Disease relevance of salicin

• E. coli K12 strains chi342LD cannot grow on salicin but derivatives with two mutations in the bgl operon, an excision of IS150 (formally called IS103) from bglF and a point mutation or insertion in bflR, grow rapidly on this sugar [1].
• Growth of Azospirillum irakense KBC1 on the aryl beta-glucoside salicin requires either salA or salB [2].
• One of these genomospecies contains strains that are negative in indole, salicin, and esculin reactions (biogroup 1) and has been named Proteus penneri [3].
• Identification by bacteriophages was compared with species identification by prereduced anaerobically sterilized biochemical testing with salicin as the differentiating test [4].
• However, with the addition of cellobiose and salicin disks and the inclusion of methyl red to the Minitek test and the use of the Voges-Proskauer test and gas production in EC medium at elevated temperature as standard tests, the identification of these Enterobacteriaceae from meats would be greatly facilitated [5].

Psychiatry related information on salicin

• Next, we determined whether this pattern of stimulus-generalization could be explained by salicin and aristolochic acid generating distinct ensemble, rate, temporal, or spatiotemporal codes [6].

High impact information on salicin

• As salicin is not mutagenic, it has been suggested that excision mutations in bglF might serve only to create the potential for a secondary selectively advantageous mutation [1].
• We show here, however, that these double mutants can be accounted for by spontaneous mutation to intermediate genotypes in non-growing populations, coupled with slow growth of some of these intermediates on salicin, which enables their populations to reach a size where secondary mutations allowing rapid growth on salicin become common [1].
• AtSUC9 showed low substrate specificity, similar to AtSUC2 (At1g22710), and transported a wide range of glucosides, including helicin, salicin, arbutin, maltose, fraxin, esculin, turanose, and alpha-methyl-d-glucose [7].
• Escherichia coli does not use beta-glucoside sugars; however, mutations in several loci can activate the cryptic bgl operon and permit growth on the beta-glucoside sugars arbutin and salicin [8].
• A salicin+ arbutin+ cellobiose+ mutant has been isolated from a strain which is deleted for the both the bgl and cel operons [9].

Chemical compound and disease context of salicin

• The ECOR collection of natural Escherichia coli isolates was screened to determine the proportion of strains that carried functional, cryptic and nonfunctional genes for utilization of the three beta-glucoside sugars, arbutin, salicin and cellobiose [10].
• We placed 43 isolates belonging to the Proteus vulgaris complex into proposed DNA groups (genomovars) using five previously recommended tests (tests for esculin hydrolysis, production of acid from salicin, L-rhamnose fermentation, and elaboration of DNase and lipase) [11].
• In Bacillus subtilis, aryl-beta-glucosides such as salicin and arbutin are catabolized by the gene products of bglP and bglH, encoding an enzyme II of the phosphoenolpyruvate sugar-phosphotransferase system and a phospho-beta-glucosidase, respectively [12].
• The Eubacterium aerofaciens group was divided into four groups by fermentation patterns of sucrose and cellobiose, and were further divided into 16 sub-groups by fermentation patterns of aesculin, salicin and amygdalin [13].
• A modified version of sorbitol MacConkey medium containing cefixime and tellurite (CT-SMAC medium) was produced by adding salicin and 4-methylumbelliferyl-beta-D-galactopyranoside to CT-SMAC medium; this medium was designated CT-SSMAC medium and was used to isolate Escherichia coli O157:H7 from radish sprouts [14].

Biological context of salicin

• Escherichia coli K12 does not metabolize beta-glucosides such as arbutin and salicin because of lack of expression of the bglBSRC operon, which contains structural genes for transport (bglC) and hydrolysis (bglB) of phospho-beta-glucosides [15].
• A newly observed phenotype of pgl strains is a lowered frequency of appearance of Bgl+ mutants that can utilize the beta-glucoside salicin [16].
• A phylogeny based upon groEL gene sequences was discordant with rhamnose or salicin fermentation data for many taxa, and no reliable phenotypic correlations could be established [17].
• Functional analysis of the bglF and bglA products revealed that they are simultaneously required for uptake, phosphorylation and breakdown of methyl beta-glucoside, salicin and arbutin [18].
• Similarly, the accumulation of salicin, salicortin, chlorogenic acid (+)-catechin, proanthocyanidins, and unknowns varied significantly according to source (tissue, individual, or clone), and in most cases the environmental (within-clonal) variation was nearly as high as the genetic variation (between-clones) [19].

Anatomical context of salicin

• Penetration of methylhexoses and salicin into the NaCl-expanded periplasm appeared to be 85 and 50%, respectively, of that of pentoses, whereas penetration of the saccharides of Mr larger than 340-400 was negligibly small [20].
• The permeability of glycosides (salicin, arbutin, glycyrritin, p-nitrophenyl-beta-D-glucopyranoside, p-nitrophenyl-beta-D-galactopyranoside, p-nitrophenyl-beta-D-lactopyranoside, and p-nitrophenyl-beta-D-maltopyranoside) and their aglycons through human erythrocyte membrane was investigated [21].
• These drugs and also flufenamic acid and salicin show a similar antagonism of the action of PGF2alpha with isolated rabbit non-pregnant myometrium [22].

Associations of salicin with other chemical compounds

• Transcription of bvrB was induced by cellobiose and salicin but not by arbutin [23].
• (iv) All tests for carbohydrate fermentation except for raffinose and salicin were read after the addition of 2 to 3 drops of 0.025% phenol red (pH 7.2) [24].
• Using computer-generated random list, 114 patients were allocated to receive a daily dose of herbal extract containing 240 mg of salicin [PAID (phyto-anti-inflammatory drug) group] and 114 were allocated to receive 12.5 mg of the synthetic COX-2 inhibitor rofecoxib [NSAID (non-steroidal anti-inflammatory drug) group] [25].
• Of these, assimilation of L-glycine and isobutyrate as sole carbon source, acid production from salicin and D-sucrose, and aesculin hydrolysis were of diagnostic value [26].
• An application is shown for monitoring the glycoside salicin and its hydrolysis product saligenin in a commercially available willow bark product that is used for making tea [27].

Gene context of salicin

• Escherichia coli K12 strain chi 342LD requires two mutations in the bgl (beta-glucosidase) operon, bglR0----bglR+ and excision of IS103 from within bglF, in order to utilize salicin [28].
• When introduced into wild-type E. coli it allows this organism to use cellobiose, arbutin and salicin; it also complements bglB and bglC mutants of Escherichia coli indicating that arbutin and salicin utilization is due to the products of the pBEC2 cloned genes [29].
• RA trial: Patients were randomized to receive willow bark extract, corresponding to 240 mg salicin/day (n = 13) or placebo (n = 13) [30].
• This gene encodes the phospho-beta-glucosidase involved in cleavage of the sugars cellobiose, salicin and arbutin [31].
• Two moderate-quality trials utilizing Salix alba (White willow bark) found moderate evidence for short-term improvements in pain and rescue medication for daily doses standardized to 120 mg or 240 mg salicin with an additional trial demonstrating relative equivalence to 12.5 mg per day of rofecoxib [32].

Analytical, diagnostic and therapeutic context of salicin

• Pharmacokinetics of salicin after oral administration of a standardised willow bark extract [33].
• Determination of salicin and related compounds in botanical dietary supplements by liquid chromatography with fluorescence detection [34].
• Further purification was achieved by affinity chromatography using a Sepharose 4B matrix to which oxidized salicin was coupled through adipic dihydrazide [35].

References