¿El licopeno puede eliminar los efectos perjudiciales de la hiperoxia en los cerebros inmaduros? / Can lycopene eliminate the harmful effects of hyperoxia in an immature brain?

Objetivos: Al ser un antioxidante, el licopeno protege a las células contra el daño causado por los radicales libres, fortalece los enlaces intercelulares y mejora el metabolismo celular. Este estudio analiza los efectos del licopeno sobre los trastornos neurodegenerativos por hiperoxia en ratas recién nacidas a término. Métodos: Estas ratas se dividieron en cuatro grupos: grupo 1 de referencia con normoxia, grupo 2 con normoxia + licopeno, grupo 3 de referencia con hiperoxia y grupo 4 con hiperoxia + licopeno. Los grupos 1 y 2 se supervisaron en condiciones de aire ambiental, y los grupos 3 y 4 se supervisaron con un nivel de oxígeno > 85 % O2. Los grupos 2 y 4 recibieron inyecciones intraperitoneales de licopeno de 50 mg/kg/día; los otros grupos recibieron inyecciones intraperitoneales de aceite de maíz con el mismo volumen. Las ratas se sacrificaron en el día 11, después de 10 días con hiperoxia. Se extrajeron los cerebros, y se evaluaron los parámetros del sistema oxidativo. Resultados: Se detectaron lesiones cerebrales por hiperoxia en sustancia blanca, regiones corticales y tálamo. Aumentó la cantidad de células apoptóticas y disminuyó la cantidad de células PCNA positivas en los grupos 3 y 4, comparados con el grupo 1. No se observó una mejora significativa en la cantidad de células apoptóticas y células PCNA positivas en los grupos 3 y 4; además, aumentó la apoptosis. Conclusión: Se halló que el licopeno no mostró efectos terapéuticos para el daño cerebral en ratas recién nacidas. Además, se demostró que el licopeno podría causar efectos tóxicos.

Objectives. In addition to protecting cells against free radical harm thanks to its anti-oxidant nature, lycopene strengthens the bonds among cells and improves cell metabolism. This study focuses on analyzing therapeutic effects of lycopene in hyperoxia-induced neurodegenerative disorders in newborn rats. Methods. Term newborn rats were divided into four groups as the normoxia control group (group-1), normoxia+lycopene group (group-2), hyperoxia control group (group-3) and hyperoxia+lycopene group (group-4). Group-1 and group-2 were monitored in room air while the group-3 and group-4 were monitored at > 85% O2. The group-2 and group-4 were injected with lycopene intrapertioneally (i.p. ) at 50mg/kg/day while the other groups were injected with corn oil i.p. at the same volume. The rats we sacrificed on the 11th day following the 10-day hyperoxia. The brains were removed and oxidant system parameters were assessed. Results. Injury resulting from hyperoxia was detected in the white matter, cortical regions, and thalamus of the brains. It was observed that the number of apoptotic cells increased and the number of proliferating cell nuclear antigen (PCNA) positive cells decreased in the groups-3 and 4 compared to the group-1. No significant improvement in the number of apoptotic cells and PCNA positive cells was observed in the groups-3 and 4, and apoptosis increased as well. Conclusion. This study found that lycopene, did not show any therapeutic effects for brain damage treatment in newborn rats. In addition, this study demonstrated that lycopene might lead to toxic effects.

Can lycopene eliminate the harmful effects of hyperoxia in an immature brain? / ¿El licopeno puede eliminar los efectos perjudiciales de la hiperoxia en los cerebros inmaduros?

OBJECTIVES: In addition to protecting cells against free radical harm thanks to its anti-oxidant nature, lycopene strengthens the bonds among cells and improves cell metabolism. This study focuses on analyzing therapeutic effects of lycopene in hyperoxia-induced neurodegenerative disorders in newborn rats. METHODS: Term newborn rats were divided into four groups as the normoxia control group (group-1), normoxia+lycopene group (group-2), hyperoxia control group (group-3) and hyperoxia+lycopene group (group-4). Group-1 and group-2 were monitored in room air while the group-3 and group-4 were monitored at > 85% O2. The group-2 and group-4 were injected with lycopene intrapertioneally (i.p. ) at 50mg/kg/day while the other groups were injected with corn oil i.p. at the same volume. The rats we sacrificed on the 11th day following the 10-day hyperoxia. The brains were removed and oxidant system parameters were assessed. RESULTS: Injury resulting from hyperoxia was detected in the white matter, cortical regions, and thalamus of the brains. It was observed that the number of apoptotic cells increased and the number of proliferating cell nuclear antigen (PCNA) positive cells decreased in the groups-3 and 4 compared to the group-1. No significant improvement in the number of apoptotic cells and PCNA positive cells was observed in the groups-3 and 4, and apoptosis increased as well. CONCLUSIONS: This study found that lycopene, did not show any therapeutic effects for brain damage treatment in newborn rats. In addition, this study demonstrated that lycopene might lead to toxic effects.

Objetivos: Al ser un antioxidante, el licopeno protege a las células contra el daño causado por los radicales libres, fortalece los enlaces intercelulares y mejora el metabolismo celular. Este estudio analiza los efectos del licopeno sobre los trastornos neurodegenerativos por hiperoxia en ratas recién nacidas a término. Métodos: Estas ratas se dividieron en cuatro grupos: grupo 1 de referencia con normoxia, grupo 2 con normoxia + licopeno, grupo 3 de referencia con hiperoxia y grupo 4 con hiperoxia + licopeno. Los grupos 1 y 2 se supervisaron en condiciones de aire ambiental, y los grupos 3 y 4 se supervisaron con un nivel de oxígeno > 85 % O2. Los grupos 2 y 4 recibieron inyecciones intraperitoneales de licopeno de 50 mg/kg/día; los otros grupos recibieron inyecciones intraperitoneales de aceite de maíz con el mismo volumen. Las ratas se sacrificaron en el día 11, después de 10 días con hiperoxia. Se extrajeron los cerebros, y se evaluaron los parámetros del sistema oxidativo. Resultados: Se detectaron lesiones cerebrales por hiperoxia en sustancia blanca, regiones corticales y tálamo. Aumentó la cantidad de células apoptóticas y disminuyó la cantidad de células PCNA positivas en los grupos 3 y 4, comparados con el grupo 1. No se observó una mejora significativa en la cantidad de células apoptóticas y células PCNA positivas en los grupos 3 y 4; además, aumentó la apoptosis. Conclusión: Se halló que el licopeno no mostró efectos terapéuticos para el daño cerebral en ratas recién nacidas. Además, se demostró que el licopeno podría causar efectos tóxicos.

The Effects of Long-Term Diabetes on Ghrelin Expression in Rat Stomachs.

BACKGROUND: Ghrelin is a hormone which has effects on the secretion of growth hormone, the gastrointestinal system, the cardiovascular system, cell proliferation and the reproductive system. OBJECTIVES: This study focused on relative ghrelin and GHS-R1a gene expression in the stomach of long-term diabetic rats. MATERIAL AND METHODS: A total of 36 male Wistar albino rats were divided into four groups: a control group, one-month diabetic rats, two-month diabetic rats and three-month diabetic rats. Diabetes was induced by streptozotocin STZ (40 mg/kg i.p). The rats were decapitated under ketamine anesthesia and their stomach tissues were removed. Tissue ghrelin expression, ghrelin and GHS-R mRNA levels were then compared using immunohistochemistry and qRT-PCR. RESULTS: After one month of diabetes, the number of ghrelin-immunopositive cells decreased significantly compared to those of the control rats. However, the ghrelin-immunopositive cells increased numerically in the two- and three-month diabetic rats compared to those of the control rats. It was also observed that there were high levels of ghrelin mRNA in the one- and two-month diabetic rats, and a subsequent decrease of ghrelin mRNA levels in the three-month diabetic rats compared to the control rats. However, ghrelin receptor mRNA expression levels decreased in the one-month diabetic rats, and ghrelin levels subsequently increased in the two- and three-month diabetic rats compared to the control rats. CONCLUSIONS: The two- and three-month diabetic rats became cachectic due to the large amount of weight lost. The authors therefore concluded that ghrelin-immunopositive cells increased in these rats due to their cachectic state.

The effects of streptozotocin-induced diabetes on ghrelin expression in rat testis: biochemical and immunohistochemical study.

INTRODUCTION: Ghrelin is a hormone which has effects on the secretion of growth hormone, gastrointestinal system, cardiovascular system, cell proliferation and reproductive system. The present study we focused on the relation between ghrelin and GHS-R1a gene expression and the regulation of their expression in the testes of diabetic rats. MATERIAL AND METHODS: 40 male Wistar albino rats were divided into four groups: control, and sampled 4, 8 and 12 weeks after induction of diabetes by streptozotocin (STZ) intraperitoneal injection (40 mg/kg). The rats were decapitated under ketamine anesthesia and their testes were removed. Blood was obtained from heart and serum follicle stimulating hormone (FSH), luteinizing hormone (LH), and testosterone levels were measured by ELISA. Tissue ghrelin and GHS-R mRNA levels were determined by qRT-PCR, while ghrelin protein expression was studied by immunohistochemistry. Histopathological damage scores were also assessed. RESULTS: Eight weeks after diabetes induction serum FSH level was increased, whereas LH and testosterone concentrations decreased. The ghrelin and GHS-R1a gene expression and ghrelin immunohistochemistry score first tended to increase after first four weeks of diabetes, and then tended to decrease. Ghrelin-immunopositive cells were detected in Leydig cells in all groups of rats, however, not in the germinal epithelium. Congestion of vessels and hemorrhage, formation of the vacuoles in spermatogonia and spermatocytes, desquamation of spermatids in the lumen and disorganization of seminiferous tubule germinal epithelium were observed in testis of all the diabetic rats. In addition, mean testicular biopsy score and mean seminiferous tubule diameter were getting lower in diabetic animals. CONCLUSION: Our results suggest that diabetes affects ghrelin expression in rat testis.