scholarly journals Brain Levels of Catalase Remain Constant through Strain, Developmental, and Chronic Alcohol Challenges

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Dennis E. Rhoads ◽  
Cherly Contreras ◽  
Salma Fathalla

Catalase (EC 1.11.1.6) oxidizes ethanol to acetaldehyde within the brain and variations in catalase activity may underlie some consequences of ethanol consumption. The goals of this study were to measure catalase activity in subcellular fractions from rat brain and to compare the levels of this enzyme in several important settings. In the first series of studies, levels of catalase were compared between juvenile and adult rats and between the Long-Evans (LE) and Sprague-Dawley (SD) strains. Levels of catalase appear to have achieved the adult level by the preadolescent period defined by postnatal age (P, days) P25–P28, and there were no differences between strains at the developmental stages tested. Thus, variation in catalase activity is unlikely to be responsible for differences in how adolescent and adult rats respond to ethanol. In the second series of studies, periadolescent and adult rats were administered ethanol chronically through an ethanol-containing liquid diet. Diet consumption and blood ethanol concentrations were significantly higher for periadolescent rats. Catalase activities remained unchanged following ethanol consumption, with no significant differences within or between strains. Thus, the brain showed no apparent adaptive changes in levels of catalase, even when faced with the high levels of ethanol consumption characteristic of periadolescent rats.

2002 ◽  
Vol 93 (3) ◽  
pp. 1123-1130 ◽  
Author(s):  
Alfin G. Vicencio ◽  
Oliver Eickelberg ◽  
Michael C. Stankewich ◽  
Michael Kashgarian ◽  
Gabriel G. Haddad

Long-term effects of hypoxia are largely due to its modulatory effects on proliferation and differentiation of epithelial and endothelial cells, processes also regulated by the transforming growth factor (TGF)-β system. We investigated the effects of hypoxia on the TGF-β system in rat lungs from different developmental stages. Sprague-Dawley rats were exposed to 9.5% oxygen during either the first 2 wk of life or adulthood. Analysis revealed an arrest of alveolarization in hypoxic postnatal day 14 rats. Bioactive TGF-β levels in bronchoalveolar lavage fluid were increased in these animals, and Western blot analysis revealed upregulation of TGF-β receptor (TβR) I and II. None of these changes was observed in hypoxic adults. Hypoxia did, however, lead to decreased expression of TβRIII in both postnatal day 14 and adult rats. Immunohistochemical analysis localized TβRI-III predominantly to bronchiolar and alveolar epithelium; these patterns did not change with hypoxia. Thus we observed changes in TGF-β activity and TβR isotype expression in rat lung that parallel the arrest in alveolarization seen with chronic hypoxia in early development. These alterations may partly explain the morphological changes observed in hypoxia.


1976 ◽  
Vol 68 (2) ◽  
pp. 235-239 ◽  
Author(s):  
J. C. BUTTE ◽  
RYOKO KAKIHANA ◽  
E. P. NOBLE

SUMMARY In the present study the circadian changes which occur in the levels of corticosterone in the brain and plasma in Sprague–Dawley rats are reported. The levels of corticosterone in the brain were found to have a daily trough and crest with timing similar to that observed for the plasma steroid. In addition, the effect of histamine stress on the corticosterone content of the particulate and the soluble fractions at the trough and crest was examined. The levels of both brain fractions were significantly higher 20 min after histamine injection. The time of day at which the stress was applied was not a significant factor in the magnitude of the stress response.


F1000Research ◽  
2019 ◽  
Vol 8 ◽  
pp. 1372 ◽  
Author(s):  
Liam Koehn ◽  
Mark Habgood ◽  
Yifan Huang ◽  
Katarzyna Dziegielewska ◽  
Norman Saunders

Background: A major concern for clinicians in prescribing medications to pregnant women and neonates is the possibility that drugs might have damaging effects, particularly on long-term brain development. Current understanding of drug permeability at placental and blood-brain barriers during development is poor. In adults, ABC transporters limit many drugs from entering the brain; however, little is known about their function during development. Methods: The transfer of clinically relevant doses of paracetamol (acetaminophen), digoxin and cimetidine into the brain and cerebrospinal fluid (CSF) was estimated using radiolabelled drugs in Sprague Dawley rats at three developmental stages: E19, P4 and adult. Drugs were applied intraperitoneally either acutely or following chronic exposure (for five days). Entry into brain, CSF and transfer across the placenta was measured and compared to three markers (L-glucose, sucrose, glycerol) that cross barriers by “passive diffusion”. The expression of ABC transporters in the brain, choroid plexus and placenta was estimated using RT-qPCR. Results: All three drugs entered the developing brain and CSF in higher amounts than the adult brain and CSF. Comparisons with “passive” permeability markers suggested that this might be due to age-related differences in the functional capacity of ABC-efflux mechanisms. In adult animals, chronic treatment reduced digoxin (12% to 5%, p<0.01) and paracetamol (30% to 21%, p<0.05) entry compared to acute treatment, with the decrease in digoxin entry correlating with up-regulation of efflux transporter abcb1a (PGP). In fetal and newborn animals, no gene up-regulation or transfer decreases were observed. Instead, chronic paracetamol treatment resulted in increased transfer into the fetal brain (66% to 104%, p<0.001). Conclusions: These results suggest that the developing brain may be more at risk from acute drug exposure than the adult brain due to reduced efflux capacity and at greater risk from chronic treatment due to a lack of efflux mechanism regulatory capacity.


Nutrients ◽  
2020 ◽  
Vol 12 (6) ◽  
pp. 1847 ◽  
Author(s):  
Thomas Horman ◽  
Maria F. Fernandes ◽  
Maria C. Tache ◽  
Barbora Hucik ◽  
David M. Mutch ◽  
...  

There is mounting evidence that diets supplemented with polyunsaturated fatty acids (PUFA) can impact brain biology and functions. This study investigated whether moderately high-fat diets differing in n-6/n-3 fatty acid ratio could impact fatty acid composition in regions of the brain linked to various psychopathologies. Adult male Sprague Dawley rats consumed isocaloric diets (35% kcal from fat) containing different ratios of linoleic acid (n-6) and alpha-linolenic acid (n-3) for 2 months. It was found that the profiles of PUFA in the prefrontal cortex, hippocampus, and hypothalamus reflected the fatty acid composition of the diet. In addition, region-specific changes in saturated fatty acids and monounsaturated fatty acids were detected in the hypothalamus, but not in the hippocampus or prefrontal cortex. This study in adult rats demonstrates that fatty acid remodeling in the brain by diet can occur within months and provides additional evidence for the suggestion that diet could impact mental health.


1991 ◽  
Vol 10 (6) ◽  
pp. 439-444 ◽  
Author(s):  
D.C. Purves ◽  
I.J. Garrod ◽  
A.D. Dayan

The effect of hexachlorophene (HCP; 2,2'-methylenebis (3,4,6-trichlorophenol), cuprizone (CPZ; bicyclohexone oxaldihydrazone) and triethyl tin (TET; triethyl tin sulphate) in producing vacuoles in the brain of the Sprague-Dawley rat has been quantified by image analysis of the extent of the spongy change in the white matter. The state of the astrocytes was assessed by immunocytochemical staining for glial fibrillary acidic protein (GFAP). HCP and TET caused a dose-related spongiosis, but cuprizone had no significant effect on the brain. With chronic HCP treatment, the spongiosis was accompanied by astrocyte hypertrophy and proliferation, and the extent of the gliotic reaction was related to the dose of HCP. The results demonstrate that HCP can produce and maintain astrocyte proliferation in the rat brain. Such an agent was required for use in an investigation of a putative tumour promoter in the rat.


1987 ◽  
Vol 26 (03) ◽  
pp. 131-134 ◽  
Author(s):  
S. Jinnouchi ◽  
K. Watanabe ◽  
T. Ueda ◽  
K. Kinoshita ◽  
T. Yamaguchi ◽  
...  

The biodistribution of N-isopropyl-p-iodoamphetamine (IMP) was studied in the rat brain.131 l-labelled IMP was injected intravenously in awake animals. Activities in the brain of Sprague-Dawley rats were 2.68–3.22 (% dose/g) in the cortex and 0.59–0.66 (% dose/g) in the white matter at 1 min p. i. Activities in the cortex were slightly increased at 60 min p. i., while activities in the white matter increased markedly at 60 min and 6 h p. i. Therefore, the cerebral cortex-to-white matter ratio decreased from 5 to 1 within 60 min after injection. Autoradiograms of the rat brain at 1–10 min p. i. showed high contrasts. Activities were high in the cortex and low in the white matter, but homogeneous at 60 min – 6 h. IMP seems to be a useful agent for cerebral perfusion imaging in the early phase after injection. Knowledge of biodistribution of this agent is considered to be indispensable for the interpretation of images.


1965 ◽  
Vol 43 (7) ◽  
pp. 1091-1098 ◽  
Author(s):  
Shozo Nakazawa ◽  
Takao Hara ◽  
Komei Ueki

The effects of X-irradiation on the metabolism of rat brain, liver, and spleen have been studied. C14-Glucose incorporation into protein of the brain of newborn rats was affected significantly by total body X-irradiation (250 r each day for 4 days). C14-Leucine incorporation into protein of the brain, liver, and spleen of adult rats was also reduced by total body X-irradiation (300 r each day for 4 days).X-irradiation of the head (500 r each day for 6 days) affected C14-leucine incorporation into protein of rat brain and liver, but it did not affect that of spleen.X-irradiation in vitro (5000 r) did not have any effect on protein metabolism of rat brain. The mode of action of X-irradiation on protein metabolism is discussed.


2020 ◽  
Vol 22 (1) ◽  
pp. 77-86 ◽  
Author(s):  
M. I. Airapetov ◽  
S. O. Eresko ◽  
E. R. Bychkov ◽  
A. A. Lebedev ◽  
P. D. Shabanov

Recent studies have provided strong evidence that long-term ethanol consumption leads to activation the mechanisms of neuroimmune signaling. Recently, much attention has been focused on the study of toll-like receptors (Toll-like receptors, TLRs), which play one of the key roles in the mechanisms of activation of the innate immune system in brain structures subsequently ethanol consumption. It is known that the activation of TLRs leads to the release of many proinflammatory cytokines with the resulting neuroinflammatory process. There are suggestions that TLRs may also be involved in the modulation of neurotransmitter systems of the brain, thereby contributing to the formation of pathological dependence on ethanol. The goal of our work was to study the level of expression the genes of TLRs (TLR3, TLR4, TLR7) and pro-inflammatory cytokine genes (IL-1β, CCL2) in the rat brain (amygdala, hippocampus, medial entorhinal cortex, striatum) under conditions of prolonged alcoholization and on different periods of alcohol withdrawal, which was previously not studied by researchers. Prolonged alcoholization of rats with ethanol did not lead to changes in levels mRNA of TLRs in the studied structures of the rat brain, with the exception of a small increase in the level of TLR3 mRNA in the hippocampus of prolonged alcoholized rats and a slight increase in the level of TLR3 mRNA in mEC. However, gene expression of TLRs undergoes changes in all the structures of the rat brain studied by us at different periods of alcohol withdrawal. The increased level of expression of both TLRs and proinflammatory genes in the period of alcohol withdrawal in the rat brain hippocampus deserves special attention, which indicates the presence of a persistent neuroinflammatory process in this brain structure in the period of alcohol withdrawal, which is probably supported with the participation of TLR-dependent signaling. The study of the mechanisms of inflammatory process activation by TLR-dependent signaling in different brain structures can open new targets for drug exposure. Such drugs can be used in the treatment of alcoholism.


1988 ◽  
Vol 64 (5) ◽  
pp. 1829-1836 ◽  
Author(s):  
S. Adler ◽  
V. Simplaceanu ◽  
C. Ho

Buffering capacity of most tissues is composed of both rapid and slow phases, the latter presumably due to active acid extrusion. To examine the time course of brain buffering the brain pH of Sprague-Dawley rats was measured using 31P-nuclear magnetic resonance. The effect on brain pH of 30- or 58-min exposures to 20% CO2 followed by 30- or 38-min recovery periods, respectively, was studied. Brain pH reached its lowest value after a 15-min exposure to elevated CO2, thereafter slowly and steadily increasing. During recovery brain pH rose rapidly in the first 5 min exceeding control brain pH by 0.08 pH units. Brain pH fell during the next 30 min despite increases in blood pH and decreases in blood CO2 tension. Calculated intrinsic brain buffering rose steadily threefold during the last 40 min of CO2 exposure and during the final 30 min of recovery. These data show that in rat brain there is a temporally late buffering process, most likely active acid extrusion, requiring greater than 30 min for full activation and at least 30 min for discontinuation.


1971 ◽  
Vol 122 (1) ◽  
pp. 13-18 ◽  
Author(s):  
R. A. Hawkins ◽  
D. H. Williamson ◽  
H. A. Krebs

1. Ketone-body utilization in fed and starved adult and suckling rats has been investigated by measuring arterio-venous differences across the brain. Venous blood was collected from the confluence of sinuses and arterial blood from the femoral artery in adult rats and by cardiac puncture in suckling rats. 2. During starvation the arterio-venous difference of ketone bodies increased in proportion to their concentrations in the blood and reached a value of 0.16mm at 48h. At a given concentration of the respective ketone bodies the arterio-venous differences of acetoacetate were about twice those of 3-hydroxybutyrate. 3. Fed rats in which the concentrations of ketone bodies were raised by intravenous infusion of sodium acetoacetate had the same arterio-venous differences as starved rats at corresponding ketone-body concentrations. Thus the ability of the rat brain to utilize ketone bodies is independent of the nutritional state. 4. The concentrations of glucose, acetoacetate and 3-hydroxybutyrate were much lower in the brain than in the arterial blood. The measured (blood concentration)/(brain concentration) ratio was 4.4 for glucose, 4.5 for acetoacetate and 8.1 for 3-hydroxybutyrate in 48h-starved rats. 5. The mean arterio-venous difference of glucose across the brain was 0.51mm in fed rats and 0.43mm in 96h-starved rats. 6. Conversion of glucose into lactate rose from negligible values in the fed state to 0.2mm after 48h starvation and decreased to zero after 96h starvation. 7. In 16–22-day-old suckling rats the arterio-venous differences of ketone bodies across the brain were also proportional to the ketone-body concentration, but they were about 3–4 times greater than in adult rats at the same blood ketone-body concentration. 8. Arterio-venous differences of glucose were about the same in adult and suckling rats. 9. The brain of fed suckling rats formed more lactate from glucose than fed adult rats. 10. The results indicate that ketone bodies are major metabolic fuels of the brain of the suckling rat under normal conditions.


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