RESUMEN
Recent intervention studies revealed that supplementation with retinoids resulted in a higher incidence of lung cancer. Recently the causal mechanism has begun to be clarified. We report here that retinol caused cellular DNA damage probably involving cellular iron accumulation. Retinol (7 microM) significantly induced DNA single strands breaks, DNA fragmentation and production of 8-oxo-7, 8-dihydro-2'-deoxyguanosine in cultured Sertoli cells. In contrast, lower doses seemed not to induce single-strands break in this experimental model. The breaks in DNA were inhibited by an iron scavenger; and 7 microM retinol treatment modulated iron turnover leading to iron accumulation, suggesting that iron ions were required for the retinol cellular effects. These findings suggest that retinol-induced DNA damage was associated with the modulation of iron turnover, and these characteristics could be responsible for the increased incidence of lung cancer associated with retinoids supplementation.
Asunto(s)
Daño del ADN , Desoxiguanosina/análogos & derivados , Hierro/metabolismo , Células de Sertoli/metabolismo , Vitamina A/toxicidad , 8-Hidroxi-2'-Desoxicoguanosina , Animales , Línea Celular , Fragmentación del ADN , Desoxiguanosina/metabolismo , Quelantes del Hierro/farmacología , Masculino , Ratas , Ratas WistarRESUMEN
Relata-se o diagnóstico de linfoma primário no sistema nervoso central em um cão Labrador Retrievier, de 10 anos de idade, que apresentava episódios convulsivos, incoordenação nos membros posteriores, head tilt, ataxia e sensibilidade diminuída no lado esquerdo. Constataram-se alterações laterais esquerdas, como ausências de propriocepção e de posicionamento tátil, alterações posteriores nas provas de carrinho de mão e de reação ao pulo e diminuição da extensão da postura e hemilocomoção. No líquido cefalorraquidiano (LCR), houve predomínio de linfócitos atípicos, caracterizados pela presença de anisocitose e anisocariose, nucléolos evidentes e anisonucleose, basofilia e microvacuolização citoplasmáticas, mitoses atípicas e corpúsculos linfoglandulares, compatíveis com linfoma, confirmado pelo exame histológico e imunocitoquímico, o qual revelou origem T, com expressão CD3+ e CD79-. A tomografia computadorizada não foi conclusiva e evidenciou diversas áreas hipodensas e intensificação de contraste na região de sulcos e giros do parênquima encefálico. A coleta do LCR foi essencial na rapidez do diagnóstico definitivo, indicando a natureza rara desta lesão primária.
A primary lymphoma in the central nervous system in a 10 year-old Labrador Retriever presenting seizures, hind limb incoordination, head tilt, ataxia and decreased sensitivity on the left side was reported. Regarding postural reactions, there were changes in the left side such as proprioceptive and tactile positioning defects, and in the posterior reaction tests such as wheelbarrowing and limb hopping, along with a reduction in the extensor postural thrust reaction and hemi-walking response. A cerebrospinal fluid (CSF) analysis showed a predominance of atypical lymphocytes characterized by pleocytosis, marked anisocytosis and anisokaryosis, evident nucleoli and anisonucleosis, cytoplasmic basophilia and microvacuolation, atypical mitotic figures and lymphoglandular bodies. These findings were compatible with lymphoma, which was confirmed by histopathology and immunocytochemistry that showed a T-cell origin, with CD3 + and CD79- expression. A computed tomography scan was inconclusive and showed several hypodense areas and a contrast enhancement in the sulci and gyri region of the brain parenchyma. The CSF analysis was essential for a quicker definitive diagnosis, indicating the nature of this rare primary injury.
Asunto(s)
Animales , Perros , Leucemia-Linfoma Linfoblástico de Células Precursoras/diagnóstico , Leucemia-Linfoma Linfoblástico de Células Precursoras/veterinaria , Linfoma de Células T/veterinaria , Líquido Cefalorraquídeo , Neoplasias Encefálicas/veterinaria , Sistema Nervioso Central/anomalías , Sistema Nervioso Central/lesiones , Técnicas de Diagnóstico Neurológico/veterinariaRESUMEN
A case of extrahepatic portal hypertension and gastric variceal bleeding due to portal vein occlusion, most probably secondary to chronic pancreatitis, was treated by percutaneous transhepatic angioplasty. After the portal angioplasty there was marked clinical improvement, with control of the variceal bleeding and significant reduction of the pressure gradient within the portal system.