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J A Holguín

Publications and source records attributed to J A Holguín.

13 recordsLinked to original sources
PubMed1991

Calcium transport sensitive to ruthenium red in cytochrome oxidase vesicles reconstituted with mitochondrial proteins.

We describe a calcium transport that is sensitive to ruthenium red in liposomes reconstituted with mitochondrial extracts. This system is able to build an internally negative membrane potential, which allows the electrogenic influx of Ca2+ and Sr2+. Proteins with molecular weights higher than 35 kDa were incorporated to the vesicles, and enhanced the accumulation of the cation in an energy-dependent fashion.

Animals↗
PubMed1991

Protective behavior of captopril on Hg(++)-induced toxicity on kidney mitochondria. In vivo and in vitro experiments.

Mercurials are known to induce morphological and functional modifications in kidney mitochondria. In this work we studied in vitro and in vivo the protective effect of captopril on the deleterious effect of Hg(++)-induced nonspecific membrane permeability changes to Ca++ and membrane de-energization. In vivo the administration of captopril prevented the toxic effects of mercury poisoning on membrane permeability, oxidative phosphorylation and Ca++ homeostasis. Moreover, captopril preserves kidney tissue morphology from Hg(++)-induced damage. The protective effect of captopril is most likely related to the existence of a sulfhydryl group in the drug.

Animals↗
PubMed1988

Ionophoretic and inhibitory action of the analgesic, diflunisal, on sarcoplasmic reticulum.

Diflunisal decreased the ATP-dependent transport rate and calcium accumulation by the sarcoplasmic reticulum. Inhibition of calcium transport by diflunisal was pH dependent, and a pKa of 6.7 to 6.9 was observed for the carboxylic acid group. In sealed sarcoplasmic reticulum vesicles, diflunisal at concentrations below 1 mM increased the rate of Ca2+-dependent hydrolysis of ATP; above 1 mM, the Ca2+-ATPase activity was inhibited. In purified Ca2+-ATPase, diflunisal acted only as an inhibitor. Methylation of the phenolic group of diflunisal eliminated both its analgesic and ionophoretic properties.

Animals↗
PubMed1988

Mitochondrial calcium release as induced by Hg2+.

Addition of Hg2+ to mitochondria of rat kidney induces efflux of intramitochondrial Ca2+. This reaction is accompanied by a diminution of the NAD(P)H/NAD(P) ratio and a decrease of the internal negative membrane potential. These effects were enhanced by dithiothreitol. The binding of mercuric ions to mitochondria saturates with a maximal binding of 9 nmol min-1 mg-1. The stoichiometry between Ca2+ released and Hg2+ bound showed that in the presence of dithiothreitol, the binding of approximately 1 nmol of Hg2+/mg of protein suffices to induce the release of the accumulated Ca2+. In the electrophoretic analysis of Hg-labeled mitochondrial proteins it was found that 203Hg2+ bound mainly to proteins that have molecular masses of 20 and 30 kDa. It is proposed that Hg2+-induced Ca2+ release is due to modification of--SH groups of these latter proteins.

Animals↗
PubMed1987

Metabolite transport in mitochondria as a function of osmolarity.

The effect of increasing sucrose concentrations on some mitochondrial functions was studied. The results showed that high osmolarity inhibits oxidative phosphorylation as well as ATPase activity and ATP-dependent delta phi formation as a consequence of adenine nucleotide translocase inhibition. It is also shown that high osmolarity does not affect delta phi formation and energy-dependent Ca2+ uptake as driven by succinate oxidation. Sodium dodecyl sulphate-polyacrylamide gel electrophoresis of membrane proteins showed a different reactivity to o-phenantroline/Cu2+ as function of osmolarity. It is proposed that high sucrose concentrations induce a collapse of the matrix compartment that results in a restricted diffusion of some metabolites.

Adenine Nucleotides↗
PubMed1986

Cooperative effects of Ca2+ and Sr2+ on sarcoplasmic reticulum adenosine triphosphatase.

The intrinsic fluorescence of purified Ca-ATPase from skeletal sarcoplasmic reticulum was measured in the presence of various concentrations of Ca2+, Sr2+, and Ba2+. Ca2+ and Sr2+ induce positive cooperative fluorescence enhancement, whereas Ba2+ does not change the fluorescence of ATPase. ATP does not seem to modify the kinetic parameters of Ca2+ and Sr2+ binding to ATPase. Nevertheless, p-nitrophenylphosphate hydrolysis, activated by Ca2+ or Sr2+ at various pHs, changes the affinity and the cooperative behavior for both cations and two components appear in the Hill plots. For Ca2+, nH of 1.6 to 3.5 were obtained, and 1.06 to 1.83 for Sr2+; nH changes of the second component seem to be pH dependent. Differences in the ratio between rates of Ca2+ transport and substrate hydrolysis by sarcoplasmic reticulum were found, i.e., two for ATP and one for p-nitrophenylphosphate. For Sr2+ this ratio was one for either ATP or p-nitrophenylphosphate.

Adenosine Triphosphate↗
PubMedDate not supplied

[A system of multidimensional behavior assessment. A scale for parents of children from 6 to 11 years of age. Colombian version].

INTRODUCTION: Behavioral Assessment System for Children (BASC) has demonstrated to be useful in the diagnosis of Attention Deficit Disorder (ADD). PATIENTS AND METHODS: A randomized sample of 120 children, 6 to 11-year-old, participants from the school of the city of Medellín, Colombia, was selected. The sample was stratified by sex and two socioeconomic status (SES). Parents were asked to answer the BASC Parent Rating Scale (PRS) 6-11, authorized Spanish version. RESULTS: Cronbach's alpha coefficient was 0.85 for the clinical scale (9 items). It was 0.75 for the Adaptive Scale (3 items). A scale designed with 4 items to assess ADD (hyperactivity, attention problems, aggression, and conduct problems) showed an alpha coefficient of 0.82. Male children scored significantly higher than female (ANOVA, p < 0.05) in hyperactivity, conduct problems, and atypicality. Children from low SES scored significantly higher than children of high SES on the most of clinical measures (p < 0.05) and lower on the three adaptive measures. Cluster analysis selecting six clusters found a prevalence of 61.6% for normal male children. In the total sample there were a 4% at risk of DDA type II (inattentive) and 14% at risk of DDA type I (combined). CONCLUSIONS: BASC PRS (6-11) showed reliability and validity to assessing the behavior in Spanish speaking Colombian children.

Attention Deficit Disorder with Hyperactivity↗
PubMedDate not supplied

[Autism of unknown aetiology].

OBJECTIVE: To review the origin, development and present state of autism, pervasive developmental disorders, progress in diagnostic tools, genetic advances, neurobiological bases, the possible causes of the increased prevalence of autism and the present treatment of the autistic condition. DEVELOPMENT: Autism is a neurobiological, life-long disorder characterized by abnormal social skills, deficient verbal and not verbal communication, symbolic and imaginative play, reasoning and related complex behaviour. Autism is 4 times more frequent in males. 70% are mentally retarded (30% mild and the rest moderate and severely retarded). Approximately 25% have convulsions and around 65% inspecific EGG abnormalities. Other conditions like ADHD, anxiety, depression may be associated. RMN: increased subarachnoidal spaces, moderate ventricular enlargement, 20% have megaloencephaly. PET and 31 PMMR show increased glucose metabolism and decreased functional links with association cortex. Mental level and language are the best prognostic indices for outcome. Pathology: reduced size of nerve cells in hippocampus, subiculum, sections of the amygdala, mamillary bodies, medial septal nucleus, decreased size of cerebellar hemispheres, posterior vermis, VI VII neocerebellar lobules. Evolution: in a small group about 9-31% live independently, 11-50% attend college. CONCLUSION: Autism is a disorder of multi-factorial origin with a genetic polygenic component and the influence of environmental elements. Treatment with risperidone improves symptoms.

Activities of Daily Living↗
PubMedDate not supplied

[Effects of acidosis and alkalosis on the sarcoplasmic reticulum of the heart].

Some functions of dog cardiac sarcoplasmic reticulum have been studied in acidosis and alkalosis conditions in a range of pH from 6.0 to 7.8. Intravesicular water content at pH 6.0 is 4.7 microliter per mg of protein and diminished to 4 microliter, (15%) at pH 8.0; this correlates with a drop of 13.5% in turbidity. Ca2+-dependent ATPase has an optimal pH of 7.2 and a specific activity of 580 nanomoles of ATP hydrolyzed/min/mg protein. The activity of Basal ATPase or Mg2+-dependent is insensitive to changes of pH. Maximal calcium uptake attains 45.1 +/- 1.4 nanomoles per mg protein between pH 6.0 and 6.6. The accumulated calcium diminished progressively when pH was raised. The rate of calcium transport in steady state shows an optimal pH of 6.7. The calcium transport kinetics constants shows that reticulum has a maximal affinity for calcium between pH 6.87 and 7.02. The maximal velocity for transport diminished progressively between pH 6.1 to 7.16. During the calcium transport process pH is changed from acid to alkaline and the accumulated calcium is release proportionally to the pH increment. This effect shows to be reversible. Calcium accumulation and ATP hydrolysis are uncoupled at pH values higher than 6.6 because to the increase in the rate of calcium release. Values of pK and number of protons per mg of protein that dissociates from ionizable residues are 6.53 and 0.68 respectively for calcium dependent ATPase; 7.09 and 0.60 for calcium transport and 7.41 and 0.39 for calcium release. We conclude that the rate of transport and affinity of cardiac sarcoplasmic reticulum for calcium are optimal between pH 6.8 and 7.0 that is the reported range of intracellular pH of normal cardiac tissue. The data are in close agreement with the fall of contractility in acidosis. It is proposed a calcium release pathway sensitive to pH and different from that of calcium pump, exclusively for entrance.

Acidosis↗
PubMedDate not supplied

[Changes induced by hypertonic solutions in the transportation of calcium by the cardiac reticular sarcoplasma].

In the sarcoplasmic reticulum of the myocardium, celular organell which function is to regulate the cytoplasmic concentration of calcium in contraction and relaxation, we have studied the effect of hypertonic solutions of sucrose between 1 and 6.96 times the normal tonicity in order to observe the behavior of the internal linked or free calcium of this structure, as well as to prove the hypothesis that hypertonic solutions encourage the calcium exit of the sarcoplasmatic reticulum with the resulting signs of contractures. The following results were obtained: 1. The ATP hydrolisis and calcium transport rate are 14% and 90% respectively of the maximum speeds of 10(-5) M in calcium, while for concentrations of 10(-7) M or ess of the said cation, the transport rates and the ATPase do not reach 5% of the maximum values. 2. Between 1 and 2.54 times of the normal tonicity the calcium uptake remains between 400 and 500 nmoles of calcium/mg protein/min, the transported amount of calcium varies between 14 and 16 nmoles/mg protein and the rate of the ATP hydrolysis increases a 37% to 0.4 M in sucrose. 3. Between 0.4 and 1.2 M in sucrose of 2.54 to 6.96 times the isotonicity, the calcium transport rate velocity as well as the ATP hydrolisis are strongly inhibited. The vesicles volume minimizes and the amount of linked calcium remains within the control values, proving that the capacity of linking this cathion is independent from sarcoplasmic reticulum volume. These results show that the sarcoplasmic reticulum is involved in the contractures induced by hypertonic solutions in intact cells, since the osmolarity increase produces changes of volume which results in a decrease of the calcium transportation velocity or in an increase of the exit of said cathion.

Animals↗
PubMedDate not supplied

[Mechanism of the antiarrhythmic effect of inorganic phosphates in digitalis poisoning].

THe synergistic effects between calcium and the therapeutic and toxic actions of the cardiac glycosides have suggested that a way of treating digitalis intoxication could be through a decrease in free plasma calcium. In 1966, Burckhardt and La-Due published a study based on the inverse relationship that exists between plasma phosphates and calcium. It was shown then that potassium phosphate had a pronounced antiarrhythmic effect on digitalis induced arrhythmias. The use of potassium phosphate for this study prevented the analysis of the role of the phosphates in these effects, since the actions of potassium in digitalis toxicity precluded any conclusion. The purpose of the present paper is to study the effect of phosphates on digitalis intoxication and its possible mechanism of action. The results obtained demonstrated: 1) Phosphates have a marked antiarrhythmic effect in digitalis induced arrhythmias. 2) This effect is due to a decrease in free plasma calcium. 3) The lowering of this calcium pool occurs in the blood and is not mediated by hormonal or renal mechanisms. 4) The ions that disappear from the free calcium pool do not precipitate. 5) The use of phosphates could be useful in the treatment of some clinical cases of advanced digitalis intoxication.

Animals↗
PubMedDate not supplied

[Mechanism of the decrease in free plasma calcium produced by the administration of inorganic phosphates].

The preceding paper (published in the issue) demonstrated that the administration of sodium phosphates exerted a marked antiarrhythmic effect on several models of digitalis intoxication; this action being due to a decrease in the free calcium fraction. THe purpose of the present paper is to analyze the effects that several concentrations of phosphates have on the different calcium fractions and determine the fate of the ions that are disappearing from the calcium pool. This study was done using two models of digitalis intoxication, one in the intact dog and the other in the heart-lung preparation and two protocols in which the experiments were carried out using blood in vitro. The results show: 1) the administration of phosphates into the intact dog produces a small decrease in the total calcium content of plasma and blood. 2) the increase in phosphate concentration runs parallel to an important decrease in free calcium. 3) In the heart-lung preparation, phosphate administration markedly decreases free calcium but does not lower total calcium in plasma or blood. 4) An increase in phosphate concentration of plasma in in vitro conditions does not alter total calcium and decreases free calcium in a linear relationship with the levels of phosphates. 5) A fraction of the phosphates added to the plasma and the ions that are disappearing from the free calcium pool are binding to a plasmatic macromolecule (most probably a protein) which prevents them from precipitating.

Animals↗