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The aim of this study was to investigate the effects of binge drinking on paracetamol-induced oxidative stress in mice liver. Male Swiss mice were divided into groups: control; ethanol-treated group (E) in five sequential doses of 2 g kg-1, administered through an orogastric tube; paracetamol-treated group (P) in a dose of 300 mg kg-1, intraperitoneally and a group that received paracetamol 12 h after the last dose of ethanol (PE). Blood and liver samples were collected for the determination of oxidative stress parameters 6, 24 and 48 h after treatment. Prior binge drinking potentiated the paracetamol-induced increase in the liver malondialdehyde level 48 h after treatment in comparison with the P and E groups (17.14±1.98 vs. 13.14±0.82 and 12.99±1.18 μmol L-1, respectively, p < 0.01). Ethanol and paracetamol in combination induced a more pronounced decrease in the liver GSH level than either of the individual substances alone at all time intervals (p < 0.01). Total liver superoxide dismutase (SOD) activity was significantly lower in PE 48 h after treatment in comparison with the P and E groups (251.73±80.63 vs. 707.62±179.92 and 1179.62±147.94 U mg-1 protein, respectively, p < 0.01). The lowest MnSOD activity in the PE group was detected 48 h after treatment (86.52±28.31; 41.13±11.07 and 23.16±5.18 U mg-1 protein in the P, E and PE groups, respectively, p < 0.05). Prior binge ethanol drinking potentiates paracetamolinduced reduction of antioxidative capacity of hepatocytes due to GSH depletion and SOD activity reduction, simultaneously increasing lipid peroxidation caused by paracetamol. [ABSTRACT FROM AUTHOR]

The aim of this study was to investigate the effects of binge drinking on the prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. Male Wistar rats were used in the experiments. They were divided into the following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g kg-1, administered by an orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg kg-1, administered intraperitoneally, 4. group that received Cd 12 h after the last dose of ethanol. Blood and liver samples for determination of oxidative stress parameters, were collected 24 h after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in the serum and liver malondialdehyde levels than either of the substances alone (p<0.01). Liver manganese superoxide dismutase (MnSOD) activity was increased in both the ethanol- and Cd-treated groups (p<0.01), while liver copper/zinc superoxide dismutase (Cu/ZnSOD) activity was elevated in the Cd group only. However, when administered in combination, ethanol and Cd induced a more pronounced decrease in liver MnSOD and Cu/ZnSOD activity 24 h after treatment (p<0.01). Based on our study, it can be concluded that ethanol may act synergistically with Cd in inducing lipid peroxidation and reduction in liver SOD activity. [ABSTRACT FROM AUTHOR]

The aim of our study was to investigate the effects of binge drinking on prooxidant/antioxidant system in rat liver in acute cadmium (Cd) intoxication. In experiment male Wistar rats were used and divided into following groups: 1. control, 2. ethanol-treated group, in five subsequent doses of 2 g/kg administered by orogastric tube, 3. Cd-treated group in a single dose of 2.5 mg/kg intraperitoneally, 4. group that received Cd 12 hours after the last dose of ethanol. Blood and liver samples were collected for determination of oxidative stress parameters, 24 hours after treatment. When administered in combination, ethanol and Cd induced a more pronounced increase in serum and liver malondialdehyde level than either of these substances alone (p<0.01). Liver manganese superoxide dismutase (MnSOD) activity was increased both in ethanol and Cd-treated group (p<0.01), while liver copper/zinc superoxide dismutase (Cu/ZnSOD) activity was elevated in Cd group only. However, when administered in combination, ethanol and Cd induced a more pronounced decrease in liver MnSOD and Cu/ZnSOD activity 24 hours after treatment (p<0.01). Based on our study, it can be concluded that ethanol may act sinergistically with Cd in inducing lipid peroxidation and reduction in liver SOD activity. [ABSTRACT FROM AUTHOR]

Introduction Oxidative stress plays an important role in pathogenesis of alcoholic liver injury. The main source of free oxygen species is cytochrome P450-dependent monooxygenase, which can be induced by ethanol. Role of cytochrome P4502E1 in ethanol-induced oxidative stress Reactive oxygen species produced by this enzyme are more important in intracellular oxidative damage compared to species derived from activated phagocytes. Free radicals lead to lip id peroxidation, enzymatic inactivation and protein oxidation. Role of mitochondria in alcohol-induced oxidative stress Production of mitochondria! reactive oxygen species is increased, and glutathione content is decreased in chronically ethanol-fed animals. Oxidative stress in mitochondria leads to mitochondria! DXA damage and has a dual effect on apoptosis. Role of Kupffer cells in alcohol-induced liver injury Chronic ethanol consumption is associated with increased release of endotoxin from gut lumen into portal circulation. Endotoxin activates Kupffer cells, which then release proinflammatoty cytokines and oxidants. Role of neutrophils in alcohol-induced liver injury Alcoholic liver injury leads to the accumulation of neutrophils, which release reactive oxygen species and lysosomal enzymes and contribute to hepatocyte damage and necrosis. Role of nitric oxide in alcohol-induced oxidative stress High amounts of nitric oxide contribute to the oxidative damage, mainly by generating peroxynitrites. Role of antioxidants in ethanol-induced oxidative stress Chronic ethanol consumption is associated with reduced liver glutathione and a-tocopherol level and with reduced superoxide dismutase, catalase and glutathione peroxidase activity. Conclusion Oxidative stress in alcoholic liver disease is a consequence of increased production of oxidants and decreased antioxidant defense in the liver. [ABSTRACT FROM AUTHOR]

Introduction. The etiopathogenesis of atherosclerosis and subsequent pulmonary emphysema has not been fully elucidated. Experimental Studies Foam cells are of great importance in the development of these diseases. It is known that local cytokine secretion and modification of native lipoprotein particles, which are internalized by the vascular and alveolar macrophages via the scavenger receptors on the surfaces of these cells, lead to the formation of foam cells. Thus, the exacerbation of local inflammatory process in the vascular and lung tissue ensues due to a generation of reactive oxygen species, resulting in further lipoprotein modification and cytokine production. Accumulating evidence suggests that oxidants may facilitate the inflammatory response by impairing antiprotease function, directly attacking vascular and lung matrix proteins and by inactivating enzymes involved in elastin synthesis and vascular and lung repair. Clinical Studies Cigarette smoke is recognized as a rich source of oxidants. Nearly 90% of all patients with chronic obstructive pulmonary disease are smokers. The process of atherogenesis is also influenced by tobacco smoke. Conclusion The role of vascular and alveolar macrophages has become increasingly important in understanding the development of atherosclerosis and resulting pulmonary emphysema. [ABSTRACT FROM AUTHOR]

Introduction. Atherosclerosis is a progressive, multifactorial, diffuse, multisystemic, chronic, inflammatory disease, which is manifested by disorders of vascular, immune and metabolic system. Pathogenesis of this disease is not fully understood. Endothelial Dysfunction and Inflammatory Process. Endothelial dysfunction is recognized as the crucial step in atherogenesis. A lot of studies have confirmed the involvement of various mediators of inflammation in initial proatherogenic processes, such as the upregulation of adhesion molecules on endothelial cells, binding of low density lipoproteins to endothelium, activation of macrophages and proliferation of vascular smooth muscle cells. Fatty stain and Inflammatory Process. Fatty stain consists of foam cell accumulation. After foam cell formation, mediators of inflammation initiate a series of intracellular events that include the induction of inflammatory cytokines. Thus, a vicious circle of inflammation, modification of lipoproteins and further inflammation can be maintained in the artery. Transitory Lesion and Inflammatory Process. In transitory lesion intensive phagocytosis of oxidized low density lipoproteins additionally activates monocytes and macrophages and consequently facilitates and exacerbates the inflammatory response. Fibrotic Plaque and Inflammatory Process. Inflammatory process, matrix-degrading metalloproteinases activity, platelets aggregation and smooth muscle cells proliferation play a central role in development of fibrotic plaque. Complex Lesion and Inflammatory Process. It has been shown that inflammation is closely related to the development of atherosclerotic plaque rupture. Conclusion. The contribution of inflammatory process has become increasingly meaningful in understanding the initiation, progression and clinical manifestations of atherosclerosis. [ABSTRACT FROM AUTHOR]