RESUMO
Cells with multiple chromosomal aberrations, the so-called rogue cells, were found in blood samples from more than 100 Chernobyl accident clearance workers. A comparative analysis of frequencies of stable and unstable chromosomal aberrations in two worker groups--those with or without rogue cells was made. A higher level of unstable aberrations in persons carrying rogue cells was observed. No difference in the level of stable aberrations between the groups was seen. The possibility of low dose alpha irradiation causing the chromosomal damage is raised.
Assuntos
Aberrações Cromossômicas , Linfócitos/efeitos da radiação , Liberação Nociva de Radioativos , Adulto , Partículas alfa/efeitos adversos , Humanos , Linfócitos/ultraestrutura , Pessoa de Meia-Idade , Fatores de Tempo , UcrâniaAssuntos
Colestase/enzimologia , Metilcolantreno/farmacologia , Microssomos Hepáticos/enzimologia , Oxigenases de Função Mista/biossíntese , Oxirredutases/biossíntese , Fenobarbital/farmacologia , Animais , Ácido Desoxicólico/farmacologia , Indução Enzimática/efeitos dos fármacos , Técnicas In Vitro , Cinética , Metabolismo dos Lipídeos , Masculino , Modelos Biológicos , Consumo de Oxigênio/efeitos dos fármacos , Peróxidos/metabolismo , RatosRESUMO
The severity of the induced effect of the polycyclic hydrocarbon 3-methylcholanthrene on monooxygenase of the microsomal fraction of the liver as a function of the number of binding sites for this inducer in the active site of cytochrome P-450 was investigated. In vivo models, in which the primary bounding and metabolism of a polycyclic hydrocarbon in the microsomes is increased or sharply inhibited, are presented. It is concluded that in the mechanism of induction by 3-methylcholanthrene, the activation of synthesis of specific protein (cytochrome P-448) is accomplished not by the initial molecule of the inducer, but by products of its primary metabolism in the microsomes.
Assuntos
Hidrocarboneto de Aril Hidroxilases/biossíntese , Benzopireno Hidroxilase/biossíntese , Citocromos/metabolismo , Metilcolantreno/farmacologia , Microssomos Hepáticos/enzimologia , Animais , Sítios de Ligação , Colestase/enzimologia , Sistema Enzimático do Citocromo P-450/metabolismo , Indução Enzimática/efeitos dos fármacos , Hepatectomia , Masculino , Fenobarbital/farmacologia , RatosAssuntos
Hidrocarboneto de Aril Hidroxilases/metabolismo , Benzopireno Hidroxilase/metabolismo , Microssomos Hepáticos/fisiologia , Animais , Sistema Enzimático do Citocromo P-450/metabolismo , Indução Enzimática/efeitos dos fármacos , Cinética , Masculino , Metilcolantreno/farmacologia , Camundongos , Camundongos Endogâmicos/genética , Microssomos Hepáticos/ultraestrutura , MorfogêneseRESUMO
Functions of the liver monooxygenase system, participating in metabolism of 3,4-benzpyrene, were shown to vary significantly at different steps of carcinogenesis induced by 3,4-benzpyrene. These variations appear to be due to changes in the effect of monooxygenase-epoxide hydrase complex in rat liver microsomes.
Assuntos
Microssomos Hepáticos/enzimologia , Neoplasias/induzido quimicamente , Oxigenases/metabolismo , Aminopirina N-Desmetilase/metabolismo , Animais , Benzopireno Hidroxilase/metabolismo , Benzopirenos , Sistema Enzimático do Citocromo P-450/metabolismo , Redutases do Citocromo/metabolismo , Masculino , Neoplasias/enzimologia , Neoplasias Experimentais/induzido quimicamente , Neoplasias Experimentais/enzimologia , Ratos , Fatores de TempoRESUMO
A possibility of step-wise induction of microsomal monooxygenases after injection of phenobarbital in the presence of 3-methylcholanthrene-caused induction was studied. It was found that the ratio of the high- and low-spin types of cytochrome, rather than the position of the CO-peak of its reduced form is a criterion for functional specificity of hemoprotein. Induction by phenobarbital appears possible under conditions when the inductor binding to microsomal hemoprotein is lacking, since cytochrome P-488 has no binding sites for phenobarbital. It is assumed that under microsomal monooxygenases induction by phenobarbital activation of genome and subsequent protein synthesis are operated by the substrate rather than by products of its primary metabolism in microsomes.