RESUMO
Resumen El lactato se considera un metabolito de desecho que se produce durante la fatiga muscular. En contraste con esta visión simplista, en este trabajo se proporcionan evidencias de las múltiples y complejas funciones de este metabolito. Se muestra que: 1) el lactato es el producto final de la glucólisis, independientemente de la concentración de oxígeno en el medio en el que se encuentren las células; 2) el lactato forma parte de 2 tipos de lanzadera, una que funciona en el espacio intermembranal de la mitocondria, y otra intercelular, que se encarga de alimentar con lactato a ciertos tipos celulares, como las neuronas o el músculo cardiaco; 3) en los espermatozoides, el lactato se transporta directamente a la matriz mitocondrial y allí se oxida para producir piruvato y NADH; 4) en el hígado, el lactato participa en la oxidación del etanol a través de la generación de peróxido de hidrógeno; 5) que dependiendo de la estirpe celular, el lactato puede funcionar como agente antiinflamatorio (endocrino) o regulador de la expresión génica.
Abstract Lactate is considered to be a waste metabolite produced during muscle fatigue. In contrast with this simplistic point of view, in this review we provide evidence of the multiple and complex functions of this metabolite. We show that: 1) lactate is the final product of the glycolysis regardless the oxygen concentration in the cell 2) lactate is part of two types of shuttle, one that functions in the intermembrane space of the mitochondrion, and another intercellular, which is responsible for feeding lactate to certain cell types, such as neurons or heart muscle, 3) in sperm, lactate is transported directly to the mitochondrial matrix and there it is oxidized to produce pyruvate and NADH, 4) in the liver, lactate participates in the oxidation of ethanol through the generation of hydrogen peroxide, 5) Depending on the cell line, lactate can function as anti-inflammatory agent (endocrine) and/or a regulator of gene expression.
RESUMO
It is known the deleterious effects of diabetes on embryos, but the effects of diabetes on placenta and its mitochondria are still not well known. In this work we generated a mild hyperglycemia model in female wistar rats by intraperitoneal injection of streptozotocin in 48 hours-old rats. The sexual maturity onset of the female rats was delayed around 6-7 weeks and at 16 weeks-old they were mated, and sacrificed at day 19th of pregnancy. In placental total tissue and isolated mitochondria, the fatty acids composition was analyzed by gas chromatography, and lipoperoxidation was measured by thiobarbituric acid reactive substances. Membrane fluidity in mitochondria was measured with the excimer forming probe dipyrenylpropane and mitochondrial function was measured with a Clark-type electrode. The results show that even a chronic mild hyperglycemia increases lipoperoxidation and decreases mitochondrial function in placenta. Simultaneously, placental fatty acids metabolism in total tissue is modified but in a different way than in placental mitochondria. Whereas the chronic mild hyperglycemia induced a decrease in unsaturated to saturated fatty acids ratio (U/S) in placental total tissue, the ratio increased in placental mitochondria. The measurements of membrane fluidity showed that fluidity of placenta mitochondrial membranes increased with hyperglycemia, showing consistency with the fatty acids composition through the U/S index. The thermotropic characteristics of mitochondrial membranes were changed, showing lower transition temperature and activation energies. All of these data together demonstrate that even a chronic mild hyperglycemia during pregnancy of early reproductive Wistar rats, generates an increment of lipoperoxidation, an increase of placental mitochondrial membrane fluidity apparently derived from changes in fatty acids composition and consequently, mitochondrial malfunction.