RESUMO
Synthetic alpha-melanocyte-stimulating hormone (alpha-MSH) was found to bind to the plasma membrane of the HM6A human melanoma cell line, using an immunocytochemical method. When treated with 10(-7) to 10(-9) M alpha-MSH, melanoma cells exhibited an increase of intracellular cyclic adenosine 3':5'-monophosphate, followed by stimulation of tyrosinase activity. Significant inhibition of DNA synthesis measured by [3H]thymidine uptake and inhibition of cell growth was found. A retrovirus expression was detected in the supernatant of HM6A cells as assayed by the KC cell syncytium-forming test. In he presence of 10(-7) M alpha-MSH, the number of syncytium-forming units was increased 15-fold. These results demonstrate that alpha-MSH modulates human melanoma differentiation and virus expression in vitro.
Assuntos
Hormônios Estimuladores de Melanócitos/farmacologia , Melanoma/metabolismo , Diferenciação Celular , Linhagem Celular , Membrana Celular/metabolismo , AMP Cíclico/análise , AMP Cíclico/metabolismo , DNA/biossíntese , Humanos , Hormônios Estimuladores de Melanócitos/metabolismo , Monofenol Mono-Oxigenase/metabolismo , Ligação Proteica , Retroviridae/efeitos dos fármacosRESUMO
The kinetics of 131I-labelled insulin distribution in heart, liver, kidneys and urinary bladder of rabbits were studied in vivo by gamma-camera techniques combined with plasma measurements (glucose concentrations and chromatographic separation of insulin and its degradation products). The distribution space of radioiodinated insulin differed from the vascular bed delineated by radioiodinated serum albumin. During a 20-min gamma-camera recording, radioactive degradation products only appeared in the plasma after 10-12 min. Previous administration of a 10 000-fold excess of unlabelled insulin and 5 ml glucose (20%) did not modify the evolution of 131I-labelled insulin cardiac invasion and the subsequent linear decrease of radioactivity. Conversely, wash-out of radioactivity from the liver and kidney was accelerated after preadministration of this excess of unlabelled hormone, binding in these organs accounting for this acceleration. Urinary bladder filling was imaged later than cardiac, hepatic or renal labelling and was only accelerated by polyuria induced by glucose injection, independent of preadministration of unlabelled hormone.