RESUMO
Carbohydrates are the integral parts of glyco-conjugates and play an important role in cellular functions. 2-Deoxy-D-glucose (2-dGlc) is a sugar analogue of glucose and mannose and is reported to inhibit the lipid-linked saccharide formation involved in N-linked glycosylation of proteins. Administration of 2-dGlc (1 mg/100 g body weight) produced a decrease in the tissue total glycosaminoglycans level. We found that the activity of the enzymes involved in the biosynthesis of precursors of glycosaminoglycans (GAG) decreased, but that of the degrading enzymes increased. Thus, the decreased levels of GAG in tissues in 2-dGlc-administered rats occurs via enhanced degradation as well as decreased synthesis.
Assuntos
Animais , Arteriosclerose/etiologia , Arilsulfatases/metabolismo , Catepsina D/metabolismo , Desoxiglucose/farmacologia , Dieta Aterogênica , Glucuronidase/metabolismo , Glutamina-Frutose-6-Fosfato Transaminase (Isomerizante)/metabolismo , Glicosaminoglicanos/metabolismo , Glicosilação/efeitos dos fármacos , Hialuronoglucosaminidase/metabolismo , Hipercolesterolemia/complicações , Masculino , Especificidade de Órgãos , Precursores de Proteínas/metabolismo , Processamento de Proteína Pós-Traducional/efeitos dos fármacos , Ratos , Ratos Sprague-Dawley , Uridina Difosfato Glucose Desidrogenase/metabolismo , beta-N-Acetil-Hexosaminidases/metabolismoRESUMO
Administration of glucocorticoid (1, 2 and 4 mg) in excess leads to degeneration of epididymides as supported by cellular degeneration, sperm density and morphometric measurements. Zinc level increased statistically after 1, 2 and 4 mg hydrocortisone treatment while copper increased after 1 and 2 mg treatment. Cholesterol, protein and leucine aminopeptidase levels increased and decreased significantly in caput and cauda respectively. Activity of alkaline phosphatase reduced significantly while the treatment of hydrocortisone at different doses elevated acid phosphatase, aryl sulphatase and lactate dehydrogenase activities. Evidently, these changes are as a result of onset of cellular degeneration leading to impairment of metabolic/secretory activity of epididymal cells. The possible involvement of pituitary-testis axis in hydrocortisone induced epididymal degeneration and functional inhibition has been discussed.
Assuntos
Fosfatase Ácida/metabolismo , Fosfatase Alcalina/metabolismo , Animais , Arilsulfatases/metabolismo , Cobre/metabolismo , Epididimo/efeitos dos fármacos , Hidrocortisona/toxicidade , L-Lactato Desidrogenase/metabolismo , Leucil Aminopeptidase/metabolismo , Masculino , Ratos , Ratos Sprague-Dawley , Zinco/metabolismoRESUMO
Arylsulphatases A, B and C were found to be inhibited in liver and kidney tissues under lead acetate-treated conditions (both in vivo and in vitro) in rats. When lead acetate-treated animals (in vivo) were supplemented with ferric ammonium citrate (in vivo), a remarkable recovery was found in the activities of all arylsulphatases A, B and C whereas ferric ammonium citrate itself had no effect on the activities of arylsulphatases. When both the in vivo and in vitro lead acetate-treated arylsulphatases were supplemented with the purified ferritins (in vitro) it was observed that lead-induced inhibition of the activities of arylsulphatases was successfully reversed. It was also found that ferritins were able to bind a large quantity of lead. These results indicated that ferritins were directly involved for reactivation of arylsulphatases which were inhibited by lead. It was well established that a response to iron administration in rats was an immediate de novo stimulation of ferritin biosynthesis. Iron might therefore protect the enzymatic activities of arylsulphatases by enhancing the level of ferritin in liver and kidney tissues which is known to bind a large quantity of lead thereby ameliorating their toxic effects in the living system.