RESUMO
The electron microscopic changes of the nephron structural components under conditions of dimethylhydrazine (DMH)-induced carcinogenesis with the development of colorectal adenocarcinoma in situ were evaluated. Destructive changes in epitheliocytes of proximal and distal tubules of the nephron, microcirculation disturbances in renal corpuscles and tubular structure are evidences of disorder in urine formation stages. Ðdministration of cytostatics aggravates the degree of destructive changes in the kidney. The application of carbon enterosorbent of IV generation "Carboline" for chronic neoplastic endotoxemia correction in combination with chemotherapy components significantly reduces the structural changes of the cortical substance of the kidneys, activates processes of reparative regeneration. The normalization of the morphological structure of the nephron components is an indication of the recovery of the test organ functions.
Assuntos
Adenocarcinoma/terapia , Antineoplásicos/toxicidade , Carbono/uso terapêutico , Neoplasias do Colo/terapia , Doxorrubicina/toxicidade , Metotrexato/toxicidade , Néfrons/efeitos dos fármacos , 1,2-Dimetilidrazina , Adenocarcinoma/induzido quimicamente , Adenocarcinoma/patologia , Adsorção , Animais , Neoplasias do Colo/induzido quimicamente , Neoplasias do Colo/patologia , Masculino , Microcirculação , Néfrons/irrigação sanguínea , Néfrons/ultraestrutura , RatosRESUMO
In experiments on white male rats it was shown that repeated administrations of nitric oxide precursors L-arginine and L-arginine L-glutamate do not alter the activity of cytolysis enzymes, reduce lipid peroxidation that correlates with indices of antioxidant protection, increase enzymatic activity in mitochondria and reduce endotoxemia. NO-synthase blockade by L-NAME increases endotoxemia, inhibits detoxification process in the liver, reduces the activity of electron transport enzymes in mitochondria, activation of lipids peroxodation reducing protective reserves of antioxidant system that is accompanied by low levels of NO2- in blood and liver.
Assuntos
Arginina/farmacologia , Dipeptídeos/farmacologia , Fígado/efeitos dos fármacos , Mitocôndrias Hepáticas/efeitos dos fármacos , Doadores de Óxido Nítrico/farmacologia , Óxido Nítrico/biossíntese , Alanina Transaminase/sangue , Animais , Arginina/metabolismo , Aspartato Aminotransferases/sangue , Dipeptídeos/metabolismo , Transporte de Elétrons/efeitos dos fármacos , Complexo IV da Cadeia de Transporte de Elétrons/metabolismo , Injeções Intraperitoneais , Peroxidação de Lipídeos/efeitos dos fármacos , Fígado/enzimologia , Masculino , Mitocôndrias Hepáticas/enzimologia , Oxigenases de Função Mista/metabolismo , NG-Nitroarginina Metil Éster/metabolismo , NG-Nitroarginina Metil Éster/farmacologia , Nitratos/sangue , Óxido Nítrico/agonistas , Óxido Nítrico/antagonistas & inibidores , Doadores de Óxido Nítrico/metabolismo , Óxido Nítrico Sintase/metabolismo , Nitritos/sangue , Ratos , Ratos Wistar , Succinato Desidrogenase/metabolismoRESUMO
There was proved in experimental investigations, conducted on white male rats, that nitric oxide (NO) play the leading role in ischemic preconditioning (IPC) while ischemic-reperfusion affection of the liver. Protective effect of IPC is presented in reduction of the cytolysis processes activity, lipoperoxydation, endotoxicosis severity, improvement in indices of hepatocytic bioenergetic state, mitochondrial transport of electrons and microsomal enzyme system. Increase in the NO end metabolites content, raising of eNOS activity and lowering of iNOS activity proves the NO role in IPC pathogenesis, and it is clear, that its changes in dynamics correlates with reduction of the anti-inflammatory cytokins content.
