Mitochondrial damage in galactosamine-induced liver intoxication in rats

Mitichondria isolated from livers of rats which received D-galactosamine (375 mg/kg body wt., four times) demonstrated a marked decrease in respiratory control ratios, the ADP/O ratios, and state 3 respiration rates and an increase in state 4 respiration rates. The aberration was profound with site I being altered prior to sites II and III. Quantitation of phospholipids revealed a reduction of total phospholipids per mg protein with decreases in phosphatidylcholine and phosphatidylethanolamine contents. Caldiolipin was the only phospholipid which remained unaltered. Fatty acid composition was altered in these phospholipids; caldiolipin was altered most severely, showing reductions in linoleic and arachidonic acids, and an elevation in saturated fatty acids and in some other small components of fatty acids. In phosphatidylethanolamine, palmitic acid decreased, whereas stearic and docosahexonoic acids increased. These changes were smaller in phosphatidylcholine fatty acids. These mitochondria were also characterized by an altered composition in high molecular weight polypeptide components. By experiments with normal mitochondria in vitro, galactosamine, but not other aminohexoses, was proved to be an uncoupling agent of the oxidative phosphorylation system. Electron microscopic observation demonstrated that both in vivo and in vitro treatments with galactosamine induced marked disorganization of mitochondral structures. These results suggest that mitochondrial damage is also included in galactosamine-induced hepatic lesion.     

Differences in the Optical Response of MSU and CPP Crystals During Magnetic Orientation: Possibility of Diagnosing Gout and Pseudogout

Pseudogout is crystalline arthritis. It has a similar clinical picture to that of gout, and it is difficult to distinguish the two diseases using conventional analysis methods. However, it is important to identify the different crystals responsible for these two cases because the treatment strategies are different. In a previous study, we reported magnetic orientation of monosodium urate (MSU) crystals, which are the causative agent of gout, at the permanent magnet level. In this study, we investigated the effect of an applied magnetic field on calcium pyrophosphate (CPP) crystals, which are the causative agent of pseudogout, and the difference in the magnetic responses of CPP and MSU crystals. We found that the CPP crystals were oriented in a magnetic field on milli-Tesla order because of the anisotropy of the diamagnetic susceptibility. In addition, the CPP crystals exhibited different anisotropic magnetic properties from those of MSU crystals, which led to a characteristic difference between the orientations of the two crystals. That is, we found that the causative agents of gout and pseudogout responded differently to a magnetic field. This report suggests that the discrimination between CPP and MSU by optical measurements is possible by application of magnetic fields appropriately. © 2023 Bioelectromagnetics Society.     

Continuous fluorometric assay of Ca2+ transport by liposomes with Quin 2 entrapped: effect of phospholipase A2 and unsaturated long-chain fatty acids

The amount of free calcium in the cytoplasm is important in stimulation coupled with a number of cellular functions. The putative ionophoretic action of membrane lipid metabolites on Ca2+ offers convenient explanation of the stimulation-coupled mobilization of cytoplasmic Ca2+. To analyze the ionophoretic action of the lipid metabolites, we devised a sensitive method to study Ca2+ transport that uses liposome-entrapped Quin 2. A calcium ionophore, A23187, increased the fluorescence intensity of the Ca2+-Quin 2 complex as a function of Ca2+ transport into liposomes. A similar Ca2+ flux into the liposomes was induced by phospholipase A2 (PLA2) and by various long-chain fatty acids in liposomes that consist of phospholipids containing unsaturated fatty acids. The potencies of the fatty acids for Ca2+ transport is inversely correlated with their melting points. The oxidized products of the unsaturated fatty acids increased the Ca2+ and nonspecific permeability of the biological membranes. These results suggest that stimulation-coupled PLA2 activation might mediates the mobilization of cytoplasmic Ca2+.     

Simultaneous administration of TRH and sulpiride caused additive but not synergistic PRL responses in normal subjects.

In order to study the mode of action of TRH and sulpiride in man, we administered TRH (500 micrograms, iv) and sulpiride (DA D2 receptor antagonist, 100 mg, im) simultaneously to 6 normal females (20-21 yr). Normal females showed significantly greater PRL increments and AUC in response to the combined administration compared to a single administration of each agent (P < 0.05-0.01), while the increment and AUC in response to the combination did not exceed the sum of those responses to a single administration. In contrast, the combined administration of TRH and sulpiride did not elicit an enhanced response of plasma TSH. These results indicate that the sites of action of TRH and sulpiride might be different from each other, and these agents work additively with no interaction in human lactotrophs.     

Some clinical and epizootological observations of infectious sialoadenitis in rats.

Epizootological and clinical observation was made of infectious sialoadenitis ocurring at a rat facility. The disease occurred mostly among animals 8 to 64 weeks of age without specific relevance with sex and age, and clinical signs disappeared within 5 days after the onset. Morbidity rates and duration of epizootics ranged from 13 to 100% and from 5 to 32 days, respectively. Most rats having severe clinical signs of sialoadenitis showed decrease in food uptake, body weight loss and remarkable disorders of estrous cycles.     

Carbohydrate-Dependent Biological Activities of Glycosylated Human Interferon-β on Human Hepatoblastoma Cells In Vitro

To evaluate the relationship between the sugar chain structure and biological activity, fibroblast-derived glycosylated human interferon-β, Chinese hamster ovary cell-derived glycosylated recombinant human interferon-β and Escherichia coli-derived unglycosylated recombinant human interferon-β were evaluated using human hepatoblastoma cells in vitro. Native fibroblast interferon-β expressed more cell-growth inhibitory action, 2′5′-oligoadenylate synthetase induction, and the inhibition of hepatitis B virus DNA replication than its asialoform and two recombinant interferon-βs. These results showed that the sugar chain structure of human interferon-β affects its biological activity on human hepatoblastoma cells.