• Archives of Pharmacal Research
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• v.22 no.3
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• pp.317-319
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• 1999

Anticomplementary activity of hederagenin and related saponins isolated from Dipsacus asper was investigated in vitro. HN saponin F (3) was most potent with $IC_{50}$ value of$ 3.7{\times}10^{-5} M$ followed by 3-O-${\beta}-D-glucopyranosyl-(1{\rightarrow} 3)-{\alpha}-L-rhamnopyranosyl-(1{\rightarrow}2)-{\beta}-L-arabinopyranosyl$ hederagenin $28-O-{\beta}-D-glucopyranosyl-(1{\rightarrow}6)-beta$-D-glucopyrano side (8), $3-O-{\beta}-L-arabinopyranosyl$ hederagenin $28-O-{\beta}-D-glucopyranosyl-(1{\rightarrow}6)-{\beta}-D-glucopyranoside$ (5), dipsacus saponin A (4), and hederagenin (1) on the classical pathway (CP) of complement system, while the saponins 3-5 did not show the inhibition of hemolysis and rather increase the hemolysis on the alternative pathway (AP). However, all of C-3 monodesmosides [prosapogenin CP (2), dipsacus saponin B (6), and dipsacus saponin C (7)] evoked hemolysis directly on the erythrocytes.

• Archives of Pharmacal Research
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• v.28 no.12
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• pp.1400-1404
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• 2005

The aim of the present study was to develop the aqueous parenteral formulation containing propofol using o/w microemulsion systems. Propofol itself was chosen as the oil phase and its content was fixed to 1$\%$, w/w. Pseudoternary phase diagrams were constructed to obtain the concentration range of surfactant and cosurfacatnt and the optimum ratio between them for microemulsion formation. Consequently, the suitability of the chosen microemulsion system as a parenteral formulation was evaluated from the stability and hemolysis tests on that. Among the surfactants and cosurfactants screened, the mixture of Solutol HS 15-ethyl alcohol (5/1) showed the largest o/w mocroemulsion region in the phase diagram. When 1 $\%$ (w/w) of propofol was solubilized with 8$\%$ (w/w) of Solutol $HS^{circledR}$??? 15-ethyl alcohol (5/1), the average droplet size (150 nm) and the content of propofol in the systems were not significantly changed at 40$^{circ}C$ for 8 weeks. The hemolysis test showed that this formulation was nontoxic to red blood cells. In conclusion, propofol was successfully solubilized with the o/w microemulsion systems.

• Journal of The Korean Society of Clinical Toxicology
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• v.19 no.1
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• pp.59-63
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• 2021

Copper sulfate is widely used as a fungicide and pesticide. Acute copper sulfate poisoning is rare but potentially lethal in severe cases. Copper sulfate can lead to cellular damage of red blood cells, hepatocytes, and myocytes. Toxic effects include intravascular hemolysis, acute tubular necrosis and, rhabdomyolysis. A 76-year-old man presented with vomiting and epigastric pain. He had ingested a copper-containing fungicide (about 13.5 g of copper sulfate) while attempting suicide 2 hours prior to presentation. From day 3 at the hospital, laboratory findings suggesting intravascular hemolysis were noted with increased serum creatinine level. He was treated with a chelating agent, dimercaptosuccinic acid (succimer). His anemia and acute kidney injury gradually resolved with a 19-day regimen of succimer. Our case suggests that succimer can be used for copper sulfate poisoning when other chelating agents are not available.

• Journal of Pharmacopuncture
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• v.25 no.4
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• pp.344-353
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• 2022

Objectives: Auraptene is the most abundant natural prenyloxycoumarin. Recent studies have shown that it has multiple biological and therapeutic properties, including antioxidant properties. Erythrocytes are constantly subjected to oxidative damage that can affect proteins and lipids within the erythrocyte membrane and lead to some hemoglobinopathies. Due to the lack of sufficient information about the antioxidant effects of auraptene on erythrocytes, this study intended to evaluate the potential of this compound in protecting radical-induced erythrocytes damages. Methods: The antioxidant activity of auraptene was measured based on DPPH and FRAP assays. Notably, oxidative hemolysis of human erythrocytes was used as a model to study the ability of auraptene to protect biological membranes from free radical-induced damage. Also, the effects of auraptene in different concentrations (25-400 µM) on AAPH-induced lipid/protein peroxidation, glutathione (GSH) content and morphological changes of erythrocytes were determined. Results: Oxidative hemolysis and lipid/protein peroxidation of erythrocytes were significantly suppressed by auraptene in a time and concentration-dependent manner. Auraptene prevented the depletion of the cytosolic antioxidant GSH in erythrocytes. Furthermore, it inhibited lipid and protein peroxidation in a time and concentration-dependent manner. Likewise, FESEM results demonstrated that auraptene reduced AAPH-induced morphological changes in erythrocytes. Conclusion: Auraptene efficiently protects human erythrocytes against free radicals. Therefore, it can be a potent candidate for treating oxidative stress-related diseases.

• Journal of Applied Biological Chemistry
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• v.52 no.1
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• pp.28-32
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• 2009

The bacterial toxin, tolaasin, causes brown blotch disease on the cultivated mushrooms by collapsing fungal and fruiting body structure of mushroom. Cytotoxicity of tolaasin was evaluated by measuring hemolytic activity because tolaasins form membrane pores on the red blood cells and destroy cell structure. While we investigated the inhibitions of hemolytic activity of tolaasin by $Zn^{2+}$ and $Cd^{2+}$, we found that $Ni^{2+}$ is another antagonist to block the toxicity of tolaasin. $Ni^{2+}$ inhibited the tolaasin-induced hemolysis in a dose-dependent manner and its Ki value was $\sim10$ mM, implying that the inhibitory effect of $Ni^{2+}$ is stronger than that of $Cd^{2+}$. The hemolytic activity was completely inhibited by $Ni^{2+}$ at the concentration higher than 50 mM. The effect of $Ni^{2+}$ was reversible since it was removed by the addition of EDTA. When the tolaasin-induced hemolysis was suppressed by the addition of 20 mM $Ni^{2+}$, the subsequent addition of EDIA immediately initiated the hemolysis. Although the mechanism of $Ni^{2+}$ -induced inhibition on tolaasin toxicity is not known, $Ni^{2+}$ could inhibit any of fallowing processes of tolaasin action, membrane binding, molecular multimerization, pore formation, and massive ion transport through the membrane pore. Our results indicate that $Ni^{2+}$ inhibits the pore activity of tolaasin, the last step of the toxic process.

• Journal of Korean Academy of Nursing
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• v.42 no.3
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• pp.443-451
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• 2012

Purpose: This study was done to compare the rates of hemolysis and repeated sampling in blood samples obtained by a syringe needle versus a vacuum tube needle. Methods: A randomized, prospective study was used to evaluate the differences between the two blood sampling methods. The study group consisted of patients seen in the emergency department (ED) for blood sampling to determine electrolyte level. ED patients were randomly assigned to either the syringe group or the vacuum tube group. All blood samples were collected by experienced ED nurses and hemolysis was determined by experienced laboratory technologists. Data were analyzed using Fisher's exact test and binary logistic regression. Results: One hundred forty-five valid samples were collected (74 in the syringe group versus 71 in the vacuum tube group). 5 of 74 (6.8%) blood samples in the syringe group and 8 of 71 (11.3%) in the vacuum tube group hemolyzed. Repeated blood sampling occurred for 2 of 74 (2.7%) and 3 of 71 (4.2%) in each group respectively. There were no significant differences in rates of hemolysis and repeated sampling between two groups (B=1.97, p=.204; B=2.36, p=.345). Conclusion: Venipuncture with syringe needles can be recommended for ED nurses to obtain blood samples.

• Journal of Applied Biological Chemistry
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• v.61 no.3
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• pp.213-217
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• 2018

Tolaasin secreted by Pseudomonas tolaasii is a peptide toxin and causes brown blotch disease on the cultivated mushrooms by collapsing cellular and fruiting body structure. Toxicity of tolaasin was evaluated by measuring hemolytic activity because tolaasin molecules form membrane pores on the red blood cells and destroy cell membrane structure. In the previous studies, we found that tolaasin cytotoxicity was suppressed by $Zn^{2+}$ and $Ni^{2+}$. $Ni^{2+}$ inhibited the tolaasin-induced hemolysis in a dose-dependent manner and its $K_i$ value was 1.8 mM. The hemolytic activity was completely inhibited at the concentration higher than 10 mM. The inhibitory effect of $Zn^{2+}$ on tolaasin-induced hemolysis was increased in alkaline pH, while that of $Ni^{2+}$was not much dependent on pH. When the pH of buffer solution was increased from pH 7 to pH 9, the time for 50% hemolysis ($T_{50}$) was increased greatly by $100{\mu}M$ $Zn^{2+}$; however, it was slightly increased by 1 mM $Ni^{2+}$ at all pH values. When the synergistic effect of $Zn^{2+}$ and $Ni^{2+}$ on tolaasin-induced hemolysis was measured, it was not dependent on the pH of buffer solution. Molecular elucidation of the difference in pH-dependence of these two metal ions may contribute to understand the mechanism of tolaasin pore formation and cytotoxicity.

• Membrane Journal
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• v.15 no.3
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• pp.224-232
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• 2005

The use of the lung assist device (LAD) would be well suited for acute respiratory failure (ARF) patients, combining the simplicity of mechanical ventilation with the ability of extracoporeal membrane oxygenators (ECMO) to provide temporary relief for the natural lungs. This study's specific attention was focused on the effect of membrane vibration in the LAD. Quantitative experimental measurements were performed to evaluate the performance of the device, and to identify membrane vibration dependence on blood hemolysis. We tried to decide upon excited frequency band of limit hemolysis when blood hemolysis came to through a membrane vibration action. The excited frequency of the module type 5, consisted of 675 hollow fiber membranes, showed the maximum gas transfer rate. We concluded that the maximum oxygen transfer rate seemed to be caused by the occurrence of maximum amplitude and the transfer of vibration to hollow fiber membranes. It was excited up to $25{\pm}5$ Hz at each blood flow rate of module type 5. We found that this frequency became the 2nd mode resonance riequency of the flexible in blood flow. Blood hemolysis was low at the excited frequency of $25{\pm}5$ Hz. Therefore, we decided that limit hemolysis frequency of this LAD was $25{\pm}5$ Hz.

• The Korean Journal of Physiology
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• v.17 no.2
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• pp.135-142
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• 1983

$PGE_2$ and $PGF_{2{\alpha}}$ are known to act similarly in a number of animal tissues. They both facilitate regression of corpus luteum(Poyser, 1972; Fuch et al, 1974; Coudert et at, 1974) and stimulate contraction of uterine muscle (Laudanski et al, 1977; Porter et al, 1979; Hollingsworth et al, 1980). It is, however, not known whether these two prostaglandins exert similar actions in osmotic fragility of erythrocytes (Rasmussen et al, 1975) and $PGF_{2{\alpha}}$ alters conformation of membrane proteins (Meyers aud Swislocki, 1974). The former effect may not be mediated through changes in c- AMP concentration in the cell, since the adenylate cyclase activity in human erythrocyte is extremely low (Rodan et al, 1976; Sutherland et al, 1962) and the latter effect implies that physical state (or fluidity) of the membrane is altered by $PGF_{2{\alpha}}$. The present study was undertaken to elucidate mechanisms of action of $PGE_2$ and $PGF_{2{\alpha}}$ on the human erythocyte membrane by examining their effects on osmotic fragility and $Ca^{++}$ binding to the membrane fragments. The results are summarized as follows: 1) $PGE_2$ and $PGF_{2{\alpha}}$ increased osmotic fragility at concentrations above $10^{11}\;M$, the effect being similar for both hormones. The concentration of NaCl for 100% hemolysis was $1/16{\sim}1/17\;M$ in the presence of $10^{11}\;M\;PGE_2$ or $PGF_{2{\alpha}}$ and 1/18 M in the absence of the hormone (control). 2) When erythrocytes were suspended in 1/15 M NaCl solution, $44.2{\pm}4.3%$ of cells were hemolyzed. Addition of $10^{12}\;M\;PGE_2$ or $PGF_{2{\alpha}}$ did not increase hemolysis. When the concentration of the hormones was increased to $10^{11}\;M$, however the degree of hemolysis increased markealy to about 80%. No further increase in hemolysis was observed at concentration of the hormones above $10^{11}\;M$. 3) The additional hemolysis due to $10^{11}\;M\;PGE_2$ and $PGF_{2{\alpha}}$ appeared to he identical regardless of absence or presence of $Ca^{++}\;(0.5{\sim}10\;mM)$ in the suspending medium. 4) In the absence of prostaglandin, the binding of $Ca^{++}$ to the erythrocyte membrane increased curvilinearly as the $Ca^{++}$ concentration increased up to 5 mM above which it leveled off. A similar dependence of $Ca^{++}$ binding on the $Ca^{++}$ concentration was observed in the presence of $10^{11}\;M\;PGE_2$ or $PGF_{2{\alpha}}$, however, the amount of $Ca^{++}$ bound at a given $Ca^{++}$ concentration was significantly higher than in the absence of the hormones. 5) As in the hemolysis, $PGE_2$ and $PGF_{2{\alpha}}$ did not affect the $Ca^{++}$ binding at a concentration of $10^{12}\;M$, but increased it by about 100% at concentration above $10^{11}\;M$. These result indicate that both tile osmotic fragility of erythrocyte and the $Ca^{++}$ binding to the erythrocyte membrane are similarly enhanced by $PGE_2$ and $PGF_{2{\alpha}}$, but these two effects are not causally related. It is, therefore, concluded that the prostaglandin-induced hemolysis is not directly associated with alterations of the $Ca^{++}$ content in the membrane.

• Journal of Chest Surgery
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• v.47 no.2
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• pp.133-136
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• 2014

Cold agglutinins are predominately immunoglobulin M autoantibodies that react at cold temperatures with surface antigens on the red blood cell. This can lead to hemagglutination at low temperatures, followed by complement fixation and subsequent hemolysis on rewarming. Development of hemagglutination or hemolysis in patients with cold agglutinins is a risk of cardiac surgery under hypothermia. In addition, there is the potential for intracoronary hemagglutination with inadequate distribution of cardioplegic solutions, thrombosis, embolism, ischemia, or infarction. We report a patient with incidentally detected cold agglutinin who underwent normothermic cardiac surgery with warm blood cardioplegia.