ABSTRACT
Activities of glucose-6-phosphate dehydrogenase (G-6-PDH) and malate dehydrogenase were measured in the blood of 38 patients with acute nonepidemic parotitis and the status of glutathione antioxidant system assessed. The predominance of free-radical processes in the mechanisms of impairment of the parotid gland was confirmed. Increased level of lipid peroxidation products and decompensation of glutathione antioxidant system were found to be due to incompetence of the malate shuttle and low activity of G-6-PDH. A conclusion is made about the necessity of revising current approaches to prevention and therapy of acute nonepidemic parotitis.
Subject(s)
Antioxidants , Glutathione/blood , Parotitis/blood , Acute Disease , Adolescent , Adult , Aged , Female , Glucosephosphate Dehydrogenase/blood , Humans , Lipid Peroxidation , Male , Malondialdehyde/blood , Middle Aged , Pancreatitis/bloodABSTRACT
Activities of lysosomal enzymes (acid phosphatase, beta-galactosidase, cathepsin D) were measured in the blood of 38 patients with acute nonepidemic parotitis, caused by surgical diseases of the abdominal organs, and the status of glutathion antioxidant system studied. When appearing in the blood, lysosomal enzymes were found to join the chain cytolytic process or local proteolysis reactions, thus possibly becoming an important pathogenetic component in the development of acute parotitis induced by surgical diseases of the abdominal organs. The authors come to a conclusion about contribution of lysosomal enzymes to the mechanisms of impairment of the parotid gland, an increased level of these enzymes in the blood being indicative of pathologic changes on tissues. The authors emphasize that current approaches to pathogenetic treatment of acute nonepidemic parotitis should be revised.
Subject(s)
Abdomen/surgery , Clinical Enzyme Tests , Hydrolases/blood , Lysosomes/enzymology , Parotitis/diagnosis , Acute Disease , Adolescent , Adult , Aged , Clinical Enzyme Tests/statistics & numerical data , Female , Humans , Lipid Peroxidation , Male , Middle Aged , Parotitis/etiologyABSTRACT
Effects of prostaglandin I2 of the content of lipid peroxidation products and the activity of glutathione antioxidative system were studied in 60 dogs in whom acute nonepidemic parotitis was induced. Prostaglandin I2 was found to enhance the reactions of protective inhibition of metabolism with reduction of peroxidation level and activation of the antioxidative system, this permitting the cell to preserve its structural intactness. A conclusion is made about the possibility of using prostaglandin I2 for the prevention and therapy of acute nonepidemic parotitis.
Subject(s)
Epoprostenol/therapeutic use , Periodontitis/drug therapy , Postoperative Complications/drug therapy , Acute Disease , Animals , Antioxidants , Disease Models, Animal , Dogs , Drug Evaluation, Preclinical , Lipid Peroxidation/drug effects , Periodontitis/metabolism , Postoperative Complications/metabolism , Time FactorsABSTRACT
Effects of prostaglandin F2 on the major components of the antioxidative system (levels of malonic dialdehyde and lipid peroxides, activities and content of glutathione enzymes and nonenzymes (glutathione peroxidase, glutathione reductase, and NADPH (NADH), oxidized and reduced glutathione) were studied in experiments with 60 dogs in which acute nonepidemic parotitis was modeled. A varying capacity of the cells of the parotid gland to resist the detrimental effects of the disease and specific features of prostaglandin F2 effect on this capacity were revealed: injection of prostaglandin F2 stimulated both lipid peroxidation and the activity of the antioxidative system and led to cellular injury in the presence of a relatively high level of cellular metabolism, preserving cellular viability on condition of inhibited rate of metabolic reactions, this being the principal factor for the parotid gland, among other factors determining the cytoprotective effect.
Subject(s)
Antioxidants , Dinoprost/pharmacology , Lipid Peroxidation/drug effects , Parotid Gland/drug effects , Parotitis/drug therapy , Acute Disease , Animals , Dinoprost/therapeutic use , Disease Models, Animal , Dogs , Drug Evaluation, Preclinical , Pancreatitis/drug therapy , Pancreatitis/metabolism , Parotid Gland/metabolism , Parotitis/metabolismABSTRACT
The major constituents of acinar cell auto-oxidative system in acute postoperative parotitis were determined in experiments on 32 dogs. Two types of cellular reactions were identified: free-radical processes with increased levels of lipid peroxidation products and insufficiency of enzymatic and nonenzymatic glutathion antioxidants and reaction of defense metabolism inhibition. A conclusion is made about the necessity of altering the current methods for prevention and therapy of postoperative parotitis.
Subject(s)
Parotid Gland/metabolism , Parotitis/metabolism , Postoperative Complications/metabolism , Acute Disease , Animals , Antioxidants , Disease Models, Animal , Dogs , Lipid Peroxidation , Time FactorsABSTRACT
Blood levels of lipid peroxidation products, glutathion enzymatic and nonenzymatic antioxidants were measured in 58 patients with parotid gland involvement in acute surgical diseases of the abdominal organs. The authors prove the predominance of free-radical processes in the mechanisms of cellular injury initiated by inflammation mediators and proteolytic enzymes. A conclusion is made on the necessity of altering the methods of prevention and therapy of acute postoperative parotitis.
