ABSTRACT
La encefalopatía por hipoxia es causa de discapacidad y requiere de nuevas estrategias terapéuticas. El pirofosfato de tiamina (PPT) es un cofactor esencial de enzimas fundamentales en el metabolismo de la glucosa, cuya disminución puede conducir a la falla en la síntesis de ATP y a la muerte celular. El objetivo de este estudio fue determinar si la administración de PPT, puede reducir el daño celular en un modelo de hipoxia neonatal en ratas. Animales de 11 días de edad fueron tratados con PPT (130 mg/kg) en dosis única o solución salina, una hora antes del protocolo de hipoxia o al término de ésta. Los cerebros fueron colectados para la evaluación del daño celular. Además, se tomaron muestras sanguíneas para evaluar los indicadores gasométricos de presión de dióxido de carbono (PaCO2) y de oxígeno (PaO2) en sangre arterial y pH. Los resultados muestran que la administración de PPT previa a la inducción de hipoxia, reduce el daño celular y restablece los indicadores gasométricos. Estos datos indican que el uso de PPT reduce el daño inducido por la hipoxia en animales neonatos.
Hypoxic encephalopathy is a leading cause of disability and requires new therapeutic strategies. Thiamine pyrophosphate (TPP) is an essential cofactor of fundamental enzymes involved in glucose metabolism. TPP reduction may lead to ATP synthesis failure and cell death. The objective of this study was to determine if TPP administration can reduce cellular damage in a model of neonatal hypoxia in rats. Eleven day old animals were treated with TPP (130 mg/kg) as a single dose or with saline solution one hour before the hypoxia protocol or after ending the protocol. The brains were collected to evaluate cellular damage. Blood samples were also collected to evaluate arterial oxygen tension (PaO2), carbon dioxide tension (PaCO2) and acidity (pH). The results showed that TPP administration previous to hypoxia induction reduces cellular damage and reestablishes arterial blood gases. These data indicate that TPP use reduces the damage induced by hypoxia in neonatal animals.
Subject(s)
Animals , Male , Rats , Thiamine Pyrophosphate/administration & dosage , Apoptosis/drug effects , Protective Agents/administration & dosage , Hypoxia/drug therapy , Oxygen/blood , Thiamine Pyrophosphate/pharmacology , Blood Gas Analysis , Brain Diseases/prevention & control , Rats, Wistar , Protective Agents/pharmacology , Disease Models, Animal , Hydrogen-Ion Concentration , Animals, NewbornABSTRACT
BACKGROUND: Ozone is an environmental pollutant that has widely documented deleterious effects on exposed organisms. In Mexico City, this pollutant frequently reaches concentrations that surpass safe health limits. In addition, it has been reported that the prevalence of malnutrition remains high in our childhood population. This experiment was carried out to determine whether malnutrition is a factor contributing to an increase in the risk of damage associated with ozone exposure. METHODS: Using an experimental animal model, 21-day-old rats fed normally or with induced malnutrition were subchronically exposed to 0.5 ppm of ozone or fresh air, respectively, for 30 days. At the end of this period and using HPLC, serotonin concentrations were measured in four areas of the brain: cortex, hemispheres, cerebellum, and medulla oblongata. RESULTS: Malnourished animals had a significant weight deficit beginning at 28 days with respect to well-fed animals. Among the well-fed animals, this phenomenon is seen at 35 days in exposed and non-exposed animals. In the four regions of the brain, malnourished animals show low serotonin concentrations with respect to well-nourished animals. In the cerebellum, there was an interaction between the nutritional factor and ozone exposure, while in the medulla oblongata both factors acted independently. CONCLUSIONS: Our results suggest a multiplicative effect from the nutritional factor and ozone exposure in the changes observed concerning serotonergic metabolism.
