsis increases the risk of the liver injury development. According to the research works, coenzyme Q10 exhibits hepatoprotective properties in vivo as well as in vitro. Current work aimed at investigating the protective impacts of coenzyme Q10 against liver injury in septic BALB/c mice. The male BALB/c mice were randomly segregated into 4 groups: the control group, the coenzyme Q10 treatment group, the puncture and cecal ligation group, and the coenzyme Q10+cecal ligation and puncture group. Cecal ligation and puncture was conducted after gavagaging the mice with coenzyme Q10 during two weeks. Following 48 h postcecal ligation and puncture, we estimated hepatic biochemical parameters and histopathological changes in hepatic tissue. We evaluated the expression of factors associated with autophagy, pyroptosis, and inflammation. Findings indicated that coenzyme Q10 decreased the plasma levels in alkaline phosphatase, alanine aminotransferase, and aspartate aminotransferase in the cecal ligation and puncture group. Coenzyme Q10 significantly inhibited the elevation of sequestosome-1, interleukin-1

Topics: Alanine Transaminase; Animals; Autophagy; Beclin-1; Body Weight; Disease Models, Animal; Gene Expression Regulation; Immunohistochemistry; Inflammation; Interleukin-6; Liver; Liver Diseases; Male; Mice; Mice, Inbred BALB C; Pyroptosis; Sepsis; Tumor Necrosis Factor-alpha; Ubiquinone; Up-Regulation

We hypothesized that the mitochondrial-targeted antioxidant, mitoquinone (mitoQ), known to have mitochondrial uncoupling properties, might prevent the development of obesity and mitigate liver dysfunction by increasing energy expenditure, as opposed to reducing energy intake. We administered mitoQ or vehicle (ethanol) to obesity-prone C57BL/6 mice fed high-fat (HF) or normal-fat (NF) diets. MitoQ (500 µM) or vehicle (ethanol) was added to the drinking water for 28 weeks. MitoQ significantly reduced total body mass and fat mass in the HF-fed mice but had no effect on these parameters in NF mice. Food intake was reduced by mitoQ in the HF-fed but not in the NF-fed mice. Average daily water intake was reduced by mitoQ in both the NF- and HF-fed mice. Hypothalamic expression of neuropeptide Y, agouti-related peptide, and the long form of the leptin receptor were reduced in the HF but not in the NF mice. Hepatic total fat and triglyceride content did not differ between the mitoQ-treated and control HF-fed mice. However, mitoQ markedly reduced hepatic lipid hydroperoxides and reduced circulating alanine aminotransferase, a marker of liver function. MitoQ did not alter whole-body oxygen consumption or liver mitochondrial oxygen utilization, membrane potential, ATP production, or production of reactive oxygen species. In summary, mitoQ added to drinking water mitigated the development of obesity. Contrary to our hypothesis, the mechanism involved decreased energy intake likely mediated at the hypothalamic level. MitoQ also ameliorated HF-induced liver dysfunction by virtue of its antioxidant properties without altering liver fat or mitochondrial bioenergetics.

Topics: Animals; Diet, High-Fat; Dietary Fats; Liver Diseases; Male; Mice; Mice, Inbred C57BL; Mitochondria, Liver; Organophosphorus Compounds; Ubiquinone; Weight Gain

Mitochondrial reactive oxygen species generation has been implicated in the pathophysiology of ischemia-reperfusion (I/R) injury; however, its exact role and its spatial-temporal relationship with inflammation are elusive. Herein we explore the spatial-temporal relationship of oxidative/nitrative stress and inflammatory response during the course of hepatic I/R and the possible therapeutic potential of mitochondrial-targeted antioxidants, using a mouse model of segmental hepatic ischemia-reperfusion injury. Hepatic I/R was characterized by early (at 2 h of reperfusion) mitochondrial injury, decreased complex I activity, increased oxidant generation in the liver or liver mitochondria, and profound hepatocellular injury/dysfunction with acute proinflammatory response (TNF-α, MIP-1α/CCL3, MIP-2/CXCL2) without inflammatory cell infiltration, followed by marked neutrophil infiltration and a more pronounced secondary wave of oxidative/nitrative stress in the liver (starting from 6 h of reperfusion and peaking at 24 h). Mitochondrially targeted antioxidants, MitoQ or Mito-CP, dose-dependently attenuated I/R-induced liver dysfunction, the early and delayed oxidative and nitrative stress response (HNE/carbonyl adducts, malondialdehyde, 8-OHdG, and 3-nitrotyrosine formation), and mitochondrial and histopathological injury/dysfunction, as well as delayed inflammatory cell infiltration and cell death. Mitochondrially generated oxidants play a central role in triggering the deleterious cascade of events associated with hepatic I/R, which may be targeted by novel antioxidants for therapeutic advantage.

Topics: Animals; Antioxidants; Cyclic N-Oxides; Dose-Response Relationship, Drug; Inflammation; Liver Diseases; Male; Mice; Mice, Inbred C57BL; Mitochondria, Liver; Organophosphorus Compounds; Oxidative Stress; Reactive Oxygen Species; Reperfusion Injury; Ubiquinone

To describe the clinical and biological findings of two Japanese siblings with novel MPV17 gene mutations (c.451insC/c.509C > T) manifesting hepatic mitochondrial DNA depletion syndrome.. We observed these brothers and sought to determine the efficacy of treatment targeting respiratory chain complex II for the younger brother.. A 3-month-old boy had presented with profound liver dysfunction, failure to thrive, and watery diarrhea. Although he was then placed on a carbohydrate-rich diet, his liver function thereafter fluctuated greatly in association with viral infections, and rapidly deteriorated to liver failure. He underwent liver transplantation at 17 months of age but died at 22 months of age. The younger brother, aged 47 months at the time of this writing, presented with liver dysfunction from 8 months of age. His transaminase levels also fluctuated considerably fluctuations in association with viral infections. At 31 months of age, treatment with succinate and ubiquinone was initiated together with a lipid-rich diet using ketone milk. Thereafter, his transaminase levels normalized and never fluctuated, and the liver histology improved.. These cases suggested that the clinical courses of patients with MPV17 mutations are greatly influenced by viral infections and that dietary and pharmaceutical treatments targeting the mitochondrial respiratory chain complex II may be beneficial in the clinical management of MPV17 mutant patients.

Topics: Carnitine; Child, Preschool; Electron Transport Complex II; Fatal Outcome; Humans; Infant; Liver; Liver Diseases; Liver Transplantation; Male; Membrane Proteins; Mitochondrial Proteins; Succinic Acid; Ubiquinone

Studies were carried out to examine the anti-oxidative effect(s) of oral coenzyme Q10 supplementation (10 mg/kg b.w./day) in rats treated per os with either sodium nitrite (10 mg/kg b.w./day) or saline (control) for 14 days. Results showed that sodium nitrite increases thiobarbituric-acid reactive substances (TBARS in rat small intestinal mucosa and liver, and the agent did not have any effect(s) on the total anti-oxidant status (TAS) and lipid peroxidation of rat blood. Pretreatment of nitrite-poisoned rats with coenzyme Q10 mitigated TBARS and increased TAS in animal blood. Coenzyme Q10 has been found to be a promising anti-oxidant agent in sodium nitrite-induced lipid peroxidation.

Topics: Animals; Antioxidants; Carcinogens; Chemical and Drug Induced Liver Injury; Coenzymes; Intestine, Small; Lipid Peroxidation; Liver; Liver Diseases; Male; Nitrates; Oxidation-Reduction; Pilot Projects; Rats; Rats, Wistar; Thiobarbituric Acid Reactive Substances; Ubiquinone

Ubiquinol-10 and ubiquinone-10 were measured in plasma of patients with several pathologies known to be associated with increased oxidative stress. Plasma ubiquinol-10, expressed as a percentage of total ubiquinol-10 + ubiquinone-10, was found to be significantly lower in hyperlipidaemic patients and in patients with liver diseases than in age-matched control subjects. In contrast, no decrease in ubiquinol-10 was detected in plasma of patients with coronary heart disease and Alzheimer's disease. Except for ubiquinol-10, no other lipophilic antioxidant was found to be decreased in patients with liver diseases. These data suggest that the level of ubiquinol-10 in human plasma may serve as a marker for liver dysfunction, reflecting its diminished reduction by the liver rather than increased consumption by oxidants.

Topics: Adult; Aged; Alzheimer Disease; Biomarkers; Cholesterol; Coronary Disease; Humans; Hyperlipidemias; Liver Diseases; Middle Aged; Models, Biological; Oxidative Stress; Reference Values; Reproducibility of Results; Triglycerides; Ubiquinone

We have applied our method for the simultaneous detection of plasma ubiquinol-10 (reduced form) and ubiquinone-10 (oxidized form) (S. Yamashita and Y. Yamamoto, Anal. Biochem. 250, 66-73, 1997) to plasmas of normal subjects (n = 16) and patients with chronic active hepatitis (n = 28), liver cirrhosis (n = 16), and hepatocellular carcinoma (n = 20) to evaluate the pressure of oxidative stress in these patients. The average ubiquinone-10 percentages (+/- S.D.) in total ubiquinone-10 and ubiquinol-10 in the four groups were 6.4 +/- 3.3, 12.9 +/- 10.3, 10.6 +/- 6.8, and 18.9 +/- 11.1, respectively, indicating a significant increase in ubiquinone-10 percentage in patient groups in comparison to normal subjects. These results and a significant decrease in the plasma ascorbate level in patient groups indicate that oxidative stress is evident after the onset of hepatitis and the subsequent cirrhosis and liver cancer.

Topics: Adult; Aged; Aged, 80 and over; Antioxidants; Ascorbic Acid; beta Carotene; Biomarkers; Carcinoma, Hepatocellular; Carotenoids; Cholesterol; Cholesterol Esters; Female; Hepatitis, Chronic; Humans; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Lycopene; Male; Middle Aged; Oxidative Stress; Ubiquinone; Vitamin E

S-Allylmercaptocysteine (SAMC), one of the water-soluble organosulfur compounds in ethanol extracts of garlic (Allium sativum L.), has been shown to protect mice against acetaminophen (APAP)-induced liver injury. In this study, we examined the mechanisms underlying this hepatoprotection. SAMC (100 mg/kg, p.o.) given 2 and 24 hr before APAP administration (500 mg/kg, p.o.) suppressed the plasma alanine aminotransferase activity increases 3 to 12 hr after APAP administration significantly. The hepatic reduced glutathione levels of vehicle-pretreated mice decreased 1 to 6 hr after APAP administration, but SAMC pretreatment suppressed the reductions 1 to 6 hr after APAP administration significantly. These inhibitory effects of SAMC were dose-dependent (50-200 mg/kg) 6 hr after APAP administration. As SAMC pretreatment (50-200 mg/kg) suppressed hepatic cytochrome P450 2E1-dependent N-nitrosodimethylamine demethylase activity significantly in a dose-dependent manner, we suggest that one of its protective mechanisms is inhibition of cytochrome P450 2E1 activity. SAMC pretreatment also suppressed the increase in hepatic lipid peroxidation and the decrease in hepatic reduced coenzyme Q9 (CoQ9H2) levels 6 hr after APAP administration. The hepatic CoQ9H2 content of the SAMC pretreatment group was maintained at the normal level. Therefore, we suggest that another hepatoprotective mechanism of SAMC may be attributable to its antioxidant activity.

Topics: Acetaminophen; Alanine Transaminase; Animals; Chemical and Drug Induced Liver Injury; Coenzymes; Cysteine; Cytochrome P-450 CYP2E1; Glucuronosyltransferase; Glutathione; Lipid Peroxidation; Liver; Liver Diseases; Male; Mice; Proteins; Sulfhydryl Compounds; Sulfotransferases; Ubiquinone; Vitamin E

Ubiquinol-10, the reduced form of ubiquinone-10 (coenzyme Q10), is a potent lipophilic antioxidant present in nearly all human tissues. The exceptional oxidative lability of ubiquinol-10 implies that it may represent a sensitive index of oxidative stress. The present study was undertaken to assess the hypothesis that the level of ubiquinol-10 in human plasma can discriminate between healthy subjects and patients who are expected to be subjected to an increased oxidative stress in vivo. Using a newly developed method, we measured plasma ubiquinol-10 in 38 hyperlipidaemic patients with and without further complications, such as coronary heart disease, hypertension, or liver disease, and in 30 healthy subjects. The oxidizability of plasma samples obtained from hyperlipidaemic patients was found to be increased in comparison with control subjects, suggesting that the patients were subjected to a higher oxidative stress in vivo than the controls. Plasma ubiquinol-10, expressed as a percentage of total ubiquinol-10 + ubiquinone-10 or normalized to plasma lipids, was lower in the patients than in controls (P = 0.001 and 0.008, respectively). The proportion of ubiquinol-10 decreased in the order young controls > aged controls > hyperlipidaemic patients without complications > hyperlipidaemic patients with complications (P = 0.003). A negative correlation was found between the proportion of ubiquinol-10 and plasma triglycerides. The hyperlipidaemic patients with hypertension had a lower proportion of ubiquinol-10 than subjects without. When the study population was divided into smokers and non-smokers, plasma ubiquinol-10 was found to be reduced amongst smokers, independently of whether it was expressed as a percentage of total ubiquinol-10 + ubiquinone-10 (P = 0.006) or normalized to plasma lipids (P = 0.009). These data suggest that the level of ubiquinol-10 in human plasma may represent a sensitive index of oxidative stress in vivo especially indicative of early oxidative damage. Measuring plasma ubiquinol-10 can be proposed as a practical approach to assess oxidative stress in humans.

Topics: Adult; Alcohol Drinking; Amidines; Antidotes; Body Mass Index; Coronary Disease; Female; Humans; Hyperlipidemias; Hypertension; Lipid Peroxidation; Lipoxygenase; Liver Diseases; Male; Middle Aged; Oxidation-Reduction; Oxidative Stress; Regression Analysis; Risk Factors; Smoking; Spectrophotometry; Triglycerides; Ubiquinone

Oxidative stress is defined as a disturbance in the prooxidant-antioxidant balance in favor of the former and has been suggested to be a relevant factor in aging as well as in different pathological conditions, such as heart attack, diabetes, and cancer. Ubiquinol is very sensitive against oxygen radicals and gives ubiquinone as an oxidation product. Therefore, the ratio of ubiquinol to ubiquinone should be a good marker of oxidative stress because of its definition. A method for the simultaneous detection of ubiquinol-10 and ubiquinone-10 in human plasma is described. Heparinized human plasma was mixed with 5 volumes of methanol and 10 volumes of hexane. After vigorous shaking and centrifugation, the hexane phase (5 microliters) was injected immediately and directly on to reverse-phase HPLC equipped with an on-line reduction column and an electrochemical detector in order to avoid the oxidation of ubiquinol to ubiquinone. It was found that the ratio of ubiquinol-10 to ubiquinone-10 was about 95/5 in human plasma from healthy donors. A significant increase in the oxidized form (ubiquinone-10) content was observed in plasmas of patients with hepatitis, cirrhosis, and hepatoma when compared with normal subjects, suggesting increased oxidative stress in these patients.

Topics: Biomarkers; Carcinoma, Hepatocellular; Chromatography, High Pressure Liquid; Coenzymes; Electrochemistry; Hepatitis; Hexanes; Humans; Liver Cirrhosis; Liver Diseases; Liver Neoplasms; Oxidation-Reduction; Oxidative Stress; Reactive Oxygen Species; Solvents; Ubiquinone; Vitamin E

The effect of coenzyme Q10 (CoQ10) on hepatocyte injury during endotoxin (ET) shock in rats was studied with special reference to the role of polymorphonuclear neutrophils (PMN). ET shock was induced by intravenous administration of 5 mg/kg ET, and CoQ10 was given at 20 mg/kg once or 3 times orally or intravenously. We examined plasma glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and glutamate dehydrogenase (GLDH) levels, superoxide production by PMN, the phagocytic activity of PMN, the cytotoxicity of PMN to liver cells, and histological changes in the liver. The CoQ10-treated rats showed lower levels of GOT, GPT, and GLDH than rats treated with ET only. When compared to the group given ET only superoxide production by PMN induced by 2-methyl-6-phenyl-3,7-dihydroimidazol [1,2-alpha]pyrazin-3-one (MCLA) was significantly inhibited in the group given CoQ10 intravenously and 3 times orally, but there was no significant difference in the group given CoQ10 once orally. However, the level of superoxide production by PMN stimulated by phorbol myristate acetate (PMA) was lower in all CoQ10-treated rats than in those given ET only. There was no difference in either peripheral PMN counts or PMN phagocytes between the CoQ10-treated group and the group given ET only. Histologically, the hepatocyte injury in all groups that received CoQ10 was milder than that in the ET-only group. No hepatocyte cytotoxicity by PMN was observed in any group that received CoQ10. These results suggest that both intravenous and oral administration of CoQ10 can modulate the endotoxin-activated PMN, and is useful for preventing hepatocyte injury during ET shock.

Topics: Animals; Coenzymes; Disease Models, Animal; Liver Diseases; Male; Neutrophils; Phagocytosis; Rats; Rats, Wistar; Shock, Septic; Superoxides; Ubiquinone

This study was performed to determine whether oxidative stress contributed to the initiation or progression of hepatic injury produced by acetaminophen (APAP). Treatment of fasted mice with APAP (400 mg/kg, I.P.) led to hepatic injury as indicated by a marked elevation of plasma alanine aminotransferase (ALT). APAP caused an increased amount of thiobarbituric acid-reactive substance (TBARS), which was accompanied by a loss of reduced forms of coenzyme Q9 (CoQ9H2) and coenzyme Q10 (CoQ10H2) functioning as antioxidants. APAP also markedly decreased hepatic reduced glutathione (GSH) levels. Pretreatment with CoQ10 (5 mg/kg, I.V.) reduced hepatic TBARS levels to 30% and plasma ALT levels to 26% of placebo pretreatment levels without affecting hepatic GSH levels at 3 h of APAP treatment. alpha-Tocopherol (alpha-Toc) (20 mg/kg, I.V.) pretreatment also reduced hepatic TBARS levels to 13% and plasma ALT levels to 27% of placebo pretreatment levels without affecting hepatic GSH levels. These results suggest that oxidative stress followed by lipid peroxidation might play a role in the pathogenesis of APAP-induced hepatic injury, and pretreatment with lipid-soluble antioxidants such as CoQ10 and alpha-Toc can limit hepatic injury produced by APAP.

Topics: Acetaminophen; Alanine Transaminase; Animals; Coenzymes; Glutathione; Lipid Peroxidation; Liver; Liver Diseases; Male; Mice; Mice, Inbred ICR; Oxidation-Reduction; Thiobarbituric Acid Reactive Substances; Ubiquinone; Vitamin E

Topics: Animals; Free Radicals; Glutathione; Ischemia; Liver; Liver Diseases; Mitochondria, Liver; Rats; Reperfusion Injury; Ubiquinone; Vitamin E; Xanthine Dehydrogenase; Xanthine Oxidase

Topics: Adenosine Triphosphate; Animals; Glutathione; Ischemia; Kidney; Lipid Peroxides; Liver; Liver Diseases; Male; Mice; Mice, Inbred ICR; Rats; Rats, Inbred Strains; Reperfusion Injury; Shock, Septic; Ubiquinone; Vitamin E

Intraperitoneal injection of endotoxin (lipopolysaccharide, [LPS]) to mice at a dose of 15 mg/kg of body weight resulted in a survival rate of 31% 48 hours after administration. Simultaneous intramuscular administration of (10 mg/kg) coenzyme Q10 (CoQ10) increased the survival rates of LPS-administered mice to 69.7%. When LPS administration was increased to 30 mg/kg, no survivors were observed in the placebo group. Simultaneous intravenous injection of CoQ10 (10 mg/kg) or alpha-tocopherol (20 mg/kg) restored the survival rate to 52.9% or 42.9%, respectively. The adenosine triphosphate (ATP) level in the liver, which is the best index of the energy state, decreased gradually to 70% of the control ATP level 24 hours after LPS (15 mg/kg) administration. The lipid peroxide level in the liver increased fivefold 16 hours after LPS administration and then decreased to the control level in 8 hours. Simultaneous treatment of mice with antioxidants, such as CoQ10 or alpha-tocopherol, completely suppressed the lipid peroxide level in the liver and preserved the hepatic ATP level in the normal range. These results indicate that LPS induced hepatic damage in mice because of lipid peroxidation and that antioxidants suppressed lipid peroxidation, preserved energy metabolism in the liver, and enhanced survival of endotoxin-administered mice.

Topics: Adenosine Triphosphate; Animals; Antioxidants; Coenzymes; Lipid Peroxides; Lipopolysaccharides; Liver Diseases; Male; Malondialdehyde; Mice; Models, Biological; Shock, Septic; Ubiquinone; Vitamin E

Topics: Aged; Chronic Disease; Coenzymes; Female; Heart Diseases; Humans; Liver Diseases; Male; Middle Aged; Ubiquinone

Topics: Biopsy; Diagnostic Errors; Dihydrolipoamide Dehydrogenase; Esterases; Histocytochemistry; Humans; Laparotomy; Liver; Liver Diseases; Liver Neoplasms; Methods; NADH, NADPH Oxidoreductases; Oxidoreductases; Postoperative Complications; Ubiquinone

Topics: Age Factors; Albumins; Animals; Body Weight; Cystine; Dietary Carbohydrates; Dietary Proteins; Liver; Liver Diseases; Liver Regeneration; Methionine; Necrosis; Selenium; Ubiquinone; Vitamins; Yeast, Dried

Topics: Coenzymes; Liver Diseases; Oxidation-Reduction; Oxidoreductases; Succinate Dehydrogenase; Succinic Acid; Tetrazolium Salts; Ubiquinone