• Journal of Microbiology and Biotechnology
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• v.30 no.3
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• pp.382-390
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• 2020

Periplanetasin-4 is an antimicrobial peptide with 13 amino acids identified in cockroaches. It has been reported to induce fungal cell death by apoptosis and membrane-targeted action. Analogs were designed by substituting arginine residues to modify the electrostatic and hydrophobic interactions accordingly and explore the effect of periplanetasin-4 through the increase of net charge and the decrease of hydrophobicity. The analogs showed lower activity than periplanetasin-4 against gram-positive and gram-negative bacteria. Similar to periplanetasin-4, the analogs exhibited slight hemolytic activity against human erythrocytes. Membrane studies, including determination of changes in membrane potential and permeability, and fluidity assays, revealed that the analogs disrupt less membrane integrity compared to periplanetasin-4. Likewise, when the analogs were treated to the artificial membrane model, the passage of molecules bigger than FD4 was difficult. In conclusion, arginine substitution could not maintain the membrane disruption ability of periplanetasin-4. The results indicated that the attenuation of hydrophobic interactions with the plasma membrane caused a reduction in the accumulation of the analogs on the membrane before the formation of electrostatic interactions. Our findings will assist in the further development of antimicrobial peptides for clinical use.

• Toxicological Research
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• v.22 no.4
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• pp.315-322
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• 2006

TALP-32 is highly basic protein with a molecular weight of 32 kDa purified from human term placenta. Some basic proteins such as defensins and cecropins are known to induce cell death by increasing membrane permeability and some of them are under development as an anticancer drug especially targeting multi-drug resistant cancers. Therefore, we investigated cytotoxic effect and mechanism of TALP-32 When HeLa cell was incubated with TALP-32, cytotoxicity was increased in time and dose dependent manner. As time goes by, HeLa cells became round and plasma membrane was ruptured. Increase of plasma membrane permeability was determined with LDH release assay. Also in transmission electron microscopy, typical morphology of necrotic cell death, such as cell swelling and intracellular organelle disruption was observed, but DNA fragmentation and caspase activation was not. And necrotic cell death was determined with Annexin V/Pl staining. The cytotoxicity of TALP-32 was minimal and decreased or RBC and Hep3B respectively. These data suggests that TALP-32 induces necrosis on rapidly growing cells but not on slowly growing cells implicating the possibility of its development of anticancer peptide drug.

• Childhood Kidney Diseases
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• v.7 no.1
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• pp.16-22
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• 2003

Purpose : Minimal Change Disease(MCD) is the most common primary nephrotic syndrome in children. Some suggested that tumor necrosis factor-${\alpha}$ ($TNF-{\alpha}$) are involved in the pathogenesis of MCD. This study was done to see the changes of plasma and urinary $TNF-{\alpha}$, and their effects on the permeability of glomerular basement membrane. Methods : Study patients consisted of 19 biopsy-proven MCD children aged 2-15 years old. Both plasma and urinary $TNF-{\alpha}$ were measured. Employing the Millicell system, $TNF-{\alpha}$ were screened for the permeability factors. Results : Urinary $TNF-{\alpha}$ during relapse was significantly increased(P<0.01). No significant change was seen in the plasma $TNF-{\alpha}$ during relapse when compared to those in remission and the healthy controls. Furthermore, in the in vitro Millicell system, $TNF-{\alpha}$ did not produce a significant change in albumin permeability. Conclusion : Therefore, it seems that $TNF-{\alpha}$ may not play a disease-specific role in the pathogenesis of MCD.

• Archives of Pharmacal Research
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• v.19 no.4
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• pp.264-268
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• 1996

Panax-ginseng saponin has been known to exert various pharmacological effects on cellular metabolism. This study was performed to determine the effect of ginseng saponin on gap junction channel-mediated intercellular communication, using an established in vitro system of reconstituted gap junction channels. Gap junction channels are a specialized plasma membrane fraction, which are permeable to relatively large water-soluble molecules. The sucrose permeable property of reconstituted gap junction channels was completely inhibited with 0.1 % (w/v) of ginseng saponin. We also compared the effect of ginseng saponin with that of Triton X-100, a nonionic detergent, on the same system. Triton X-100 showed significantly different effect on sucrose-permeability of gap junction channel from that was affected by ginseng saponin. The structures of liposomes containing gap junction channels was significantly destroyed by Triton X-100.

• The Korean Journal of Physiology
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• v.25 no.2
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• pp.179-188
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• 1991

Effect of a sulfhydryl reagent, p-chloromercuribenzoic acid (PCMB), on the transport of succinate was studied in brush border (BBMV) and basolateral (BLMV) membrane vesicles isolated from rabbit renal cortex. PCMB induced an irreversible inhibition of the $Na^+-dependent$ succinate uptake in a dose-dependent manner with $IC_{50}$ of 55 and $65\;{\mu}M$ in BBMV and BLMV, respectively. The inhibitory effect of PCMB was prevented by a pretreatment of vesicles with dithiothreitol. PCMB did not increase $Na^+$ permeability at concentrations inhibiting succinate uptake. The PCMB inhibition of succinate uptake was due to a change in Vmax, but not in Km. When membrane vesicles were pretreated with PCMB in the presence of unlabelled succinate, the inhibitory effect was significantly reduced. In both BBMV and BLMV, succinate uptake was inhibited by various sulfhydryl reagents with the inhibitory potency of following order: $HgCl_2$>DTNB>PCMBS>PCMB. These results suggest that sulfhydryl groups are essential for dicarboxylate transport and that they may be located at or near substrate binding sites of the transporters in renal brush border and basolateral membranes.

• Proceedings of the Korean Society of Toxicology Conference
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• 2001.05a
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• pp.22-40
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• 2001

Apoptosis is characterized by DNA fragmentation, chromatin condensation and plasma membrane blebbing. These apoptotic processes have been mainly associated with genetic mechanisms. Recently, these processes have been also associated with mitochondrial events that include the release of cytochrome c and Diablo/SMAC by modulation of mitochondrial membrane permeability.(omitted)

• Journal of the Korean Chemical Society
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• v.22 no.5
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• pp.304-310
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• 1978

The relative permeabilities, distribution coefficients and diffusion coefficient of some salts which are important components in blood plasma through a poly(HEMA) membrane were measured. The crosslinker which was used for preparing the membrane was tetraethylene glycol dimethacrylate(TEGDMA), the weight percentage of the latter was about 2.8. We found that the diffusion coefficients ($D_m$) of the solutes decrease exponentially with increasing molecular weight, and also that $D_m$'s decrease linearly (except urea) with cylindrical radius (a). These facts were explained by a sieve pore flow model. The relative permeability and diffusion coefficient of urea at various temperature were larger than those of other solutes such as glycine, ${\beta}$-alanine, D-glucose, saccharose and maleic acid. The result indicates that the poly(HEMA) membrane might be suitable for hemodialysis application.

• Journal of Applied Biological Chemistry
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• v.66
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• pp.311-319
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• 2023

Caveolin-1 (Cav-1) is the main structural component of the caveolae on the plasma membrane, which regulates various cellular processes, including cell growth, differentiation, and endocytosis. Although a recent study demonstrated that Cav-1 might be involved in diabetes-associated inflammation, its exact role in the intestine was unclear. In this study, we examined the intestinal expression of Cav-1 in diabetic conditions. We also investigated its effect on lipopolysaccharide (LPS)-induced inflammation by expressing this protein in human intestinal Caco-2 cells lacking Cav-1. We observed that increased Cav-1 levels and decreased expression of tight junction proteins affected intestinal permeability in high-fat diet-induced diabetic mice. When Caco-2 cells were treated with LPS, Cav-1 enhanced the NF-κB signaling. Moreover, LPS reduced the expression of tight junction proteins while it increased cell-cell permeability and reactive oxygen species generation in Caco-2 cells and this effect was amplified by cav-1 overexpression. LPS treatment promoted phosphorylation of tyrosine-14 (Y14) on Cav-1, and the LPS-induced NF-κB signaling was suppressed in cells expressing non-phosphorylatable Cav-1 (tyrosine-14 to phenylalanine mutant), which reduced intestinal barrier permeability. These results suggest that Cav-1 expression promotes LPS-induced inflammation in Caco-2 cells, and phosphorylation of Y14 on Cav-1 might contribute to the anti-inflammatory response in LPS-induced NF-κB signaling and cell permeability.

• The Korean Journal of Pharmacology
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• v.18 no.2
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• pp.69-77
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• 1982

$Na^+,\;K^+-ATPase$ is a component of plasma membrane in almost all animal cell, and maintains ionic distribution and membrane potential of normal cell. In the mechanism of adrenergic transmission, it is relatively well known that drug-receptor combination leads to stimulate adenylate cyclase and so on. In the cholinergic transmisison, the mechanism is not well known but is simply interpreted as the change of membrane permeability results from acetylcholine receptor interaction. To study the relationship between cholinergic transmission and membrane $Na^+,\;K^+-ATPase$, the effect of carbachol on $Na^+,\;K^+-ATPase$ activity in rabbit erythrocyte membrane is studied. The results are summarized as follows. 1) Total ATPase, $Mg^{+2}-ATPase$ and $Na^+,\;K^+-ATPase$ of rabbit erythrocyte membrane show maximum activities at 1mM of tris-ATP. 2) Total ATPase activity tends to increase when treated with carbachol $(10-^{-9}M-10^{-3}M)$. 3) The $Mg^{+2}-ATPase$ activity also tends to increase when treated with carbachol $(10-^{-9}M-10^{-3}M)$. 4) The $Na^+,\;K^+-ATPase$ activity is inhibited when treated with carbachol $(10-^{-9}M-10^{-7}M)$. It is suggested that the inhibition of $Na^+,\;K^+-ATPase$ by cholinergic drugs may be considered as one part of mechanism of cholinergic transmission.

• Journal of Microbiology and Biotechnology
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• v.17 no.9
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• pp.1573-1578
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• 2007

An increasing number of applications is being developed for the use of nanoparticles in various fields. We investigated possible toxicities of nanoparticles in cell culture and in mice. Nanoparticles tested were Zn (300 nm), Fe (100 nm), and Si (10-20, 40-50, and 90-110 nm). The cell lines used were brain, liver, stomach, and lung from humans. In the presence of nanopaticles, mitochodrial activity decreased zero to 15%. DNA contents decreased zero to 20%, and glutathione production increased zero to 15%. None of them showed a dose dependency. Plasma membrane permeability was not altered by nanoparticles. In the case of Si, different sizes of the nanoparticles did not affect cytotoxicity. The cytotoxicity was also shown to be similar in the presence of micro-sized ($45\;{\mu}m$) Si particles. Organs from mice fed with nanoparticles showed nonspecific hemorrhage, lymphocytic infiltration, and medullary congestion. A treatment with the micro-sized particle showed similar results, suggesting that the acute in vivo toxicity was not altered by nano-sized particles.