RESUMEN
Subtle neurological disturbances have been described in organophosphorus intoxication. Experimental studies have reported neuronal necrosis, particularly in animals experiencing seizures. The objective of the present work was to investigate if in rats (without seizures) exposed to an organophosphate agent, morphological changes occur in specific regions of the brain. The animals received 2.5 or 5.0 mg/kg methamidophos once a week for 2 months and were decapitated after 2 months 7 days of drug administration. We observed atrophy of the molecular layer of the parietal cortex without neuronal loss in specific cerebral regions. This would be due to atrophy or loss of neuronal ramifications but without neuronal loss.
Asunto(s)
Encéfalo/efectos de los fármacos , Encéfalo/patología , Inhibidores de la Colinesterasa/toxicidad , Compuestos Organotiofosforados/toxicidad , Animales , Atrofia , Corteza Cerebral/efectos de los fármacos , Corteza Cerebral/patología , Inhibidores de la Colinesterasa/administración & dosificación , Masculino , Microscopía/métodos , Neuronas/efectos de los fármacos , Neuronas/patología , Compuestos Organotiofosforados/administración & dosificación , Lóbulo Parietal/efectos de los fármacos , Lóbulo Parietal/patología , Ratas , Ratas WistarRESUMEN
The authors studied the effects of nicotine in developing skeletal muscles of rats. Pregnant Wistar rats received an enteral dose of nicotine (2.5, 5.0 or 10mg/kg, respectively, in groups G2, G5, and G10) from the 10th to the 18th or 20th days of pregnancy. Myotube atrophy was observed mainly in 20-day-old fetuses of G10. Twenty-day-old control fetus and of G2 and G5 had a high sarcoplasmic expression of desmin (weaker in G10). Vimentin expression was similar in 18-day-old fetuses of the control, G2, and G5 groups, but it was weaker in 20-day-old fetuses of the G2 and G5 groups. This would indicate an acceleration of the maturation pattern of vimentin expression in these intoxicated fetus. In conclusion, high doses of nicotine induce myotube atrophy and decrease of the expression of intermediate filaments, whereas relatively low doses of nicotine (G2 and G5) induce an early decrease of vimentin expression with no myofiber atrophy.
Asunto(s)
Fibras Musculares Esqueléticas/efectos de los fármacos , Músculo Esquelético/citología , Músculo Esquelético/crecimiento & desarrollo , Nicotina/farmacología , Agonistas Nicotínicos/farmacología , Animales , Desmina/metabolismo , Femenino , Inmunohistoquímica , Fibras Musculares Esqueléticas/metabolismo , Músculo Esquelético/efectos de los fármacos , Embarazo , Ratas , Ratas Wistar , Receptores Nicotínicos/efectos de los fármacos , Receptores Nicotínicos/metabolismo , Vimentina/metabolismoRESUMEN
We have described that administration of seeds or parts of the seed of Senna occidentalis (coffee senna) for long periods, induces histochemical changes in the skeletal muscles of hens and rats that are characteristic of a mitochondrial myopathy--as decrease of SDH and COX activity, with some COX negative fibers. In this experimental model of mitochondrial myopathy, as in many human mitochondrial diseases, there is a random distribution of COX negative fibers. Some fibers are completely COX negative while others are partially negative and others are completely positive. In the present work we have studied the distribution of COX negative mitochondria at transmission electron microscopy in skeletal muscle of rats in this experimental myopathy. In myofibers of intoxicated animals the expression of COX was heterogeneous. The histochemical reaction was observed in the internal membrane (more evident in mitochondrial cristae) of all mitochondria of some myofibers, while it was almost absent in other myofibers. In these myofibers the great part of the mitochondria were negative for COX reaction while other ones had a weak expression of this enzyme (dot or focal expression of COX). Our results indicated that the COX mitochondrial activity is heterogeneously impaired in myofibers of rats intoxicated with S. occidentalis. These abnormalities remember those observed in some types of human mitochondrial myopathies.
Asunto(s)
Deficiencia de Citocromo-c Oxidasa , Mitocondrias/efectos de los fármacos , Fibras Musculares Esqueléticas/efectos de los fármacos , Músculo Esquelético/efectos de los fármacos , Semillas/toxicidad , Senna , Dieta , Modelos Animales de Enfermedad , Mitocondrias/enzimología , Mitocondrias/ultraestructura , Miopatías Mitocondriales/enzimología , Miopatías Mitocondriales/etiología , Miopatías Mitocondriales/patología , Fibras Musculares Esqueléticas/enzimología , Fibras Musculares Esqueléticas/ultraestructura , Músculo Esquelético/enzimología , Músculo Esquelético/ultraestructura , Plantas Medicinales , Extracto de Senna/toxicidad , Senna/químicaRESUMEN
The objective of the present investigation was to study the expression of the proliferation marker Ki-67 in cervical intraepithelial lesions in women with AIDS. We studied 18 low-grade cervical intraepithelial lesions (Lo-CIN) and 8 high-grade cervical intraepithelial lesions (Hi-CIN ) in AIDS patients and 18 Lo-CIN and 14 Hi-CIN in patients from the general population. Positive Ki-67 nuclei were counted. A significantly higher number of Ki-67-positive cells (p < 0.001) was found in Lo-CIN of AIDS patients (mean 29.18 +/- 10.44) as compared with Lo-CIN of general-population women (mean 17.08 +/- 7.40), whereas no significant difference in positive Ki-67 nuclei was observed in the Hi-CIN of AIDS patients and of patients from the general population (p > 0.05). We conclude that the proliferative potential of cervical cells in Lo-CIN - as studied by the expression of the proliferation marker Ki-67 - is higher in AIDS patients than in the general population.