• Journal of Microbiology and Biotechnology
• /
• 제26권12호
• /
• pp.2043-2050
• /
• 2016

Exploring novel antibiotics is necessary for multidrug-resistant pathogenic bacteria. Because the probiotics in soybean food have antimicrobial activities, we investigated their effects on multidrug-resistant Acinetobacter baumannii. Nineteen multidrug-resistant A. baumannii strains were clinically isolated as an experimental group and 11 multidrug-sensitive strains as controls. The growth rates of all bacteria were determined by using the analysis for xCELLigence Real-Time Cell. The combination of antibiotics showed synergistic effects on the strains in the control group but no effect on the strains in the experimental group. Efflux pump gene adeS was absent in all the strains from the control group, whereas it exists in all the strains from the experimental group. Furthermore, all the strains lost multidrug resistance when an adeS inhibitor was used. One strain of probiotics isolated from soybean food showed high antimicrobial activity for multidrug-resistant A. baumannii. The isolated strain belongs to Bacillus subtilis according to 16S RNA analysis. Furthermore, E. coli showed multidrug resistance when it was transformed with the adeS gene from A. baumannii whereas the resistant bacteria could be inhibited completely by isolated Bacillus subtilis. Thus, probiotics from soybean food provide potential antibiotics against multidrug-resistant pathogenic bacteria.

• Archives of Pharmacal Research
• /
• 제19권5호
• /
• pp.353-358
• /
• 1996

E. coli 11 and E. coli 101, clinical isolates of Escherichia coli were resistant to various quinolones, especially MICs to norfloxacin of both strains were higher than 100 mg/ml. In the presence of carbonyl cyanide m-chlorophenylhydrazone, a proton gradient uncoupler, norfloxacin uptake in both strains was increased, suggesting that an efflux system play an important role in the norfloxacin resistance. Outer membrane proteins of the susceptible and resistant strains which could affect the route of norfloxacin entry into cells were different. When quinolone resistance determining region(QRDR) of gyrA was amplified using PCR and cut with Hinf I, QRDR in the susceptible strain yielded two fragments while QRDRs in E. coli 11 and E. coli 101 yielded only one uncut fragment. When DNA sequence of QRDR was analyzed, there were two mutations as Ser-83 and Asp-87 in both resistant strains. these residues were changed to Leu-83 and Asn-87, respectively. These results showed that the norfloxacin resistance of E. coli 11 and E. coli 101 was resulted from multiple changes-an altered DNA gyrase A subunit, a change in route of drug entry, and reduction in quinolone concentration inside cells due to an efflux system.

• 약학회지
• /
• 제60권1호
• /
• pp.1-7
• /
• 2016

The aim of this study was to investigate the prevalence of quinolone resistant E. coli from retail meat and to characterize the resistant determinants. Determination of minimum inhibitory concentration, the sequence analysis of gyrA, gyrB, parC, and parE quinolone resistance determining regions (QRDR), the presences of plasmid mediated quinolone resistance (PMQR) and the expression of efflux pump genes were investigated. Of the total 277 retail meat samples, 67 coli form bacteria were isolated. 15 of 67 isolates showed nalidixic acid resistance and 7 of 15 nalidixic acid resistant isolates were also resistant to ciprofloxacin, moxifloxacin and levofloxacin. 11 of 15 nalidixic acid resistant strains were isolated from chicken, 2 of 15 were isolated from beef and 2 of 15 were isolated from pork samples. 11 of 15 nalidixic acid resistant strains have single mutation at codon 87 (D87N or D87G) in gyrA, 2 of 11 gyrA mutants have double mutations at codon 86 and 87 (L86A and L87I) in parC with mutations at codon 434+445+465 or 429 in gyrB. 2 of 15 resistant isolates harbored qnrS, a PMQR determinant. Over expression of the acrB gene, efflux pump gene (3.93~16.53 fold), was observed in 10 of 15 resistant isolates.

• International Journal of Oral Biology
• /
• 제38권2호
• /
• pp.61-65
• /
• 2013

Erythromycin is a macrolide antibiotic and inhibits bacterial protein synthesis by stimulating the dissociation of the peptidyl-tRNA molecule from the ribosomes during elongation. The use of macrolides has increased dramatically over the last few years and has led to an increase in bacterial resistance to these antibiotics. Bacterial resistance to erythromycin is generally conferred by the ribosome methylation and/or transport (efflux) protein genes. Among the identified erythromycin-resistant genes, erm(B) (erythromycin methylation) and mef(A) (macrolide efflux) are generally detectable in erythromycin-resistant streptococcal species. The distribution of these genes in oral streptococcal isolates has been reported in studies from other countries but has not been previously examined in a Korean study. We here examined by PCR the presence of erm(B) and mef(A) in oral streptococci isolated from Korean dental plaques. Among the 57 erythromycin-resistant strains tested, 64.9% harbored erm(B) whereas 40.4% were positive for mef(A). Eleven isolates had both the erm(B) and mef(A) genes. Twenty six isolates had only erm(B) and 12 isolates had only mef(A). Eight of the 57 strains examined were negative for both genes.

• The Korean Journal of Physiology
• /
• 제23권1호
• /
• pp.23-34
• /
• 1989

Gentamicin (GM) is a polybasic, aminoglycoside antibiotic used frequently for the treatment of serious gram-negative infections. The major limiting factors in the clinical use of GM as well as other aminoglycoside antibiotics are their nephrotoxicity and ototoxicity. The primary mechanism of cell injury in aminoglycoside toxicity appears to be the disruption of normal membrane function and the inhibition of $Na^{+}-K^{+}$ ATPase activity. There are both indirect and direct evidences which suggests that the effect of aminoglycoside antibiotics on $Na^{+}-K^{+}$ ATPase may explain, or contribute to, their toxicity. It has been shown that aminoglycoside reduce total ATPase activity (Kaku et al., 1973) and $Na^{+}-K^{+}$ ATPase activity (linuma et al., 1967) in the stria vascularis and spiral ligament of the guinea-pig cochlea. Lipsky and Lietman (1980) reported that aminoglycoside antibitoics inhibited the activity of $Na^{+}-K^{+}$ ATPase in microsomal fractions of the cortex and medulla of the guinea-pig kidney, isolated rat renal tubule and human erythrocyte ghosts. The present invstigation was undertaken to elucidate the mechanism of GM on human erythrocytes by examining its effect on $Na^{+}-K^{+}$ ATPase activity, actives sodium and potassium transport across red blood cell and $^{3}H-ouabain$ binding to red blood cell membranes. The results obtained are summarized as follows: 1) CM inhibited significantly both the activity of total ATPase and $Na^{+}-K^{+}$ ATPase at all concentrations tested. 2) GM inhibited active $^{22}Na$ efflux across red blood cell. When ouabain is present, the rate of $^{22}Na$ efflux was completely inhibited. When both GM and ouabain were added, the inhibitory effect of active $^{22}Na$ efflux was more pronounced. 3) Active $^{86}Rb$ influx was inhibited significantly by GM. In the presence of ouabain, the rate of $^{86}Rb$ influx is markedly inhibited. But $^{86}Rb$ influx is not appreciably altered by the presence of both GM and ouabain. 4) In the presence of GM, $^{3}H-ouabain$ binding to red blood cell membrane increased. From the above results, it may be concluded that the inhibition of active sodium and potassium transport across red blood cell by gentamicin appears to be due to the inhibition of $Na^{+}-K^{+}$ ATPase activity and an increase in ouabain binding to red blood cell membranes.

• Journal of Microbiology and Biotechnology
• /
• 제8권4호
• /
• pp.388-398
• /
• 1998

A bacterium which is resistant to both mercury and cadmium, and also capable of utilizing phenol as a carbon and energy source, was isolated from the Kumho River sediments near Kangchang Bridge, Taegu, Korea. The isolate was labeled Pseudomonas sp. KM10 and characterized. The bacteria grew in 4 mM $CdCl_2$and in $70{\mu}M$ $HgCl_2$. The bacteria efficiently removed over 90% of 1 g/l phenol within 30 h. In the presence of 1.250 g/l phenol, the growth of the microorganism was slightly retarded and the microorganism could not tolerate 1.5 g/l phenol. Curing of plasmid from the bacteria was carried out to generate a plasmidless strain. Subsequent experiments localized the genes for phenol degradation in plasmid and the genes for mercury resistance and cadmium resistance on the chromosome. Dot hybridization and Southern hybridization under low stringent conditions were performed to identify the DNA homology. These results showed significant homologies between the some sequence of the chromosome of Pseudomonas sp. KM10 and merR of Shigella flexneri R 100, and between the some sequence of the chromosome of Pseudomonas sp. KM10 and cadA of Staphylococcus aureus pI258. The mechanism of cadmium resistance was efflux, similar to that of S. aureus pI258 cadA, and the mechanism of mercury resistance was volatilization, similar to that of S. flexneri R100 mer.

• 한국작물학회:학술대회논문집
• /
• 한국작물학회 2005년도 춘계학술발표회 요지
• /
• pp.188-189
• /
• 2005

• 한국생명과학회:학술대회논문집
• /
• 한국생명과학회 2007년도 제48회 학술심포지움 및 추계국제학술대회
• /
• pp.78.2-78.2
• /
• 2007

See Full Text

• The Korean Journal of Physiology and Pharmacology
• /
• 제22권2호
• /
• pp.215-223
• /
• 2018

Intracellular $Ca^{2+}$ mobilization is closely linked with the initiation of salivary secretion in parotid acinar cells. Reactive oxygen species (ROS) are known to be related to a variety of oxidative stress-induced cellular disorders and believed to be involved in salivary impairments. In this study, we investigated the underlying mechanism of hydrogen peroxide ($H_2O_2$) on cytosolic $Ca^{2+}$ accumulation in mouse parotid acinar cells. Intracellular $Ca^{2+}$ levels were slowly elevated when $1mM\;H_2O_2$ was perfused in the presence of normal extracellular $Ca^{2+}$. In a $Ca^{2+}-free$ medium, $1mM\;H_2O_2$ still enhanced the intracellular $Ca^{2+}$ level. $Ca^{2+}$ entry tested using manganese quenching technique was not affected by perfusion of $1mM\;H_2O_2$. On the other hand, $10mM\;H_2O_2$ induced more rapid $Ca^{2+}$ accumulation and facilitated $Ca^{2+}$ entry from extracellular fluid. $Ca^{2+}$ refill into intracellular $Ca^{2+}$ store and inositol 1,4,5-trisphosphate ($1{\mu}M$)-induced $Ca^{2+}$ release from $Ca^{2+}$ store was not affected by $1mM\;H_2O_2$ in permeabilized cells. $Ca^{2+}$ efflux through plasma membrane $Ca^{2+}-ATPase$ (PMCA) was markedly blocked by $1mM\;H_2O_2$ in thapsigargin-treated intact acinar cells. Antioxidants, either catalase or dithiothreitol, completely protected $H_2O_2-induced$ $Ca^{2+}$ accumulation through PMCA inactivation. From the above results, we suggest that excessive production of $H_2O_2$ under pathological conditions may lead to cytosolic $Ca^{2+}$ accumulation and that the primary mechanism of $H_2O_2-induced$ $Ca^{2+}$ accumulation is likely to inhibit $Ca^{2+}$ efflux through PMCA rather than mobilize $Ca^{2+}$ ions from extracellular medium or intracellular stores in mouse parotid acinar cells.

• 한국생물물리학회:학술대회논문집
• /
• 한국생물물리학회 2001년도 학술 발표회 진행표 및 논문초록
• /
• pp.46-46
• /
• 2001

Evidence has suggested that an anion channel blocker, 4, 4'-diisothiocyanatostilbene-2, 2' disulfonic acid (DIDS) could trigger Ca release from skeletal sarcoplasmic reticulum (SR) by binding to a 30 kDa SR protein. Since the high molecular weight $Ca^{2＋}$ release channel (CRC)/ryanodine receptor (RyR) is the main SR protein that conducts $Ca^{2＋}$ efflux in skeletal muscles, the relationship between CRC and the 30kDa protein remains to be elucidated.(omitted)