Search PubMed⌕ Search

Biomedical subjects

A Y Sun

Publications and source records attributed to A Y Sun.

88 records · Page 5Linked to original sources
PubMed1976

Aging and in vivo norepinephrine-uptake in mammalian brain.

In order to examine the cellular effect of aging in the central nervous system, the regional distribution and the dynamic aspects of catecholamine metabolism in the brain were investigated. Results indicated that the endogenous norepinephrine (NE) content is lower in hypothalamus and brain stem of older rats (25 mo. n = 6) than younger rats (12 mo. n = 6). We have also observed in these animals that the age pigments were apparently absent in the brain tissue of young rats but become a very distinct feature for the old rats and that the catecholamine strong vesicles appear to be less dense in the nerve terminals of old as compared with the young ones. 3H-NE was administered intracerebrally to mice of different age groups (4, 8, 12, 21 and 24 months) and the NE-uptake activity was examined by measuring the radioactive NE inside the isolated synaptosomes 5 min after 3H-NE injection. The result indicated that the young group (4 mo) has highest uptake activity. The uptake activity decrease with the older mice and reached the lowest in the age group of 21-24 mo. The decrease in NE-uptake activity may be related to the deterioration of synaptosomal membranes.

Aging↗
PubMed1976

Alcohol-membrane interaction in the brain: norepinephrine release.

The nerve endings of mouse brain were loaded with 3H-norepinephrine (3H-NE) by intraventricular injection of 3H-NE. After dissection of brain, the synaptosomal particles were isolated and used for NE-release studies. The NE release process was stimulated by K+ and Ca++ but was antagonized by Na+. Acetylcholine at low concentration also decreased the release of 3H-NE. Ethanol at low concentrations (0.1-0.5%) decreased the amount of synaptosomal NE release whereas at higher ethanol concentrations (1-4%) the NE release was increased. This biphasic response of NE release in the presence of ethanol could be the effect of ethanol on related active cation transport systems such as Ca++-transport.

Acetylcholine↗
PubMedDate not supplied

Oxidative stress and neurodegenerative disorders.

Oxidative insults, whether over-excitation, excessive release of glutamate or ATP caused by stroke, ischemia or inflammation, exposure to ionizing radiation, heavy-metal ions or oxidized lipoproteins may initiate various signaling cascades leading to apoptotic cell death and neurodegenerative disorders. Among the various reactive oxygen species (ROS) generated in the living organism, hydroxyl and peroxynitrite are the most potent and can damage proteins, lipids and nucleic acids. It appears that some natural antioxidants (tocopherol, ascorbic acid and glutathione) and defense enzyme systems (superoxide dismutase, catalase and glutathione peroxidase) may provide some protection against oxidative damage. Recent findings indicate several polyphenols and antioxidant drugs (probucol, seligilline) are effective in protecting the cells from ROS attack. Further development of these antioxidant molecules may be of value in preventing the development of neurodegenerative diseases.

Animals↗
PubMedDate not supplied

Ethanol and oxidative mechanisms in the brain.

There is strong evidence showing that chronic and excessive ethanol consumption may enhance oxidative damage to neurons and result in cell death. Although not yet well understood, ethanol may enhance ROS production in brain through a number of pathways including increased generation of hydroxyethyl radicals, induction of CYP2E1, alteration of the cytokine signaling pathways for induction of iNOS and sPLA(2), and production of prostanoids through the PLA(2)/COX pathways. Since many neurodegenerative diseases are also associated with oxidative and inflammatory mechanisms in the brain, it would be important to find out whether chronic and excessive ethanol consumption may exacerbate the progression of these diseases. There is evidence that the polyphenolic antioxidants, especially those extracted from grape skin and seed, may protect the brain from neuronal damage due to chronic ethanol administration. Among the polyphenols from grapes, resveratrol seems to have unique antioxidant properties. The possible use of this compound as a therapeutic agent to ameliorate neurodegenerative processes should be further explored.

Alcoholism↗
PubMedDate not supplied

Chronic ethanol consumption alters transbilayer distribution of phosphatidylcholine in erythrocytes of Sinclair (S-1) miniature swine.

Effects of chronic ethanol consumption on transbilayer distribution of phospholipids in the exofacial and cytofacial leaflets of erythrocytes from chronic ethanol-consuming Sinclair (S-1) miniature swine were examined. Phosphatidylcholine (PC) was predominantly located in the exofacial leaflet and phosphatidylethanolamine (PE) and phosphatidylserine (PS) located primarily in the cytofacial leaflet. Chronic ethanol consumption significantly increased PC content in the exofacial leaflet without changing bulk membrane PC composition. Ethanol-induced changes in PC distribution were specific for PC and not detected in PE or PS. There was also a significant decrease in sphingomyelin in the ethanol group. Sphingomyelin is primarily an exofacial phospholipid. The specific ethanol-induced changes in the exofacial leaflet are consistent with recent studies showing that the exofacial membrane leaflet is more susceptible to effects of ethanol as compared to the cytofacial leaflet. Such specificity of action provides a new way of viewing how ethanol alters membrane structure and function.

Animals↗
PubMedDate not supplied

Ethanol and membrane lipids.

Although ethanol is known to exert its primary mode of action on the central nervous system, the exact molecular interaction underlying the behavioral and physiological manifestations of alcohol intoxication has not been elucidated. Chronic ethanol administration results in changes in organ functions. These changes are reflective of the adaptive mechanisms in response to the acute effects of ethanol. Biophysical studies have shown that ethanol in vitro disorders the membrane and perturbs the fine structural arrangement of the membrane lipids. In the chronic state, these membranes develop resistance to the disordering effects. Tolerance development is also accompanied by biochemical changes. Although ethanol-induced changes in membrane lipids have been implicated in both biophysical and biochemical studies, measurements of membrane lipids, such as cholesterol content, fatty acid unsaturation, phospholipid distribution, and ganglioside profiles, have not produced conclusive evidence that any of these parameters are directly involved in the action of ethanol. On the other hand, there is increasing evidence indicating that although ethanol in vitro produces a membrane-fluidizing effect, the chronic response to this effect is not to change the membrane bulk lipid composition. Instead, changes in membrane lipids may pertain to small metabolically active pools located in certain subcellular fractions. Most likely, these lipids are involved in important membrane functions. For example, the increase in PS in brain plasma membranes may provide an explanation for the adaptive increase in synaptic membrane ion transport activity, especially (Na,K)-ATPase. There is also evidence that the lipid pool involved in the deacylation-reacylation mechanism (i.e., PI and PC with 20:4 groups) is altered after ethanol administration. An increase in metabolic turnover of these phospholipid pools may have important implications for the membrane functional changes. Obviously, there are other lipid-metabolizing enzyme systems that may exert similar effects but have not yet been investigated in detail. From the results of these studies, it is concluded that the multiple actions of ethanol are associated with changes in enzymic systems important in the functional expression of the membranes.

Animals↗