Disease relevance of dihydrostreptomycin

• Phage replication was sensitive to those metabolic inhibitors which inhibited the host streptococcus: these included rifampin, fluorodeoxyuridine, hydroxyurea, dihydrostreptomycin, and 6-P-hydroxyphenylazouracil [1].
• Effect of enzymatic adenylylation on dihydrostreptomycin accumulation in Escherichia coli carrying an R-factor: model explaining aminoglycoside resistance by inactivating mechanisms [2].
• Inhibition of dihydrostreptomycin binding to Mycobacterium smegmatis by monovalent and divalent cation salts [3].
• Killing of intraphagocytic Staphylococcus aureus by dihydrostreptomycin entrapped within liposomes [4].
• Effect of low concentrations of dihydrostreptomycin on drug resistance in enteric bacteria [5].

High impact information on dihydrostreptomycin

• Extracellular Ca2+ increases the free energy of the barrier nearest the extracellular side and of the binding site for dihydrostreptomycin [6].
• In vivo, where the extracellular Ca2+ concentration in the endolymph surrounding the hair bundles is < 100 microM, we predict that some 9000 dihydrostreptomycin molecules per second enter each hair cell at therapeutic drug concentrations [6].
• The aminoglycoside antibiotic dihydrostreptomycin rapidly enters mouse outer hair cells through the mechano-electrical transducer channels [6].
• Intracellularly applied dihydrostreptomycin also blocks the transducer channels, but at positive membrane potentials [6].
• This MexXY upregulation was associated with a 2- to 16-fold increase in the MICs of AGs in the S/R pairs and lower intracellular accumulation of dihydrostreptomycin [7].

Chemical compound and disease context of dihydrostreptomycin

• When normal hearing was established, aminoglycosidic antibiotics (kanamycin and dihydrostreptomycin) were given daily and hearing tests administered in order that the course of hearing loss could be closely followed [8].
• Paromomycin and dihydrostreptomycin binding to Escherichia coli ribosomes [9].
• CONCLUSIONS: Dihydrostreptomycin/penicillin G is effective for treatment of acute and persistent leptospirosis [10].
• Solutions of EDTA-Tris potentiate the effect of tetracycline, dihydrostreptomycin and penicillin when reacted with Escherichia coli [11].
• The effect of chloramphenicol and rifampicin upon degradation of dihydrostreptomycin-induced abnormal protein in Escherichia coli [proceedings] [12].

Biological context of dihydrostreptomycin

• Respiration-dependent uptake of dihydrostreptomycin by Escherichia coli. Its irreversible nature and lack of evidence for a uniport process [13].
• Effect of dihydrostreptomycin on active transport in isolated bacterial membrane vesicles [14].
• The evidence suggested that the observed kinetics was that of the energy-dependent phase I component of dihydrostreptomycin uptake [15].
• The stimulation by dihydrostreptomycin of ATP hydrolysis resulted in a suppression of the sensitivity of this activity to inhibition by oligomycin [16].
• Bioenergetics of dihydrostreptomycin transport by Escherichia coli [17].

Anatomical context of dihydrostreptomycin

• Effects of dihydrostreptomycin on ribosome function in vivo: lack of correlation between changes in ribosome patterns and growth [18].
• These data indicated that metabolism was required for dihydrostreptomycin to exert an effect on the bacterial cell membrane [14].
• Lack of accumulation of exogenous adenylyl dihydrostreptomycin by whole cells or spheroplasts of Escherichia coli [19].
• On the other hand the dihydrostreptomycin-promoted proton conduction in submitochondrial particles was suppressed by oligomycin [16].
• Interaction of the aminoglycoside antibiotic dihydrostreptomycin with the H+-ATPase of mitochondria [16].

Associations of dihydrostreptomycin with other chemical compounds

• Two liquid chromatography-tandem mass spectrometry (LC-MS/MS) methods were developed for the determination of streptomycin (STR) and its derivative dihydrostreptomycin (DHSTR) in milk and honey [20].
• It was observed that dihydrostreptomycin binds equally well to the 30-S subunit and the 70-S ribosome, and that neomycin stimulates the binding of dihydrostreptomycin to the ribosome by increasing the association constant and not by creating new binding sites [21].
• Paromomycin binding, unlike dihydrostreptomycin binding, is independent of changes in ribosome concentration but influenced by magnesium ion concentration [9].
• About half of the isolates were susceptible to dihydrostreptomycin or tetracycline in vitro, while less than 10% were susceptible to penicillin or clindamycin [22].
• The addition of 1000 units or mug of ampicillin, chloramphenicol, kanamycin, lincomycin, polymyxin, or spectinomycin per ml of extender containing 750 units penicillin and 750 mug dihydrostreptomycin per ml did not influence the fertility of frozen spermatozoa in a field test involving 19,663 first inseminations [23].

Gene context of dihydrostreptomycin

• Forty-five aminoglycoside antibiotics and related compounds were compared for their ability to induce the accumulation of dihydrostreptomycin in Escherichia coli K12 [24].
• The method includes clean-up using a Sep-Pak C18 cartridge and quantitation using dihydrostreptomycin as an internal standard [25].
• Streptomycin and dihydrostreptomycin were separated by reversed-phase ion-pair chromatography on LiChrosorb RP-18 and detected by UV absorption (195 nm) [25].
• From then on, the whole herd was examined weekly for a period of 2 months, and all cows Leptospira-positive by polymerase chain reaction were treated once with dihydrostreptomycin [26].
• These findings suggest that a single DHSM molecule or more than one CDDP molecule binds to a single MET channel [27].

Analytical, diagnostic and therapeutic context of dihydrostreptomycin

• Detection of incurred dihydrostreptomycin residues in milk by liquid chromatography and preliminary confirmation methods [28].
• Modified determination of dihydrostreptomycin in kidney, muscle and milk by HPLC [29].
• Block of the mechano-electric transduction (MET) channel by dihydrostreptomycin (DHSM) and its effects on adaptation were investigated in dissociated cochlear hair cells of the chick with a whole-cell patch-electrode voltage clamp technique [30].
• Two regimens consisted of procaine penicillin injected intramuscularly for either three or five days, and the third, the traditional Norwegian regimen, consisted of one intramuscular injection of a combination of procaine penicillin and dihydrostreptomycin followed by one intramammary treatment daily per infected quarter for four days [31].
• Again, all cows stopped shedding leptospires in the urine within 1 week after treatment with dihydrostreptomycin [26].

References