Effects of ambient temperature on free radical generation, antioxidant defenses and life span in the adult housefly, Musca domestica

Life spans of poikilotherms like the housefly are shortened by elevation of ambient temperature. The objective of this study was to examine the possible involvement of active oxygen species in temperature induced life-shortening of the adult male housefly. Effects of varied ambient temperature, 20 degrees C and 28 degrees C, on life span, cyanide-resistant respiration, H2O2 concentration, superoxide dismutase (SOD) and catalase activities and glutathione (GSH) concentration were examined. Average life span of flies raised at 28 degrees C was about 52% lower than those raised at 20 degrees C. Rate of cyanide-resistant respiration, an indicator of oxygen free radical generation, was higher in flies raised at 28 degrees C, whereas steady-state concentration of H2O2 was decreased at this temperature. Catalase activity and GSH concentration were lower at 28 degrees C while SOD activity was unaffected by the ambient temperature. Results of this study suggest that life-shortening effects of elevated ambient temperature may be due, in part, to increased oxidative stress.     

Potent Induction of Total Cellular and Mitochondrial Antioxidants and Phase 2 Enzymes by Cruciferous Sulforaphane in Rat Aortic Smooth Muscle Cells: Cytoprotection Against Oxidative and Electrophilic Stress

Sulforaphane, a cruciferous isothiocyanate compound, upregulates cytoprotective genes in liver, but its effects on antioxidants and phase 2 defenses in vascular cells are unknown. Here we report that incubation of rat aortic smooth muscle A10 cells with sulforaphane (0.25-5 muM) resulted in concentration-dependent induction of a spectrum of important cellular antioxidants and phase 2 enzymes, including superoxide dismutase (SOD), catalase, the reduced form of glutathione (GSH), glutathione peroxidase, glutathione reductase (GR), glutathione S-transferase (GST), and NAD(P)H:quinone oxidoreductase 1 (NQO1). Sulforaphane also increased levels/activities of SOD, catalase, GSH and GST in isolated mitochondria of aortic smooth muscle cells. Time-dependent sulforaphane-induced increases in the mRNA levels for MnSOD, catalase, the catalytic subunit of gamma-glutamylcysteine ligase, GR, GST-A1, GST-P1, and NQO1 were observed. Pretreatment with sulforaphane (0.5, 1, and 5 muM) protected aortic smooth muscle cells from oxidative and electrophilic cytotoxicity induced by xanthine oxidase (XO)/xanthine, H(2)O(2), SIN-1-derived peroxynitrite, 4-hydroxy-2-nonenal, and acrolein. Furthermore, sulforaphane pretreatment prevented intracellular accumulation of reactive oxygen species (ROS) after exposure of the cells to XO/xanthine, H(2)O(2), or SIN-1. Taken together, this study demonstrates that in the aortic smooth muscle cells sulforaphane at physiologically relevant concentrations potently induces a series of total cellular as well as mitochondrial antioxidants and phase 2 enzymes, which is accompanied by dramatically increased resistance of these vascular cells to oxidative and electrophilic stress.     

Age-related changes in catalase, glutathione reductase activities, the amount of glutathione in total body of oregon and vestigial Drosophila melanogaster

Natural antioxidants, free radical scavengers as catalase, glutathione reductase and glutathione are considered for aging mechanism. The objective of our study was to investigate the differences in the life span of male Oregon (w.t.) and vestigial Drosophila melanogaster, the possible role of free radical scavengers such as catalase, glutathione reductase and reduced-oxidized glutathione levels in the aging process by studying the pattern of age-related changes. The life span of male Oregon D. melanogaster is longer than that of the vestigial D. melanogaster. The beginning of the dying phase of Oregon was around 40 days, while the vestigial's around 20 days. The maximum life span was 85 days in Oregon population and 56 days in vestigial population. Age-related changes of catalase activities were similar in male Oregon and vestigial and showed a decreasing curve during aging. Glutathione reductase activity of Oregon increased slightly between 10 and 40 days, decreased sharply therafter. Glutathione reductase activity of vestigial followed a pot-shaped trend with 60% decrease during the first 40 days and followed by a sharp increase during the late part of life. The amounts of reduced glutathione (GSH) and oxidized glutathione (GSSG) increased slightly up to 40 days of age and followed a sharp decline thereafter in male Oregon D. melanogaster. In male vestigial D. melanogaster, the concentrations of GSH and GSSG remained quite stable for the nogaster, the concentrations of GSH and GSSG remained quite stable for the first 10 days, followed by a sharp decline around 20th day and increased thereafter.     

Functional modulation of antioxidant enzymes in vascular endothelial cells by glycated LDL

Reactive oxygen species (ROS) have been implicated in atherogenesis. Previous studies demonstrated that oxidized LDL (oxLDL) or glycated LDL (gly-LDL) increased the generation of superoxide from vascular endothelial cells (EC). The present study examined the effects of gly-LDL on the activation of antioxidant enzymes for the metabolism of ROS in cultured human vascular endothelial cells in comparison to oxLDL and LDL without chemical modification. Treatment with LDL, oxLDL or gly-LDL significantly increased the release of hydrogen peroxide (H(2)O(2)) from EC following 2h of incubation and the release of superoxide after 24 h of treatment. The increased release of H(2)O(2), but not superoxide, was normalized in EC treated with LDL or its modified forms. Elevated activities of superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase in EC were detected following a 24 h-treatment with the LDLs. The levels of GR activity and reduced/oxidized glutathione (GSH/GSSG) in EC treated with the lipoproteins were increased after 2 h, but were reduced after > or =24 h of incubation. Gly-LDL caused less increases in SOD, GPx or catalase activity, but more evident changes in GR activity and H(2)O(2) release compared to oxLDL or LDL. The findings suggest that exposure to glucose-modified LDL altered the activities of multiple antioxidant enzymes in cultured EC, which partially normalizes the excess generation of ROS, but reduced the intracellular reservoir of GSH.     

Changes in enzyme activities in skin fibroblasts derived from persons of various ages

We examined antioxidant enzyme activities (catalase, glutathione peroxidase, and superoxide dismutase) in cultured skin fibroblasts (passage number 2-3) derived from 30 persons of various ages. With increasing ages, catalase activity decreased, glutathione peroxidase activity increased slightly, and superoxide dismutase activity was unchanged. After UVA irradiation (4.8 joule/cm2) of the fibroblasts, only catalase activity decreased by 70%. This suggests that catalase may play an important role in the aging of human skin fibroblasts.     

Changes of platelet antioxidative enzymes during oxidative stress: the protective effect of polyphenol-rich extract from berries of Aronia melanocarpa and grape seeds

Aronia melanocarpa fruits (Rosaceae) and grape seeds (seeds of Vitis vinifera, Vitaceae) are two of the richest plant sources of phenolic substances, and they have been shown to have various biological activities. The aim of the present study was to investigate and compare the action of phenolic extracts (at concentrations 5-100?μg/mL) of two different plants, berries of A. melanocarpa (chokebbery) and grape seeds, on the activities of various antioxidative enzymes, the amount of glutathione (as an important component of redox status) in control the platelets and platelets treated with H(2)O(2) (the strong physiological oxidant) in?vitro. The properties of these two tested extracts were also compared with the action of a well characterized antioxidative and antiplatelet commercial monomeric polyphenol - resveratrol. The extract from berries of A. melanocarpa, like the extract from grape seeds, reduced the changes in activities of different antioxidative enzymes (glutathione peroxidase, superoxide dismutase, and catalase) in platelets treated with H(2)O(2). The action of the two tested plant extracts and H(2)O(2) evoked a significant increase of reduced glutathione in platelets compared with platelets treated with H(2)O(2) only. Comparative studies indicate that the two tested plant extracts had similar antioxidative properties, and were found to be more reactive in blood platelets than the solution of resveratrol.     

Comparison of metabolic rate and oxidative stress between two different strains of mice with varying response to caloric restriction

Metabolic rate and parameters associated with oxidative stress were compared in two strains of mice, one of which, C57BL/6, exhibits an extension of life span in response to caloric restriction while the other, DBA/2, shows no such effect. Metabolic rate was higher in the DBA/2 than in the C57BL/6 mice, when measured at 5-6 months of age as in vivo and in vitro rates of oxygen consumption or body temperature. There were no remarkable inter-strain differences in activities of the antioxidant enzymes, superoxide dismutase, catalase, and glutathione peroxidase or in the rates of mitochondrial superoxide anion radical generation in heart or skeletal muscles. Comparison of glutathione redox state in the heart and skeletal muscles at 3 and 20 months of age indicated that the amount of glutathione (GSH) and the GSH:GSSG (glutathione disulfide) ratio were relatively higher in the young DBA/2 mice, but there were no inter-strain differences in the older mice. The age-related elevation in the level of oxidative stress reflected by GSH:GSSG ratio was greater in the C57BL/6 than DBA/2 mice. The energy balance, indicated by the gain/loss in body weight per unit of food consumed, is higher in C57BL/6 than DBA/2 mice. It is hypothesized that the genotype-specific extension of life span by caloric restriction may involve modulation of oxidative stress produced as a result of an interplay between metabolic rate and energy balance during aging.     

CuZn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase in lymphocytes and erythrocytes in insulin-dependent diabetic children

CuZn superoxide dismutase, Mn superoxide dismutase, catalase and glutathione peroxidase activities in lymphocytes and erythrocytes were studied in 9 children with insulin-dependent diabetes mellitus (IDDM) as well as in 21 healthy children. The mean erythrocyte CuZn superoxide dismutase and glutathione peroxidase were statistically significantly lower in the IDDM group compared with the controls although almost all IDDM results fell within the mean +/- 2 SD limits of the controls. The small differences found can hardly be assigned biological significance. Erythrocyte catalase as well as lymphocyte CuZn superoxide dismutase and Mn superoxide dismutase did not differ from the controls.     

Oxidative stress in blood of patients with alcohol-related pancreatitis

To determine the possible role of oxidative stress in alcoholic pancreatitis, the authors measured the ability of blood neutrophils of 22 patients with acute and 20 patients with chronic alcoholic pancreatitis to produce superoxide anion (O2-) and hydrogen peroxide (H2O2), spontaneously and after in vitro stimulation with phorbol ester and compared it with that of neutrophils isolated from the blood of 16 healthy controls. In addition, they measured serum activities of superoxide dismutase, catalase, and the serum concentration of glutathione peroxidase (GPx). Phorbol ester-induced O2- and H2O2 production in neutrophils of patients with acute and chronic pancreatitis was greater than in controls, but these differences, except of superoxide anion production by neutrophils of patients with chronic pancreatitis, were not statistically significant because of large individual differences. Spontaneous resting production of O2- and H2O2 by neutrophils of patients with chronic pancreatitis was significantly greater than in the controls. Superoxide dismutase and catalase activity was greater in sera of both groups of patients with acute and chronic alcoholic pancreatitis than in controls, but GPx concentration was significantly less in the sera of patients with chronic pancreatitis. Impaired GPx production and increased production of O2- and H2O2 by neutrophils may result in increased lipid peroxidation and could play a role in the pathogenesis of chronic alcoholic pancreatitis.     

Enhancement of erythrocyte superoxide dismutase activity: effects on cellular oxidant defense

To delineate further the role of superoxide dismutase (SOD) in red blood cell (RBC) oxidant defense, normal human erythrocytes were osmotically lysed and resealed in the presence of varying concentrations of exogenous SOD. This resulted in a dose-dependent increase in SOD activity in the resealed erythrocytes while maintaining nearly normal RBC hemoglobin concentration (less than 10% decrease from the control value), cell volume, and cellular deformability. Surprisingly, a five- or ninefold increase in SOD activity yielded no additional protection against superoxide-generating drugs (phenazine methosulfate or menadione sodium bisulfite). No significant differences were observed between the control and SOD-loaded RBCs in O2-driven methemoglobin formation or generation of thiobarbituric acid-reactive substances. In contrast, RBCs with elevated SOD activity pretreated with sodium azide (to block catalase activity) or 1-chloro-2,4- dinitrobenzene (to deplete reduced glutathione, GSH) showed significantly enhanced methemoglobin generation in response to superoxide generating drugs. No differential response was noted between the control, control-resealed, and SOD-loaded RBCs to oxidants other than superoxide. Based on our results and other data, we conclude that elevated SOD activity may imbalance cellular oxidant defense, resulting in enhanced oxidation due to the accelerated generation of H2O2, the product of O2- dismutation. This effect is significantly exacerbated under conditions in which H2O2 catabolism is altered.     

Hormonal and local factors influence antioxidant enzyme activity of rat fetal lung cells in vitro

Monolayer cultures of fetal rat mixed lung cells respond to sublethal concentrations (50%) of oxygen by a reduced growth rate. Exposure to 95% O2 causes growth arrest and cell loss. In the presence of serum the addition of dexamethasone (5.5 nM), tri-iodothyronine (5.5 nM), or insulin (5 microU/ml) appeared to increase the cytotoxicity of 95% O2. Under growth-arrested conditions, in the absence of serum or elevated O2 concentrations, all three agents influence cellular antioxidant enzyme activities. Dexamethasone (0.055 nM) increased CuZn superoxide dismutase activity by 72% and glutathione peroxidase activity by 94%. Triiodothyronine (5.5 nM) increased CuZn superoxide dismutase activity 93%. Insulin (5 microU/ml) increased CuZn superoxide dismutase activity 90%, and catalase activity 58%. Dexamethasone, but not tri-iodothyronine or insulin, seems to have a protective effect against subsequent acute hyperoxia under serum-free conditions. Local non-hormonal factors may also influence lung cell responses to acute increases in oxygen concentrations, since cells acutely exposed to 50% or 95% O2 release a transferable factor(s) into their culture medium which increases antioxidant enzyme activities of non-hyperoxic lung cells.     

Chronic Alcohol Consumption and Cerebral Indices of Oxidative Stress: Is There a Link?

BACKGROUND: It is still difficult to define the biochemical mechanisms that cause alterations in neuronal function and plasticity and neuronal cell loss in the brains of alcohol-dependent patients. METHODS: To evaluate the extent of cerebral alcohol-induced oxidative stress ex vivo, we investigated the levels of glutathione (GSH), its oxidation product glutathione disulfide (GSSG, produced by GSH-peroxidases), and the activities of catalase and superoxide dismutases (SOD). In addition, selected brain regions from up to 22 subjects (versus controls) were studied post mortem to compare the amount of oxidized DNA-base 8-hydroxy-2'-deoxyguanosine (8-OHdG) with levels of deoxyguanosine (dG) in mitochondrial and nuclear DNA. RESULTS: The most prominent findings showed significantly decreased GSH/(GSH+2GSSG) molar redox (oxidation-reduction) ratios in the corpus mamillare and cerebellum, which appeared due to an increase in GSSG caused by chronic alcohol intake. Catalase activity was increased in only the frontal cortex, whereas decreased catalase activity was found in the corpus callosum. In contrast, neither copper-zinc-superoxide dismutase (CuZnSOD) and manganese-superoxide dismutase (MnSOD) activities nor 8-OHdG/dG molar ratios were altered, although a tendency toward higher OHdG/dG ratios in temporal and parietal cortex from alcohol-dependent patients could be detected when mitochondrial DNA was analyzed selectively. CONCLUSIONS: We propose that decreased brain GSH/(GSH+2GSSG) molar redox (oxidation-reduction) ratios in alcohol-dependent patients may reflect neural impairment due to increased peroxide production after chronic alcohol consumption. However, future experiments, investigating the activities of enzymes and cofactors involved in GSH synthesis and metabolism in the human brain, will have to validate the specificity of these results for oxidative stress.     

Modulation of the iodination reaction in normal human neutrophils and in whole blood by penicillamine, congeners and intracellular enzyme catalase and superoxide dismutase

We have demonstrated that penicillamine (PSH) has the capacity to effect phagocytic cells by its interaction with the myeloperoxidase-halide system (MPOHS). We have undertaken studies at the cellular level, measuring the activity of the MPOHS through quantitation of I125 uptake (free and bound), known as the iodination reaction (i.e., in isolated polymorphonuclear leukocytes (PMN) and in whole blood). In contrast to other studies investigating the effects of PSH on isolated myeloperoxidase (MPO), we have shown that PSH scavenges the H2O2 produced by phagocytic cells, thereby reducing the availability of H2O2 for conversion to HOI125 by myeloperoxidase. This was observed as a reduction in the level of iodination. This finding is supported by our having obtained similar results in PMN and whole blood with catalase (C), glutathione (GSH) and N-acetylcysteine (NAC) but not with penicillamine disulphide (PSSP) or superoxide dismutase. Cu2+ (8 microM) when incubated with PSH reduced the level of inhibition of the iodination reaction by the oxidation of PSH to PSSP, illustrating the importance of the free sulphydryl group for this action. Incubation of PMN or whole blood for 0 to 2 hours with PSH, with a subsequent washing of PMN prior to stimulation, showed that PSH (free) requires to be present during stimulation of phagocytic cells to have this effect on the iodination reaction. Superoxide dismutase (SOD) produced increases in the iodination reaction in stimulated PMN by increasing the availability of H2O2. In conclusion, PSH inhibits the myeloperoxidase-halide system at a cellular level by scavenging H2O2 rather than by oxidation of the myeloperoxidase enzyme. This was observed at clinically relevant concentrations of PSH.     

Superoxide dismutase, glutathione peroxidase and catalase in the red cells of patients with malignant lymphoma

Erythrocyte superoxide dismutase, glutathione peroxidase and catalase activities have been measured in patients with untreated malignant lymphomas. Marked deficiencies of superoxide dismutase (P less than 0.001) and glutathione peroxidase (P less than 0.001) were found, whereas catalase levels were normal. There was no apparent difference in enzyme activities between the different histological types of lymphoma.     

Antioxidant vitamins C and E ameliorate hyperglycaemia-induced oxidative stress in coronary endothelial cells

OBJECTIVE: Vitamins C and E have protective features in many disease states associated with enhanced oxidative stress. The aim of this study was to investigate whether vitamin(s) C and/or E modulate hyperglycaemia-induced oxidative stress by regulating enzymatic activities of prooxidant, i.e. NAD(P)H oxidase and/or antioxidant enzymes, namely endothelial nitric oxide synthase (eNOS), superoxide dismutase, catalase and glutathione peroxidase, using coronary microvascular endothelial cells (CMEC). METHODS: CMEC were cultured under normal (5.5 mM) or high glucose (22 mM) concentrations for 7 days. The enzyme activities were determined by specific assays. The levels of O(2) (-) and nitrite were measured by cytochrome c reduction and Griess assays respectively. RESULTS: Hyperglycaemia did not alter eNOS activity or overall nitrite generation, an index of NO production. However, it increased NAD(P)H oxidase and antioxidant enzyme activities (p < 0.05). Specific inhibitors of NAD(P)H oxidase, i.e. phenylarsine oxide (0.1-3 microm) and 4-(2-aminoethyl)benzenesulfonyl fluoride (5-100 microm) and vitamins C and E (0.1-1 microm) significantly reduced prooxidant and antioxidant enzyme activities in CMEC exposed to hyperglycaemia (p < 0.01). The differences in enzyme activities were independent of increases in osmolarity generated by high glucose levels as investigated by using equimolar concentrations of mannitol in parallel experiments. CONCLUSIONS: Vitamins C and E may protect CMEC against hyperglycaemia-induced oxidative stress by concomitantly regulating prooxidant and antioxidant enzyme activities.     

左旋肉碱对氧化应激损伤肾小管上皮细胞的保护作用

目的观察左旋肉碱对过氧化氢（H2O2）应激损伤人肾小管上皮细胞的保护作用,并探讨其可能机制。方法用H2O2作用于人肾小管上皮细胞系HK-2,建立肾小管上皮细胞氧化应激损伤模型;MTT法检测左旋肉碱预处理后HK-2细胞的活力;用酶化学法测定HK-2细胞超氧化物歧化酶（SOD）、谷胱甘肽过氧化物酶（GSH—Px）、过氧化氢酶（CAT）活性及总抗氧化能力（T—AOC）、丙二醛（MDA）;荧光显微镜观察及流式细胞仪测定细胞内活性氧（ROS）及HK-2细胞凋亡率。结果左旋肉碱预处理12h能抑制H2O2损伤所导致的HK-2细胞活力降低,增加细胞中SOD、GSH—Px和CAT含量,提高细胞T-AOC,降低细胞中MDA和ROS水平,抑制HK-2细胞凋亡。结论左旋肉碱对氧化应激所致的肾小管上皮细胞损伤具有保护作用,其机制可能与增强细胞抗氧化能力、减少自由基生成、抑制脂质过氧化反应及细胞凋亡有关。     

Protective factors against oxygen free radicals and hydrogen peroxide in rheumatoid arthritis synovial fluid

Oxygen free radicals are probably involved in the pathogenesis of rheumatoid arthritis (RA). The enzymes involved in protection against oxygen free radicals and H2O2 (superoxide dismutase, catalase, and glutathione peroxidase) were measured. Superoxide dismutase was not increased, glutathione peroxidase was slightly and catalase was strongly elevated in RA synovial fluid (SF) compared with control SF. Although these enzymes are present in SF, the activities are insufficient to protect against oxygen free radicals and H2O2. In contrast to transferrin, ferritin was increased in RA synovial fluid. Ceruloplasmin was also elevated. When rat liver microsomes were used as a target for oxygen free radicals, serum and SF were both protective. Gel filtration experiments showed that the fraction pattern in which there was maximal protective potential against lipid peroxidation corresponded closely to the level of ceruloplasmin. After removal of ceruloplasmin from serum or SF, about 70% of the protective capacity disappeared. It is concluded that ceruloplasmin is an important protector against oxygen free radicals.     

Rat enterocyte injury by oxygen-dependent processes.

Neutrophils migrate to areas of inflammation and, when stimulated, produce O2-, H2O2, and other reactive O2 metabolites. To assess the effects of stimulated neutrophils on enterocytes, rat enterocytes were incubated with peripheral neutrophils. To assess cell viability, trypan blue exclusion and lactate dehydrogenase and protein release were measured. When 10(6) enterocytes/mL were incubated with 2.5 x 10(5) neutrophils/mL stimulated with phorbol myristate acetate, trypan blue exclusion decreased and lactate dehydrogenase and protein release increased. With the addition of 0.10 mg/mL of superoxide dismutase, trypan blue exclusion further decreased and lactate dehydrogenase and protein release increased. This suggests that H2O2- or H2O2/O2(-)-derived metabolites are more damaging to isolated enterocytes than O2-. To test this hypothesis, enterocytes were incubated with xanthine and increasing concentrations of xanthine oxidase in the presence and absence of superoxide dismutase. With increasing concentrations of xanthine oxidase, the cell number decreased and protein release increased. With the addition of superoxide dismutase, fewer cells were present, suggesting that cell lysis occurred. Protein release was further increased by the addition of superoxide dismutase. Enterocytes were then incubated with leucine and increasing concentrations of amino acid oxidase. With increasing concentrations of amino acid oxidase, trypan blue exclusion decreased and protein and lactate dehydrogenase release increased. These effects were ameliorated by the addition of 500 IU catalase/mL. These data suggest that O2- and H2O2, whether created by stimulated neutrophils or an enzyme-generating system, are damaging to isolated enterocytes. Superoxide dismutase did not offer enterocytes protection.     

Alcohol-induced congestive cardiomyopathy in adult turkeys: Effects on myocardial antioxidant defence systems

Summary The effects of chronic intake of dietary alcohol upon left ventricular function, activities of myocardial antioxidant enzymes, reduced glutathione (GSH) content and lipoperoxidation (measured as the formation of diene conjugates and lipid-soluble fluorescence) were studied in adult domestic Nicholas turkeys. The non-invasive evaluation of left ventricular function by echocardiography revealed an impaired contractile function (the calculated fractional shortening values were 31.1±4.1% in the alcoholic group and 38.8±4.4% in the controls) and dilatation of the heart in the alcoholic birds. The changes in the non-invasive parameters of the left ventricle indicate that the adult Nicholas turkey developed congestive cardiomyopathy secondary to the ingestion of ethanol.In the hearts of normal adult turkeys, high GSH content (2.39±0.25 mol/g wet weight) and superoxide dismutase activity were found, as compared to other animals, indicating the relatively higher development of antioxidant defence systems. Compared to the controls, significant increases were noted for all the antioxidant enzymes investigated (superoxide dismutase, catalase and glutathione peroxidase) and a moderately significant decrease in the GSH content was found in the left ventricle of alcoholic birds. The changes in GSH concentration and antioxidant enzyme activities might indirectly indicate some involvement of free radicals in the pathogenesis of ethanol-induced myocardial lesion. However, the levels of in vivo lipoperoxidation in the alcoholic birds did not significantly vary from those of control turkeys. Based on these findings, it appears that the reactive oxygen radicals may play a less important role in the pathogenesis of alcohol-induced cardiomyopathy in turkeys—probably due to the higher development of myocardial antioxidant defence systems.