Biomedical subjects

L Boquist

Publications and source records attributed to L Boquist.

170 records · Page 10Linked to original sources

PubMedDate not supplied

Hyperglycemia following p-hydroxymercuribenzoate administration to mice.

p-Hydroxymercuribenzoate (PMB) administration to fed mice induced transient hyperglycemia of a few hours' duration, and an increase in mitochondrial volume and pyroantimonate precipitation in the cytoplasmic ground substance of the pancreatic islet B-cells, whereas the secretory granules were unaffected. No significant blood glucose elevation or any obvious structural alterations were observed in starved mice treated with PMB. The serum inorganic phosphate concentration was unaffected in fed mice but decreased in starved mice 10 min after PMB injection, and increased in both fed and starved mice 2 h following PMB treatment, whereas the hydrogen ion concentration was increased in both fed and straved mice 10 min after PMB administration. Mitochondrial and ionic alterations, and possible inhibited insulin release may play a role in the development of hyperglycemia in PMB-treated mice.

Animals↗

PubMedDate not supplied

Effect of alloxan on the transport of dicarboxylate, tricarboxylate, pyruvate and glutamate in isolated mouse liver mitochondria.

The effect of alloxan on anion transport in isolated mouse liver mitochondria was studied with the swelling technique. Mitochondria pre-incubated with alloxan exhibited partial inhibition of the transport of malate, citrate, pyruvate and glutamate. 2n-butylmalonate caused complete inhibition of malate transport, and the translocation of citrate was completely blocked by 1,2,3-benzenetricarboxylate, while N-ethylmaleimide inhibited glutamate transport partially. The observation that alloxan inhibits different mitochondrial anion transport mechanisms emphasizes that the drug profoundly affects mitochondrial function.

Alloxan↗

PubMedDate not supplied

Factors affecting the inhibition by alloxan, and effect of streptozotocin on phosphate transport in isolated mouse mitochondria.

The swelling technique evidenced inhibition of Pi transport in isolated mouse liver mitochondria by 1 mM or higher concentration of alloxan inhibition was found under the following conditions: preincubation at 4 degrees C, or pretreatment with Pi, glucagon, succinate, malate or pyruvate. Complete protection was observed in isolated mitochondria from mice injected with glucagon. No protection was seen under the following conditions: preincubation at 37 degrees C, addition of microsomes, or pretreatment with insulin or glucagon in the presence of glucagon antibodies. So-called light and heavy mitochondria were as sensitive to alloxan as those obtained with the routine technique. Alloxanic acid had no effect, and addition of cysteine or glutathione abolished the inhibition by alloxan. Alloxan inhibited Pi transport also in isolated lung mitochondria. The findings suggest a direct action of alloxan on mitochondrial Pi transport which is affected by the energetic state. A relationship seems to exist between protection against alloxan toxicity in vivo and protection under the present experimental conditions.

Alloxan↗

PubMedDate not supplied

p-Hydroxymercuribenzoate-induced hyperglycemia: influence of pre- and post-treatment with L-leucine, tolbutamide, D-mannoheptulose, insulin and alloxan.

The aims were to see whether p-hydroxymercuribenzoate (PMB) administration affects the serum insulin concentration in mice in vivo, whether the transitory hyperglycemia induced in fed mice by treatment with PMB is affected by L-leucine, tolbutamide, D-mannoheptulose or insulin, and whether PMB affects the B-cell toxicity of alloxan. A significant decrease in the serum insulin concentration was found 1 and 2 h following PMB injection in fed and starved mice. PMB-induced hyperglycemia was abolished by pre-treatment with L-leucine and tolbutamide, but not by pre-treatment with D-mannoheptulose, or by post-treatment with insulin. Pre-treatment of fed mice with PMB caused potentiation of the initial hyperglycemia following alloxan, but inhibited the second hyperglycemic phase. These findings indicate that PMB treatment of mice has a transient inhibitory influence upon insulin secretion, and protects against the development of alloxan diabetes.

Alloxan↗

PubMedDate not supplied

Mitochondrial changes and associated alterations induced in mice by streptozotocin administered in vivo and in vitro.

Isolated mouse liver mitochondria incubated with streptozotocin showed decreased rate and extent of Ca2+ uptake, and, dependent on the concentration of streptozotocin and the addition of alpha-ketoglutarate, glutamate, fluorocitrate or guanosine 5'-triphosphate, the retention of Ca2+ was either increased or decreased. Similar observations were made in liver mitochondria incubated with succinyl-CoA. In mitochondria isolated from the kidneys and islets of mice injected with streptozotocin, with and without additional injections of glucose and/or glucagon, the rate and extent of Ca2+ uptake were reduced and the release of accumulated Ca2+ was stimulated. Electron microscopy and X-ray microanalysis showed dislocation of Ca2+-containing precipitates from the mitochondria to the cytosol, and stereology disclosed increased mitochondrial volume in the B cells of streptozotocin-treated mice. State 3 and state 4 respiration with NAD-linked substrates was inhibited, but succinate oxidation was unaffected, in mitochondria isolated from the kidneys of mice treated with streptozotocin. In the kidneys of streptozotocin-injected mice, the concentration of succinyl-CoA was increased, that of citrate and guanosine 5'-triphosphate was decreased, that of glucose 6-phosphate, fructose 6-phosphate and fructose 1,6-diphosphate was unaffected, and the metabolite concentration ratios suggested increased mitochondrial [NAD+]/[NADH] ratio and decreased cytoplasmic [NAD+]/[NADH] ratio. It is suggested as a new hypothesis that the cytotoxicity and the diabetogenicity of streptozotocin are dependent on inhibited citric acid cycle enzyme activity (primarily that of succinyl-CoA synthetase and citrate synthetase) with altered metabolite concentrations, leading to impairment of the mitochondrial uptake of Ca2+ and the activation of the pyruvate, isocitrate and alpha-ketoglutarate dehydrogenases.

Acyl Coenzyme A↗

PubMedDate not supplied

Clinical and histopathological features of a large parapharyngeal neurilemmoma located at the base of the tongue.

Neurilemmomas of the tongue have only been sporadically reported in the literature. Vague symptoms and limited knowledge of this kind of tumor may result in long delays before diagnosis and treatment. The rarity of the lesion in this area is the main reason why we report this case of neurilemmoma. After observation of a mass in the tongue, magnetic resonance imaging showed a large tumor with central necrosis localized to the base of the tongue. Needle electromyography disclosed no nerve lesion. Fine-needle aspiration cytology was negative, whereas biopsy revealed a neurilemmoma. The tumor was surgically removed, and histopathology, including immunohistochemistry, of the resected specimen disclosed the typical neurilemmoma. The postoperative course was uneventful.

Adult↗

PubMedDate not supplied

Alloxan diabetogenicity: determinants of potentiation, protection and B-cell selectivity.

Compounds with a reported in vivo and in vitro effect on the diabetogenicity of alloxan were studied with regard to the uptake of calcium in mouse islet mitochondria, with the aim of obtaining information on the susceptibility and selectivity of alloxan toxicity. A strong correlation was found between the uptake of calcium in mouse islet mitochondria, which is believed to be associated with the activation of oxidative enzymes involved in energy production and secretion of insulin, and the protection afforded by the injection of D-glucose, D-mannose, L-leucine and glucagon, and by the in vitro administration of cyclic AMP, L-glutamine and L-leucine. The effect of D-glucose was abolished by D-mannoheptulose. A correlation was also seen between reduced mitochondrial uptake of calcium and the potentiation of alloxan cytotoxicity afforded by 1.25-dihydroxycholecalciferol, methylene blue and menadione. The observations suggest an association between functional activity and alloxan cytotoxicity. The selectivity of the cytotoxic action of alloxan is believed to be dependent on a reduced mitochondrial uptake of calcium and an associated reduction of the energy production at low functional activity in the B-cells (e.g. in starvation which is well-known to potentiate the alloxan effect).

Alloxan↗

PubMedDate not supplied

Study of isolated mitochondria incubated with labelled and non-labelled alloxan, with regard to intramitochondrial concentrations of reduced glutathione and inorganic phosphate.

Isotope technique and determination of the intramitochondrial concentration of GSH were used with the aim of studying the uptake of alloxan in isolated mouse mitochondria. A significantly decreased concentration of GSH was observed in mitochondria from liver and pancreas incubated with alloxan. This effect was significantly more marked in mitochondria depleted of Pi. Increased radioactivity was found in isolated mitochondria from liver, exocrine pancreas and endocrine pancreas incubated with 14C-2-alloxan. Even this effect was significantly more marked in Pi depleted mitochondria. Isolated liver mitochondria of the KsJ-strain of C57BL-mice possessed a significantly lower concentration of endogenous Pi than those of the 6J-strain. The findings support the view that alloxan can pass across the inner mitochondrial membrane, and suggest that the intramitochondrial concentration of Pi is one of the factors which has an influence on the uptake of alloxan in isolated mouse mitochondria.

2,4-Dinitrophenol↗