Biomedical subjects

A Y Sun

Publications and source records attributed to A Y Sun.

At least 55 records · Page 3Linked to original sources

PubMed1992

Effects of microinjection of picrotoxin into posterior hypothalamus on ventricular electric stability.

Ventricular fibrillation threshold (VFT), serum potassium, and monophasic action potentials (MAP) have been assessed before and after microinjection of picrotoxin (Pic) into posterior hypothalamus in rabbits. Pic (2 and 3 micrograms) brought about a biphasic effect on VFT, an initial decrease followed by a notable increase. Pretreatment with spinal cord transection almost abolished the descending phase, whereas pretreatment with vagotomy depressed the ascending phase significantly. Following the microinjection of Pic, serum potassium rose up to 5.0 mmol.L-1 at 30 min. The amplitude of MAP (MAPA) and Vmax were lessened in rabbits, while in vagotomized rabbits, the changes of MAP were aggravated, and the duration of MAP was shortened. Phentolamine counteracted the changes of MAP induced by Pic. These results suggested that the initial decrease of VFT caused by Pic derived mainly from the direct action and myocardial ischemia of sympathetic activation, while its subsequent elevation was caused by vagal activation and hyperkalemia.

Action Potentials↗

PubMed1991

The involvement of ethanol in the free radical reaction of 6-hydroxydopamine.

ESR spin trapping technique was used to detect and analyze free radical formation. When 6-hydroxydopamine (6-OHDA) was incubated alone or in the presence of a free radical generating system (H2O2 and FeSO4), hydroxyl free radicals were observed in a concentration-dependent manner. Glutathione was found to be the most effective scavenger of the ESR signal when compared with vitamin E or Mannitol. The addition of ethanol resulted in the formation of the pure hydroxyethyl free radicals. The amount of hydroxyethyl free radicals in the system was dependent upon the concentration of ethanol and the formation of hydroxyethyl free radicals correlated well with the extent of lipid peroxidation and the loss of enzymic activity of the membrane-bound (Na+,K+)-ATPase. We suggest that in the biological system ethanol may potentiate the neurotoxicity of 6-OHDA with the formation of hydroxyethyl free radicals, which are longer-lived and far more damaging to membranes than the hydroxyl radicals. These data lead us to further hypothesize that the neuronal degeneration caused by 6-OHDA and other compounds that generate free radicals could be potentiated in the presence of ethanol.

Cyclic N-Oxides↗

PubMed1991

Stress-induced changes of central GABAergic function in rats.

The effects of acute and repeated immobilization stress on central GABAergic function were examined in rats by evaluating the changes of the cardiovascular responses to intracerebroventricular injection of GABA. The depressor and bradycardia responses of GABA were attenuated significantly by immobilization stress for 6 h (from -5.5 +/- 0.7 kPa and -75 +/- 25 bpm to -2.3 +/- 0.9 kPa and -27 +/- 16 bpm respectively, for GABA 200 micrograms). These effects of stress were neither mimicked by administration of hydrocortisone, nor abolished by pretreatment with adrenalectomy or diazepam, but they were attenuated significantly by pretreatment with isoniazid. These results indicated that immobilization stress for long duration causes subsensitivity of central GABA receptors, in which the down-regulation mechanism may be involved.

Adrenalectomy↗

PubMed1990

A comparative blinded study in miniature swine of whole blood-, hemoglobin-, platelet-, plasma-, and lymphocyte-associated acetaldehyde as markers for ethanol intake.

Blood samples were obtained from miniature swine maintained on 0, 2, or 6 g/kg/24 hr ethanol for 8 months (N = 6 in each group). Samples from drinking pigs were taken after 8 hr of ethanol abstinence and all were coded and sent for "blinded" analysis. A fluorigenic high performance liquid chromatographic assay was used to quantify whole blood-associated acetaldehyde, hemoglobin-associated acetaldehyde, plasma-associated acetaldehyde, platelet-associated acetaldehyde, and lymphocyte-associated acetaldehyde. Detectable levels of acetaldehyde were found in each sample in both drinking and nondrinking pigs. Analysis of whole blood-associated acetaldehyde was most discriminatory in distinguishing nondrinking from drinking pigs (mean 21.4 +/- 1.0 microM for nondrinkers vs. 24.6 +/- 1.5 SD for the group consuming 2 g/kg ethanol, p = 0.001). Measurements of hemoglobin-associated acetaldehyde normalized to protein concentration (250 +/- 47 nmoles/g vs. 203 +/- 33 SD, p less than 0.05 drinking vs. nondrinking pigs) and platelet-associated acetaldehyde (0.46 0.34 vs. 0.15 +/- 0.16 nmoles/3 x 10(8) platelets, p = 0.05 drinking vs. nondrinking pigs) were also useful in discriminating drinking from nondrinking animals. Analysis of plasma-associated acetaldehyde and lymphocyte-associated acetaldehyde were not useful as markers of ethanol consumption.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetaldehyde↗

PubMed1990

Ventricular arrhythmia evoked by microinjection of picrotoxin into brain areas in rabbits.

To explore the main areas of brain responsible for arrhythmia evoked by icv picrotoxin (Pic), a very small dose of Pic (3 micrograms) was injected into different areas of brain in anesthetized rabbits. The short latency of arrhythmia was found after microinjection of Pic into posterior hypothalamus (PH, 5.6 +/- 0.9 min) and the medial part of tuberal region (7.5 +/- 2.9 min). The ventricular arrhythmia was abolished by vagotomy, iv phentolamine or diazepam, or pretreatment with adrenalectomy or vagotomy. Microinjection of phentolamine or diphenhydramine into PH prior to Pic postponed the arrhythmia. The results indicate that PH and the medial part of tuberal region are the most effective areas for Pic to induce arrhythmia, activations of both sympathoadrenomedullary and parasympathetic systems are involved in the genesis of arrhythmia.

Adrenalectomy↗

PubMed1988

Potentiation of ethanol-induced lipid peroxidation of biological membranes by vitamin C.

The hydroxyl free radical (.OH) was generated by the system of ADP-Fe++ and H2O2, trapped by 5,5-dimethyl-1-pyrroline-N-oxide (DMPO) and analyzed by electron spin resonance (ESR) spectroscopy. The addition of vitamin C to the system decreased considerably the amount of hydroxyl adduct of DMPO formed. In the presence of ethanol, the ESR spectrum observed was a composite signal of the hydroxyl and hydroxyethyl (HE) adducts of DMPO. However, in the presence of vitamin C and ethanol, pure HE adduct of DMPO was detected. We also detected the increase in lipid peroxidation in the presence of ethanol and vitamin C. These data lead us to hypothesize that in the biological system, formation of these long-lived HE free radicals may result in membrane damage due to an increase in lipid peroxidation.

Animals↗

PubMed1988

Effects of ethanol on arachidonic acid incorporation into lipids of a plasma membrane fraction isolated from brain cerebral cortex.

In the presence of ATP, MgCl2, and CoASH, somal plasma membranes isolated from rat cerebral cortex were active in transferring arachidonic acid to phosphatidylinositols, phosphatidylcholines, and triacylglycerols. Ethanol (350-525 mM) added to the incubation mixture inhibited arachidonic acid incorporation into phospholipids, while it enhanced the incorporation into triacylglycerols. Under these conditions, ethanol was found to react with arachidonic acid to form arachidonoyl ethyl ester. The incorporation of labeled arachidonic acid into glycerolipids as well as the synthesis of ethyl esters required the presence of ATP and CoASH for maximal activity. Nevertheless, each uptake process exhibited a unique pH profile. The esterification of arachidonic acid was not specific for ethanol as other aliphatic alcohols (e.g., propanol and butanol) were also able to react with labeled arachidonic acid to form the respective esters. Somal plasma membranes isolated from mice after chronic ethanol administration showed an increase in arachidonoyl transfer to both phospholipids and triacylglycerols. When these membranes were challenged with ethanol (325 mM), those isolated from the chronic ethanol group showed a greater increase in the labeling of triacylglycerols and ethyl esters than those from controls. Thus, different acyltransferases exhibite different responses to the effects of ethanol in vitro and in vivo.

Acyltransferases↗

PubMed1987

Detection of free radical formation in various tissues after acute carbon tetrachloride administration in gerbil.

alpha-phenyl N-tert-butyl nitrone (PBN) was used as a spin-trapping agent to search for free radical formation in various tissues of gerbils. A significantly large amount of free radicals was detected in liver, kidney, heart, lung and testis after a single intraperitoneal dose of CCl4. We have also detected free radical formation in the brain and blood, although the number of spins was considerably smaller than those found in the other tissues. Free radicals formed in brain tissue after an oxidative insult may give strong supporting evidence for the free radical theory of aging.

Animals↗

PubMed1987

Effects of chronic ethanol administration on rat brain phospholipid metabolism.

Alterations in brain phospholipid metabolism were observed after chronic ethanol administration for 16 days to developing rats. Animals were injected intraperitoneally with 32Pi 16 h prior to killing. Overall uptake of 32Pi by brain did not differ between the control and ethanol-treated groups, which were killed 2 h and 24 h after the last ethanol feeding. Except for an increase in the labeling of myelin after ethanol treatment, the amount of radioactivity recovered in the synaptosomal-mitochondrial and plasma membrane fractions of control and ethanol-treated groups was not different. Relative to the radioactivity of phosphatidylcholines, which indicated no change, there were increases (20-44%) in labeling of ethanolamine plasmalogens, phosphatidic acids, and phosphatidylinositols in cortical synaptosomes from the 2-h ethanol-treated group. In the plasma membrane fractions, however, increases (9-14%) in labeling of phosphatidylserines and phosphatidylinositols were observed in both 2- and 24-h ethanol-treated groups. In both membrane fractions, there was an obvious increase (44-86%) in labeling of polyphosphoinositides at 24 h after withdrawal from ethanol. Results thus indicate an adaptive increase in the biosynthesis of ethanolamine plasmalogen and brain acidic phospholipids due to chronic ethanol administration. Furthermore, the increase in labeling of polyphosphoinositides in the 24-h withdrawal group may reflect the hypoactivity associated with ethanol withdrawal.

Animals↗

PubMed1987

Ethanol effects on phospholipids and triacylglycerols of rat brain astrocyte cell line.

A homotypic population of rat brain astrocyte (RBA-1) cell line was used to investigate the effects of ethanol on uptake of [3H]-arachidonic acid and incorporation of label into phospholipids and neutral lipids in the cell. Incubation of the cells with [3H]-arachidonic acid resulted in labeling of most phospholipids and triacylglycerols, although individual phospholipids exhibited different rates for acquiring the label. Labeled arachidonate was first incorporated into phosphatidylcholines and phosphatidylinositols prior to equilibriation with other phospholipids. In short term incubation (8 hr), ethanol (128-255 mM) enhanced the incorporation of labeled arachidonate into most phospholipids. In addition, ethanol at 128 mM enhanced the labeling of the triacylglycerols, and the difference was greater with increasing time of ethanol exposure. It is concluded that ethanol enhanced the uptake and incorporation of polyunsaturated fatty acids into the cell membrane lipids. This study further indicates the feasibility of using the RBA-1 cells in culture to probe the effects of ethanol on membrane lipid metabolism.

Animals↗

PubMed1987

Effects of ethanol on acetylcholine and GABA release: differences in the role of potassium.

Ethanol inhibited electrically stimulated [3H]ACh release from cortical brain slices, but not when release was stimulated by high potassium. In contrast, ethanol was ineffective on electrically stimulated release of [14]GABA from cortical brain slices, but inhibited potassium-induced release. Ethanol also significantly inhibited potassium-stimulated [14C]GABA release from cortical synaptosomes. These data suggest that ethanol selectively inhibits GABA release from neurons by a specific effect on potassium conductance, and inhibits ACh release by a selective effect on Na+ conductance.

Acetylcholine↗

PubMed1987

Chronic ethanol effect on the acidic phospholipids of synaptosomes isolated from cerebral cortex of C57BL/6NNIA mice--a comparison with age.

A total of six groups of C57BL/6NNIA male mice at 6, 18 and 28 months of age were administered a liquid diet containing either ethanol (8 g/kg body wt/day) or an isocaloric amount of glucose for three weeks. Sixteen hours after the last ethanol feeding, homogenates of cerebral cortices were prepared for isolation of the synaptosome-mitochondrial fraction. Phospholipids were separated by two-dimensional tlc and the level of individual phospholipids was determined by assaying the lipid phosphorus content. Based on protein content, there was a decrease (18%) in the level of phosphatidylserines between samples from 6 and 28 month-old mice; no age difference was observed in other phospholipids. Ethanol consumption resulted in a three-fold increase in poly-phosphoinositide level in the 6 month-old group, but the difference diminished considerably with age. The increase in poly-phosphoinositide level suggests a link between chronic ethanol administration and the receptor-mediated signal transduction mechanism involving phosphoinositide turnover. Results further indicate that animals in the younger age group are more readily influenced by the chronic effect of ethanol than those in the older age group.

Aging↗

PubMed1986

Dolichol alters dynamic and static properties of mouse synaptosomal plasma membranes.

Dolichols are isoprenologues that are found in almost all tissues and whose biochemical function, aside from dolichol phosphate precursors, is not known. In addition, an understanding of the organizational and dynamic properties of dolichols in biological membranes has not been forthcoming. The purpose of the experiments reported here were to examine the effects of dolichol on the physical properties of mouse synaptic plasma membranes (SPM). Differential polarized phase fluorometry indicated that dolichol both fluidized and rigidified SPM. Membrane areas detected by diphenylhexatriene and trans-parinaric acid were selectively fluidized and rigidified, respectively. It also was found that the spin label, 5-doxyl stearic acid indicated that dolichol reduced membrane fluidity. These results report for the first time a structural effect of dolichol on a biological membrane.

Animals↗

PubMed1986

Changes in lipid composition of rat heart mitochondria after chronic ethanol administration.

Triacylglycerols and phospholipids of mitochondria from heart ventricular muscle were analyzed following chronic ethanol administration (2 and 10 g/kg of body weight/day) to adult rats for 21 days via intragastric intubation. Triacylglycerols were elevated 57% in the high ethanol group as compared to controls, but cholesterol level was not altered. Most of the phospholipids, including lysophospholipids, showed a small increase in level after ethanol administration. However the greatest increase (50%) occurred in ethanolamine plasmalogens. Although small changes in the acyl group composition of phosphatidylethanolamines and phosphatidylcholines were observed, the acyl group profile of cardiolipin remained unaltered. It is concluded that myocardial membranes respond to the disordering effects of ethanol by altering the synthesis of selected lipids more than through altering the phospholipid acyl group composition. Some of these changes may be responsible for altered mitochondrial functions in the myocardium.

Alcoholism↗

PubMed1985

Electroacupuncture alters catecholamines in brain regions of rats.

Electroacupuncture (EA) stimulation mediated the release of [3H]norepinephrine (NE) from synaptosomes prelabeled with [3H]NE. The pulse release of [3H]NE by EA stimulation was dependent on the presence of Ca2+. Treatment of rats with EA for 30 min at 4 Hz did not significantly alter the dopamine (DA) content in hypothalamus, cerebellum, pons, midbrain, and cerebral cortex regions, but the DA level was decreased by 20% in caudate nucleus. The NE level was found to increase by 43% in caudate nucleus and 38% in hypothalamus. The results indicate that only certain neuronal pathways are affected by the EA treatment, and that NE and DA may respond differently to such stimulation.

Acupuncture Therapy↗

PubMed1984

Increased acidic phospholipids in rat brain membranes after chronic ethanol administration.

Two types of plasma membranes isolated from rat brain cortex were used to study the membrane-perturbing properties of ethanol. Rats administered ethanol in the form of a liquid diet showed an increase in levels of phosphatidylserines, phosphatidylinositols and phosphatidic acids as compared to controls. The results present evidence that chronic ethanol treatment results in an increase in the acidic phospholipids in brain membranes. This type of membrane modification may have important implications for the function of membrane transport enzymes such as (Na+, K+)-ATPase, which also increases in activity upon chronic ethanol administration.

Alcoholism↗

PubMed1984

Ethanol consumption and serum lipid profiles in Sinclair(S-1) miniature swine.

Ethanol consumption was correlated with changes in acyl group profiles of phosphatidylcholine and triacylglycerols in serum of Sinclair(S-1) miniature boars. Serum triacylglycerols in the control pigs were high in linoleate (18:2) (48%) and low in stearate (18:0 (3%). Upon feeding with 10% (w/v) ethanol ad lib for two weeks, the proportion of 18:2 in serum triacylglycerols decreased to 12-15% with a concomitant increase in 16:0, 18:0 and 18:1. Similar, but less extensive, acyl group changes were observed in the serum phosphatidylcholine. In addition, there was a decrease in the proportion of 20:3(n-6), but a biphasic change was shown in 20:4(n-6) with respect to ethanol consumption. In general, the high ethanol consumers (7.0 g/kg/day) indicated a more rapid rate of acyl group change than the low consumers (3.8 g/kg/day). Upon withdrawal of ethanol, acyl groups of triacylglycerols rapidly returned towards the control values, whereas only small changes were observed for the recovery in phospholipids. In this situation, the low-consumer group indicated a more rapid recovery than the high-consumer group. Results indicate that with the swine model, serum lipid changes can be a useful parameter for correlating biological changes upon ethanol consumption.

Alcohol Drinking↗

PubMed1984

Effect of electroacupuncture on synaptosomal (Na+ + K+)-ATPase.

The action of electroacupuncture (EA) may be similar to analgesia by electrode stimulation or transcutaneous nerve stimulation. Since EA may directly stimulate nerve activity or indirectly enhance the release of opiate peptides and other neurotransmitter substances, we have used (Na+ + K+)-ATPase as a model to study the mechanism of action of EA. The membrane-bound (Na + K)-ATPase from purified synaptic plasma membranes inhibited slightly by high concentration of endorphin (30 microM), but not by met-enkephalin up to 6 X 10(-4) M. A single EA treatment for 30 min did not alter the (Na+ + K+)-ATPase activity in the cerebral cortex. However, when rats were treated with low (4 Hz) or high (200 Hz) frequency EA 30 min daily for 3 weeks, both (Na+ + K+)-ATPase and acetylcholinesterase were significantly elevated. The enhanced (Na+ + K+)-ATPase activity after high frequency EA was only partially blocked by i.p. injection of naloxone prior to EA during the last week of the EA treatment program. The results indicated that EA treatment may involve some other neurotransmitter pathways besides opiate peptides.

Acetylcholinesterase↗