Topic
Bekanamycin
About: Bekanamycin is a research topic. Over the lifetime, 4 publications have been published within this topic receiving 61 citations. The topic is also known as: 2'-amino-2'-deoxykanamycin & O-3-amino-3-deoxy-alpha-D-glucopyranosyl-(1->4)-O-(2,6-diamino-2,6-dideoxy-alpha-D-glucopyranosyl-(1->6))-2-deoxy-D-streptamine.
Papers
TL;DR: Aminoglycoside antibiotics including gentamicin, bekanamycin, tobramycin, lincomycin and ribostamycin have been determined by CE-EC with copper clectrodes as discussed by the authors.
Abstract: Aminoglycoside antibiotics including gentamicin, bekanamycin, tobramycin, lincomycin, neomycin, kanamycin, and ribostamycin have been determined by CE-EC with copper clectrodes. Both copper wall-jet electrodes (WJEs) and copper on-capillary electrodes (OCEs) were evaluated. The OCEs provided μM detection limits, superior stability and reproducibility (2–3% relative standard deviation in oxidation current), and a simple instrumental set-up without the need for capillary/electrode alignment. The analytical capabilities of the Cu-OCE were examined, following the optimization of CE conditions, for the seven aminoglycosides above; and the practical utility of this approach was demonstrated through the determination of aminoglycoside antibiotics in three pharmaceutical preparations.
33 citations
TL;DR: 3,4‐diaminopyridine strongly antagonized the effects of BoTx at early stages of poisoning, and the combined presynaptic effects ofBoTx and aminoglycoside antibiotics provided that transmitter release was not completely blocked by the toxin.
Abstract: Impulse-evoked transmitter release was greatly reduced at frog neuromuscular junctions 3-20 days after botulinum type A toxin (BoTx) poisoning. The reduction in transmitter release was accompanied by an increased variability in the latency between the presynaptic spike and the release of transmitter. The aminoglycoside antibiotics amikacin, gentamycin, and bekanamycin, when applied at concentrations within their therapeutic levels, markedly enhanced the blockade of transmitter release in BoTx-poisoned junctions. 3,4-diaminopyridine strongly antagonized the effects of BoTx at early stages of poisoning, and the combined presynaptic effects of BoTx and aminoglycoside antibiotics provided that transmitter release was not completely blocked by the toxin. The antagonism was apparent at all frequencies of stimulation. Since the aminoglycoside antibiotics enhanced the neuromuscular block caused by BoTx, these drugs should be avoided in patients suspected of poisoning by this toxin.
31 citations
TL;DR: The results suggested that the inhibition of lysozyme by aminoglycosides is specific and that the decreased effectiveness of a protective system against bacterial infection in the eye is highly possible when am inoglycoside antibiotics are used without prior sensitivity testing.
Abstract: • We examined biochemically the effect of six aminoglycoside antibiotics on the activity of lysozyme, acid phosphatase, and N -acetylβ-d-glucosaminidase in human tears. All six antibiotics strongly inhibited lysozyme activity, the degree of inhibition depending on the dose administered. Except for bekanamycin, antibiotics had little effect on the activity of acid phosphatase or N -acetyl-β-d-glucosaminidase. The nature of the inhibition was competitive. Other kinds of antibiotics, such as sulbenicillin or erythromycin, had no inhibitory effect on lysozyme, acid phosphatase, or N -acetyl-β-d-glucosaminidase. These results suggested that the inhibition of lysozyme by aminoglycosides is specific and that the decreased effectiveness of a protective system against bacterial infection in the eye is highly possible when aminoglycoside antibiotics are used without prior sensitivity testing.
3 citations
Journal Article•
TL;DR: Serum analysis of the guinea-pigs on day 14 post-administration as a measure of nephrotoxicity revealed that glucarolactam suppressed the elevation of BUN and serum creatinine caused by the aminoglycosides, and no difference in the in vivo antibiotic activity against bacterial infections of mice was observed between the salt and the mixture.
Abstract: Intramuscular administration of glucarolactam in the form of aminoglycoside salt to guinea-pigs protected the experimental ototoxicity caused by high dosing of aminoglycoside antibiotics. The protection was evidenced by the pinna reflex threshold and histochemical examinations of hair cells of cochlea as well as body weight gain. The degree of protection differed with the aminoglycosides, and high protection was observed for dibekacin, gentamicin, tobramycin, followed by kanamycin and bekanamycin. However, protection was weak or not observed when glucarolactam was administered as a mixture of glucarolactam potassium and aminoglycoside sulfate. Serum analysis of the guinea-pigs on day 14 post-administration as a measure of nephrotoxicity revealed that glucarolactam suppressed the elevation of BUN and serum creatinine caused by the aminoglycosides. The protective effect of glucarolactam on the aminoglycoside-induced nephrotoxicity in the dehydrated rats did not differ between the salt and the mixture. No difference in the in vivo antibiotic activity against bacterial infections of mice was observed between the salt and the mixture.
1 citations
Related Topics (5)
Performance Metrics
| Year | Papers |
|---|---|
| 1997 | 1 |
| 1989 | 1 |
| 1987 | 1 |
| 1985 | 1 |