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M Sarasua

Publications and source records attributed to M Sarasua.

5 recordsLinked to original sources
PubMed1991

Relationship between membrane fluidity and adrenoceptor binding in depression.

Membrane fluidity and adrenergic receptor binding were studied in platelets of depressed patients before and during treatment with desmethylimipramine to investigate the relationship between the alpha 2-adrenergic receptor and its membrane environment in depression. Most samples came from a previous study in which we observed higher 3H-para-aminoclonidine (3H-PAC) binding in platelets from depressed patients compared to healthy subjects. Fluidity was measured by steady state diphenylhexatriene (DPH) anisotropy in both purified plasma membranes and in intracellular membrane preparations from platelets. No differences were observed in DPH membrane fluidity, per se, indicating that fluidity changes probably do not underlie either the increased alpha 2-adrenergic receptor binding in depression or the normalization of binding during treatment. However, lower intracellular membrane fluidity was correlated with higher binding to 3H-PAC site-1 in healthy subjects, but not in depressed patients. Thus, during depression there may be a disruption in the normal relationship between the adrenergic receptor and its membrane environment.

Adrenergic alpha-Agonists↗
PubMed1991

Lithium effects on dispersed bovine parathyroid cells grown in tissue culture.

It is not clear whether hypercalcemia and hyperparathyroidism associated with lithium therapy are the result of an unmasking of preexisting disease or a direct effect of lithium on the parathyroid glands. To investigate this phenomenon, parathyroid hormone (PTH) secretion and cytosolic calcium concentrations [( Ca]i) were measured in normal and lithium-treated dispersed bovine parathyroid cells grown in tissue culture and incubated with varying concentrations of extracellular calcium [( Ca]e) (0.5 to 2.5 mmol/L). Results indicate that lithium has two effects on parathyroid secretory response: (1) a decrease in low calcium-stimulated PTH release and (2) a potentiation of PTH release at physiologic concentrations of extracellular calcium. [Ca]i was assessed by use of fura-2, a calcium-sensitive fluorescent indicator. Resting [Ca]i levels were unaffected by lithium (103 +/- 13 nmol/L in controls vs 101 +/- 5 nmol/l in lithium-treated cells, mean +/- SE). Subsequent increases in [Ca]i in response to increases in [Ca]e were significantly less in lithium-treated cells, with no difference at maximal [Ca]e. Increases in [Ca]i in response to a submaximal concentration of extracellular magnesium were also blunted in cells pretreated with lithium. In conclusion, our data suggest that, at physiologic calcium concentrations, lithium decreases parathyroid cell sensitivity to changes in [Ca]e, reducing [Ca]i levels and increasing PTH secretory response.

Animals↗
PubMed1990

Mechanisms of oxygen free radical-induced calcium overload in endothelial cells.

Unregulated increases in intracellular calcium levels with subsequent cytoskeletal disruption have been implicated in tissue injury caused by oxygen free radicals (OFRs). The purpose of these experiments was to study the kinetics of free intracellular calcium in endothelial cells on exposure to exogenous OFRs and investigate the mechanisms of this altered homeostasis. Monolayers of endothelial cells were labeled with a calcium-sensitive probe and exposed to exogenous OFRs generated with hypoxanthine and xanthine oxidase. Intracellular calcium changes were monitored dynamically by continuous measurement of fluorescence with a spectrofluorometer. A sustained rise in intracellular Ca++ levels reaching a peak at 5 minutes was observed. This effect was blocked by superoxide dismutase and catalase. Removal of calcium from the medium or chelating the extracellular calcium with ethyleneglycoldiamine tetraacetate significantly blunted the response to OFRs (p less than 0.05). Preincubation of the cells with verapamil did not alter the observed increase in Ca++i. Addition of another divalent cation (Mn++) to the medium partially blocked the rise in calcium levels (p less than 0.05). Membrane potential measurements assessed fluorometrically, with the fluorescent probe bisoxonol, demonstrate a transient hyperpolarization of the plasma membrane on exposure to OFRs, temporally associated with the rise in [Ca++]i. In summary, OFRs cause an increase of intracellular calcium in endothelial cells. This response is dependent on extracellular calcium and independent of voltage-sensitive calcium channels. The increase can be partially inhibited by other divalent cations. These results suggest that the transformation of the plasma membrane components (lipid peroxidation and cross-linking of proteins) caused by OFRs may produce cation ionophores.

Animals↗
PubMedDate not supplied

Intracellular membranes are more fluid in platelets of Alzheimer's disease patients.

We studied 12 patients with probable Alzheimer's disease versus age- and sex-matched healthy control subjects. Platelets were subfractionated into intracellular membranes and plasma membranes, and steady-state anisotropy of diphenylhexatriene was measured on the preparations as an index of membrane fluidity. Fluidity was higher in intracellular membranes from platelets of Alzheimer's patients compared to controls (P = 0.016). However, no difference was observed in purified plasma membrane's fluidity from the same patients versus controls. Neither the platelet counts, platelet volumes, percent of larger platelets, nor the amount of internal membrane protein per platelet were different between groups. There was no correlation between intracellular membrane anisotropy and severity of dementia as measured on the Mini-Mental State Exam. The results extend previous studies suggesting that there is an intracellular membrane alteration in platelets in Alzheimer's disease.

Aged↗