Indices of RNA metabolism in the brain stem of rats under superlethal exposure to ionizing radiation

A study was made of the content of hnRNA, nuclear poly(A) RNA and biosynthesis of rlnRNA in truncus cerebri of rats divided into 3 groups by the forced swimming test 6-8 min and 60 min after a short-term exposure to sparsely ionizing radiation of 100 Gy. The observed changes in the nuclear RNA metabolism can subsequently lead to the impairment of the synthesis of proteins required for normal functioning of CNS, and to the development of CNS syndrome.     

Changes in phosphoinositide metabolism in the brain of rats with different neuromuscular excitation threshold subjected to neurotic exposure and antioxidant administration

No difference was found in metabolism of phosphoinositides in rats with high (H) and low (L) levels of excitability under normal conditions. Neurotisation decreased the content of phosphotidilinositol-4,5-diphosphate and increased the phosphorus turnover rate in the brain cortex of the L rats. Oxymetacyl reduced the effect of neurotisation. This antioxidants seems to exert an effect on the brain cells functional condition in the L rats.     

Variations of brain histamine levels in germ-free and nephrectomized rats

The influence of nephrectomy on brain and peripheral tissue histamine and on brain norepinephrine, dopamine, serotonin, and 5-hydroxyindoleacetic acid was studied in germ-free and conventionally housed rats. The conventional controls had higher levels of histamine in the hypothalamus than the germ-free control animals, but no differences existed for histamine in whole brain minus the hypothalamus or in peripheral tissues. Nephrectomy increased brain histamine and 5-hydroxyindoleacetic acid levels in both germ-free and conventional rats, but had no effect on norepinephrine, dopamine or serotonin. In contrast, the histamine level in the heart of the nephrectomized germ-free animals was lower than that for germ-free controls. There were no changes in the heart or liver histamine levels of the conventional nephrectomized rats.     

Elevation of brain histamine content in protein-deficient rats.

—Male rats of the Sprague-Dawley strain (80–250 g body wt) were fed either an adequate protein diet (18% lactalbumin) or a protein-deficient diet (0.5% lactalbumin). After 5–8 weeks of receiving the low protein diet, some of the malnourished rats were rehabilitated with an adequate protein diet. The malnourished rats exhibited significant elevations in brain levels of histidine (+415%) and homocarnosine (+100%) in comparison to findings in the control animals of similar age. Associated with the elevated brain levels of histidine in malnutrition was a prominent increase in brain content of histamine (+ 150-+ 238%). The mean brain histamine levels (ng/g) in the control rats varied from 45.96 to 56.15 in several experiments. In the protein-deficient rats, values ranged from 115 to 190. Refeeding the malnourished rats with adequate protein diet elicited reversal of histidine and histamine levels to near normal values within 1 week. The increased brain content of histamine in malnutrition was attributed to enhanced rate of production resulting from increased availability of the precursor amino acid, a conclusion consistent with elevation also of the brain content of homocarnosine (γ-aminobutyryl-l -histidine) which is another major route of disposal of histidine in the brain. The relevance of these neurochemical alterations to the behavioural changes often associated with protein malnutrition, deserves some intensive examination.     

Effect of exposure to oxygen at 101 and 150 kPa on the cerebral circulation and oxygen supply in conscious rats

Hyperbaric oxygen at pressures of 300 to 500 kPa has been shown to induce changed distribution of cerebral blood flow ( _CBF) in rats, in places reducing the supply of the supplementary O₂. Thus, in the present study, the effect of hyperoxia at 101 (group 1, n = 9) and 150 (group 2, n = 9) kPa OZ on cerebral blood flow distribution and central haemodynamics was tested in conscious, habituated rats. During the control period the systolic arterial pressure (BP_s), heart rate (f _c), breathing frequency (f _b), cardiac output ( _c), arterial acid-base chemistry and glucose, as well as _CBF distribution (r _CBF) were similar in the two groups of animals. During O₂ exposure, the acid-base chemistry remained unchanged. The haemoglobin decreased in group 2, but remained unchanged in group 1. The f _c decreased rapidly in both groups during the change in gas composition, after which f _c remained constant both in group 1 and in group 2, for whom pressure was increased. The _c and f _b decreased and BP_s increased similarly in the two groups. Total _CBF and r _CBF decreased to the same extent in both groups, and the r _CBF changes were equally scattered. In group 1, breathing of pure O₂ did not increase the O₂ supply to any cerebral region except to the thalamus and colliculi after 60 min, whereas the O₂ supply to the hypothalamus decreased and remained low. In group 2, the O₂ supply was unchanged compared to the control period in all regions. These findings agree with previous observations during exposures to higher O₂ pressures. In air after O₂ exposure the acid-base chemistry remained normal. The f _c and f _b increased to higher levels than during the control period. The BP_s remained high. The brain blood flows were increased, inducing elevated O₂ supply to several brain regions compared to the control period. In conclusion, O₂ supply to the central nervous system was found to be in the main unchanged during breathing of O₂ at 101 kPa and 150 kPa.     

Glutamate metabolism in the brain of young rats exposed to organic and inorganic lead

The synthesis of glutamate and its conversion to glutamine and GABA were studied using labelled glucose in cerebral cortex, cerebellum and brainstem of rats intoxicated acutely with tetraethyl lead and chronically with lead acetate. To assess the interconversion and the synaptosomal accumulation of these amino acids, the labelling of glutamate, glutamine and GABA were measured in whole tissue and synaptosomes after giving labelled glutamate. The radioactive carbon dioxide production from labelled glutamate by brain slices was measured to evaluate the oxidation of glutamate. The tissue levels of glutamate, glutamine and GABA and the activity of glutamate decarboxylase were also measured in both conditions.In inorganic lead toxicity, even though the glutamate pool size was reduced, the glutamate-glutamine cycling between synaptosomes and astrocytes was increased. The oxidation of glutamate and the glutamate-GABA cycling were reduced. These findings suggest that brain tries to maintain the endogenous glutamate levels by decreasing the oxidation of glutamate and increasing the uptake systems and the cycling through glutamine in inorganic lead toxicity. In organic lead toxicity, the glutamate pool as well as glutamate turnover was reduced markedly resulting in complete distortion of glutamate metabolism.     

RNA metabolism in the cortex of newly weaned rats following first exposure to light

Newly weaned rats which had been kept in the darl from birth were injected intraventricularly with (6-¹⁴C) orotic acid. Experimental rats were exposed to light for 2 h and dark controls were returned to the dark environment for 2 h. It was found that after this period the relative specific activity of the RNA in the visual cortex of the former was significantly (p<0.001) higher than that of the RNA in the visual cortex of the latter. There was no significant difference in the labelling of the frontal cortex.In a second group of experiments light deprived newly weaned rats were exposed to light for periods ranging from 0–15 h prior to being given a 1 h pulse of (6-¹⁴C) orotic acid. After 1–2 h after first exposure to light the labelling of the RNA in the visual cortex was significantly increased (p<0.001) but after 3 h the labelling was not significantly different from the dark control value. This transient increase in RNA labelling after first exposure to light was not found in the frontal cortex.     

Early exposure to a high-fat diet has more drastic consequences on metabolism compared with exposure during adulthood in rats

The aim of this study was determine whether the introduction of a high-fat diet during the peripubertal phase induces significant changes in body weight control, glucose homeostasis and the parasympathetic tonus compared with the administration of this diet to adult rats. High-fat diet was offered to male Wistar rats at weaning or during adulthood. A group of rats received high-fat diet for 60 days, from weaning to 81-day-old (HF81) or from 60 to 120-day-old (HF120), whereas 2 other groups received a normal-fat diet (i. e., NF81 and NF120). We analyzed adiposity, glucose homeostasis, insulin sensitivity, and vagal nerve activity. High-fat diet increased the accumulation of adipose tissue in all of the rats, but the difference was greater in the rats that were fed the high-fat diet since weaning (p<0.001). The HF rats showed glucose intolerance with high levels of insulin secretion during the glucose tolerance test (p<0.01). Rats that were fed the high-fat diet presented severe insulin resistance, indicated by a low K itt (p<0.01). Interestingly, the HF81 rats exhibited greater insulin resistance compared with the HF120 rats (p<0.05). The recordings of vagus nerve activity showed that the HF rats had higher parasympathetic activity than the NF rats irrespective of age (p<0.01). Our results show that a high-fat diet offered to rats just after weaning or in adulthood both cause impairment of glycemic homeostasis and imbalance in parasympathetic activity. Importantly, the consumption of high-fat diet immediately after weaning has more drastic consequences compared with the consumption of the same diet during adulthood.     

Features of oxidative phosphorylation in brain mitochondria of rats with different sensitivity to oxygen insufficiency]

Oxidative phosphorylation parameters have been investigated in the isolated brain mitochondria of rats preliminary divided into non-resistant (NR) and high-resistant (HR) animals by their sensitivity to hypobaric hypoxia. During the NAD-dependent substrates oxidation it was shown that the identical effectiveness of the respiratory chain function in both groups of animals was reached at more tension of the oxidative processes. It has been established that at the identical effectiveness of the succinate oxidation by the brain mitochondria in both groups of animals compensatory potentialities of the succinate-oxidase pathway of oxidation is higher in the brain of the NR to hypoxia animals. It has been shown the regulated influence of the NAD-dependent pathway of oxidation activity on the succinate-oxidase site of respiratory chain. This influence is more expressed in the brain mitochondria of the NR animals that in the HR animals.     

Skin-flap metabolism in rats: oxygen consumption and lactate production

Overall glucose metabolism was evaluated by measuring the rate of oxygen consumption (QO2) and lactate production in the pedicle skin flaps of rats. Skin flaps exhibited increases in QO2 and lactate production in vitro. The distal portion of the flap is characterized by a greater deposition of glucose to lactate during the initial 3 days following flap elevation. The contribution of glycolysis and of the oxidative pathways to glucose metabolism in skin flaps approximates that in normal skin on day 7 postoperatively.     

Induction of metallothionein by exposure to normobaric 100% oxygen atmosphere in rats with different zinc supply

The objective of this study was to determine the effects of an oxygen enriched environment on the induction of the metalloprotein metallothionein (MT) and its relation to zinc metabolism in rats supplied with different levels of dietary zinc. Male albino rats were fed purified diets based on maize starch, egg white, saccharose and soybean oil differing in the concentration of zinc (1; 20; 100; 500 mg Zn/kg diet). At a dietary zinc supply of 1 mg/kg, the rats developed a zinc deficiency indicated by visual and biochemical parameters. At the end of the 37-day feeding period, half of the rats were exposed to 100% oxygen for 12 h.

The oxygen treatment significantly reduced plasma zinc in the zinc supplemented rats and reduced it in tendency in the zinc deficient rats. The MT concentration was increased in the zinc supplemented groups in the liver, kidney and lung. The oxygen treatment elevated the metallothionein concentration in the two high zinc supplemented groups (100 and 500 mg Zn/kg diet) in the liver. The response of the zinc concentration in plasma and of hepatic metallothionein levels to oxygen exposure indicates a role of metallothionein in zinc distribution or interactions with other trace elements to support antioxidant capacity, rather than an impact on direct scavenging activity of free radicals.     

Neuronal storage of histamine in the brain and tele-methylimidazoleacetic acid excretion in portocaval shunted rats

Rats with portocaval anastomosis (PCA), an animal model of hepatic encephalopathy (HE), have very high brain histamine concentrations. Our previous studies based on a biochemical approach indicated histamine accumulation in the neuronal compartment. In this study, immunohistochemical evidence is presented which further supports the amine localization in histaminergic neurons. These neurons become pathological in appearance with cisternae frequently seen along histaminergic fibres in many brain areas, including the hypothalamus, amygdala, substantia nigra and cerebral cortex. Such formations were not observed in sham-operated animals. The neuronal deposition is predominant, and unique for histamine. It serves as a mechanism to counterbalance excessive brain neurotransmitter formation evoked by PCA. However, there are other mechanisms. The data provided here show that there is also a significant increase in histamine catabolism in the shunted rats, as reflected by both the higher brain N-tele-methylhistamine (t-MeHA) concentration and urinary excretion of N-tele-methylimidazoleacetic acid (t-MelmAA), a major brain histamine end product. The stomach, in addition to the brain, is a site of enhanced histamine synthesis in portocavally shunted subjects. After gastrectomy or food deprivation to eliminate the contribution of the stomach, shunted rats excrete significantly more t-MelmAA, implying the role of the CNS. This last finding suggests that under strictly defined conditions, namely in parenterally fed HE patients with abnormal plasma L-histidine, the measurement of urinary t-MelmAA might provide valuable information concerning putative brain histaminergic activity.