The influence of microscopic disorder on electron paramagnetic resonance spectra of Eu(2+) ions in Pb(1-x)Ge(x)Te.

In mixed crystals, because of the different ionic radii of cations or anions and the randomness in the placement of ions of different kinds, the crystal lattice is locally deformed. Such local deformations have significant influence on the ground state splitting of magnetic ions. Because this ground state splitting is responsible for the position of the electron paramagnetic resonance (EPR) lines, microscopic disorder is one of the factors which lead to the broadening of the lines, and eventually to their disappearance. This paper is devoted to semi-quantitative analysis of the influence of microscopic disorder on EPR spectra. The theory is compared against measurements performed on mono-crystalline Pb(1-x)Ge(x)Te epitaxial layers containing Eu(2+) ions for different germanium and europium contents. With increasing germanium content we observe gradual disappearance of the EPR lines, although macroscopically, on the basis of x-ray diffraction analysis, each layer might have been considered as a perfect crystal.

Hexose diphosphates and phosphofructokinase in rat brain during development.

Fructose 2,6-diphosphate and glucose 1,6-diphosphate concentrations were determined during late gestation and over the course of suckling in rat brain cortex and cerebellum. Cortex fructose 2,6-diphosphate concentration was greatest in neonatal animals and gradually declined thereafter by 25% to reach the adult level at 15 days of age. In contrast, the glucose 1,6-diphosphate concentration increased 4-fold over the same period to reach its highest level by postnatal day 15. Neither cerebellar fructose 2,6-diphosphate nor glucose 1,6-diphosphate concentrations varied significantly. Six day cortex 6-phosphofructo-1-kinase was less sensitive to inhibition by citrate than the enzyme obtained from 15 day pups, and fructose 2,6-diphosphate was better than glucose 1,6-diphosphate at relieving the inhibition imposed by citrate at either age. It is suggested that the rise in cerebral glucose use which occurs during suckling cannot be attributed to either changes in the concentrations of fructose 2,6-diphosphate or glucose 1,6-diphosphate, or the age-related differential sensitivity of 6-phosphofructo-1-kinase toward these effectors.

Lactate genesis by rat liver and muscle during development.

Lactate has been shown to be an important fuel for brain metabolism during early postnatal development (1). In an attempt to identify the source(s) of lactate in the postnatal rat, we have studied the in vitro catabolism of glucose, galactose, fructose, alanine, glycerol, and octanoate in liver and muscle minces prepared from suckling rat pups. Whereas galactose, fructose, and octanoate were found to be lactagenic (lactate generating) in liver, glucose was the sole lactate precursor in muscle. Galactose was most effective as a hepatic lactate source at 3 d of age. Thereafter, the production of lactate from galactose decreased to reach control levels by 15 d of age. In contrast, fructose or octanoate were lactagenic throughout development. Lactate formation from galactose was completely halted by iodoacetate, inhibited by high galactose concentrations, and suppressed by fasting. The absence of oxygen increased lactate production from either fructose or octanoate, but it did not affect lactagenesis from galactose. Muscle minces produced lactate from glucose in an age-dependent manner similar to the development pattern of lactate formation from galactose by liver. Because lactose-derived galactose is readily available during suckling, it is suggested that galactose-based hepatic lactagenesis serves a unique role in maintaining the supply of lactate during early postnatal development. This hepatic capability may augment glucose-based muscle lactate synthesis at a time when lactate is a major brain fuel.

Lactate, 3-hydroxybutyrate, and glucose as substrates for the early postnatal rat brain.

The dependence of cerebral energy metabolism upon glucose, 3-hydroxybutyrate, and lactate as fuel sources during the postnatal period was investigated. The brain of 6 day old suckling pups used very little glucose, but by the 15th postnatal day glucose was the major catabolite. Hydroxybutyrate was not a major brain fuel at either 6 or 15 days of age. Its utilization accounted for only 19% of the brain's total energy needs at 15 days of age, even through blood ketone concentrations are near maximal at this time. Seventy percent of the cerebral metabolic requirements were met by lactate in animals aged 6 days. The major role played by lactate as a substrate for brain metabolism in young pups was not a result of abnormally elevated blood lactate concentrations. The slow catabolism of glucose in young brain can not be explained by low rates of influx or inadequate enzymatic capacity.

The inefficient transfer of maternally fed alcohol to nursing rats.

The growth of rat pups nursed by ethanol-drinking mothers or pups exposed daily to ethanol/vapor was monitored for the first three weeks of life. Pups nursed by mothers fed either a 6% ethanol containing liquid diet or a 10% ethanol/water mixture had significantly lower body weights after the 2nd postnatal week than controls. This decrease in pup growth occurred despite pup blood alcohol levels that did not exceed 20 mg%. Only a small fraction of the alcohol fed to mothers ever reached suckling animals. In contrast, pups exposed daily to ethanol vapor regularly achieved blood alcohol concentrations in excess of 250 mg%, but experienced only minimal growth retardation. These results suggest that maternal alcohol feeding cannot be used to study the effects of ethanol upon postnatal development.

Alkaline phosphatase activity can interfere with the enzymatic determination of triglycerides.

Unlike human plasma, rat plasma was found to contain substantial quantities of alkaline phosphatase. The large amount of phosphatase activity in rat plasma interferes with assay methods that employ orthophosphoric acid esters as substrates or reaction intermediates. Although these methods are effective when applied to human plasma samples, they cannot be used with rodent plasma.

The metabolism of D- and L-3-hydroxybutyrate in developing rat brain.

The incorporation of L- and D-3-hydroxybutyrate into rat brain protein, lipid, and amino acids during development was studied. L-3-Hydroxybutyrate was found to label brain protein and amino acids in addition to sterols and fatty acids throughout the first 32 postnatal days. Age related changes in L- and D-3-hydroxybutyrate labeling of protein and amino acids were similar. Whereas L-3-hydroxybutyrate incorporation into brain lipids rose sharply between 6-15 days of age, D-3-HOB incorporation into the lipid fraction gradually increased from birth through the age of 15 days. Incorporation by both isomers into lipid was greatest during the third week of suckling and then declined when the animals were weaned. At 15 days of age, the distribution of L-3-hydroxybutyrate into glutamate, glutamine + aspartate, and gamma-aminobutyrate was similar to that obtained with D-3-hydroxybutyrate. L-3-Hydroxybutyrate was poorly oxidized to CO2 by brain slices and mitochondria. Oxidation capacity was maximal from 15-21 days of age for both isomers. The activity of L-3-hydroxybutyrl-CoA ligase increased between 6-28 days of age, and its increase is well correlated with the developmental pattern of L-3-hydroxybutyrate incorporation and mitochondrial oxidation. L-3-Hydroxybutyrate was not detected in the blood of palmitate-injected pups or fasted adult animals. These results suggest that although L-3-hydroxybutyrate can be utilized for the synthesis of brain components during development, its negligible blood concentration precludes a significant contribution to either tissue synthesis or energy balance during the suckling period.