Disease relevance of n-butyl alcohol

• Treatment of whole viable MCA-F murine sarcoma cells from syngeneic female C3H/HeJ mice with a single-phase solution of 2.5% (vol/vol) 1-butanol yielded a crude membrane protein extract without loss of cell viability [1].
• Differential extraction of tumor-specific transplantation antigen and embryonic antigen from simian virus 40- and adenovirus 7-induced sarcoma cells of hamsters with 1-butanol and 3 M potassium chloride [2].
• [3H] gamma-aminobutyric acid, [14C] butanol, and 113mIn-labeled serum protein (transferrin) were injected simultaneously 4 s before decapitation [3].
• Differential extraction of tumor-specific antigens from two ultraviolet light-induced murine fibrosarcomas with the use of 1-butanol [4].
• Identification of cell surface cathepsin B-like activity on murine melanomas and fibrosarcomas: modulation by butanol extraction [5].

Psychiatry related information on n-butyl alcohol

• The acetate and butyrate conversion reactions in vitro were inhibited by physiological levels of acetone and butanol, and this may be another factor in the in vivo regulation of enzyme activity [6].
• When locomotor activity was the dependent variable, daily n-butanol had no effect [7].
• Moreover, alpha-(4-fluorophenyl-2-pyrimidinyl)-1-piperazine butanol (BMY 14802), a putative sigma antagonist (1-10 mg/kg i.p.), did not affect CO-induced amnesia, but when simultaneously administered with DTG, it completely prevented its effect in both tests.(ABSTRACT TRUNCATED AT 250 WORDS)[8]
• Olfaction was assessed using a butanol threshold test, the UPSIT, and a 7-item discrimination test [9].
• The objective of this study is to assess the use of n-butanol as a suitable odorant for organoleptic training of breath judges [10].

High impact information on n-butyl alcohol

• Distribution of butanol molecules along bullfrog olfactory mucosa [11].
• Oral administration of ethanol, n-butanol, or t-butanol to mice 20 minutes before injection of carbon-14-labeled nitrosonornicotine inhibited the localization of radioactivity in bronchial and salivary duct epithelium and in the liver [12].
• Therefore, the ability of butanol-extracted LPS to modulate a spectrum of C3H/HeJ B-cell functions was investigated [13].
• Both butanol-extracted (LPS-B) and phenol-extracted (LPS-P) LPS preparations activated responder C3H/St spleen cell cultures to polyclonal antibody production, while only LPS-B activated C3H/HeJ spleen cells [13].
• A cross-protective antigen(s), not detected in the CBE tumor extracts, was retained in the intact, 1-butanol-extracted SV40 and Adv-7-induced tumor cell lines after completion of the CBE extraction procedure and in similarly extracted 10-day hamster fetal cells [2].

Chemical compound and disease context of n-butyl alcohol

• Lipopolysaccharide (LPS), extracted from Escherichia coli K235 by the butanol water technique, was fractionated by gel filtration chromatography into high m.w. (LPS I) and low m.w. (LPS II) fractions [14].
• In addition, bacterial chemotactic factor-enriched butanol extracts from Escherichia coli culture filtrates can also bind to anti-f Met-Leu-Phe, affording additional evidence for the similarity in the structure of the bacterial chemotactic factor to the synthetic chemotactic peptides [15].
• Glucocerebrosidase from normal human spleen, and spleen from cases of neurologic (types 2 and 3) and nonneurologic (type 1) Gaucher's disease, was delipidated and inactivated by extraction from membranes with sodium cholate and ice-cold 1-butanol [16].
• The response of these mice to PHA, Con A, Poly I:C, 8BrcGMP, and butanol extraced E. coli K235 LPS was normal [17].
• Cells pretreated with pertussis toxin or n-butanol did not affect the cyclocommunin-induced O2*- generation [18].

Biological context of n-butyl alcohol

• Cell cycle studies revealed that n-butanol influenced not just interphase cortical microtubules but also those in the preprophase band and phragmoplast, but not those in the spindle structure [19].
• Microscopic observation of plant roots showed that butanol extract of B. japonicum strain USDA110 cultures induced for nod gene expression elicited root hair deformation, an early event in the nodulation process [20].
• Chemotaxis was also increased, as indicated by the decrease, by a factor of approximately 1/3 in the ED50 for fMet-Leu-Phe, as well as by a 1.5-fold increase in the maximal distance of migration in the presence of 0.25% butanol or 0.1% pentanol [21].
• Low doses of n-butanol (0.25%) and n-pentanol (0.1%) were nontoxic to the leukocytes yet reduced their diphenylhexatriene-induced polarization, indicating increased membrane fluidity [21].
• 1-Alcohols from methanol through 1-butanol inhibit with increasing potency the cell-cell adhesion mediated by the immunoglobulin cell adhesion molecule L1 [22].

Anatomical context of n-butyl alcohol

• The release of nascent secretory vesicles from the TGN was sensitive to 1% 1-butanol, a concentration that inhibited PLD-catalyzed formation of phosphatidic acid [23].
• Within 30 min of adding n-butanol, a potent activator of PLD, cortical microtubules were released from the plasma membrane and partially depolymerized, as visualized with four-dimensional confocal imaging [19].
• The inhibition was reversed by soluble proteins extracted with butanol from purified membranes or from intact cells [24].
• Using two enrichment procedures of the (32)P-postlabeling method, nuclease P1 digestion and butanol extraction, we found that all hepatic microsomes were competent to activate 3-NBA [25].
• The total cellular content of the fluorescent mitochondrial-specific dye rhodamine 123 (Rh-123) was quantified by butanol extraction as a function of time of exposure and dose for a variety of cell lines [26].

Associations of n-butyl alcohol with other chemical compounds

• Extraction of the purified membrane preparation with 1-butanol yielded an activity in the aqueous phase which resides in a protein probably a glycoprotein, with an estimated molecular weight of 50,000 in solution [27].
• Both bovine serum albumin and lysozyme partition between water and 1-butanol by the addition of sodium p-toluene sulfonate at pH 2 [28].
• Downregulation of phosphoinositide production by 1-butanol resulted in diminished PIP(2) in the plasma membrane and eliminated EGF-induced calpain activation [29].
• In HGF-stimulated hepatocytes, butanol prevented the formation of PA and DG [30].
• Incubation of extracted tumor cells with crude butanol extracts prepared from those cells restored the cell surface CB-like activity to that of the unextracted controls, suggesting that the increased enzyme activity observed following extraction may be due to the release of an endogenous cysteine protease inhibitor [5].

Gene context of n-butyl alcohol

• Here we demonstrate that Ste4 and Ste5 activate Kss1 during IG and in response to multiple stimuli including butanol [31].
• Conversely, inhibition of PLD1 activity by 1-butanol decreases betaAPP trafficking in both wt and PS1-deficient cells [32].
• In contrast, 1.5% butanol was found to inhibit the activation of PLD by ARF1 and also decrease PIP levels by 50% [33].
• Moreover, treatment of cells with butan-1-ol or phospholipase D1 antisense oligonucleotides inhibits translocation of PKCdelta, -epsilon, and -zeta but had no effect on the association of PKCalpha or ARF6 with phospholipase D1 [34].
• The PDGF-BB-induced activation of growth signaling was also suppressed by 1-butanol, which prevents the production of phosphatidic acid by phospholipase D (but not by t-butyl alcohol), thereby implicating PLD2 in PDGF-BB-mediated signaling in TC-135 cells [35].

Analytical, diagnostic and therapeutic context of n-butyl alcohol

• Moreover, immunization of mice with antigens from the same fractions (fraction II) of n-butanol extracts of C-C26 tumor on the gel filtration could induce the resistance against challenged C-C36 as well as against challenged C-C26 tumor growth [36].
• Administration of tumor-specific transplantation antigens extracted from viable MCA-F cells with the use of single-phase (2.5%) 1-butanol [crude butanol extract (CBE)] augmented immunity after resection of the primary MCA-F tumor [37].
• Extraction of a murine tumor-specific transplantation antigen with 1-butanol. I. Partial purification by isoelectric focusing [1].
• Based upon its ability to inhibit opiate receptor binding, a low-molecular-weight substance (600) has been isolated from human plasma by extraction into butanol and ion exchange, molecular sieve, and thin-layer chromatography [38].
• C-C26 crude butanol extract was characterized by biochemical procedures including the Sephadex G200 column, lens culinaris affinity column, and anion-exchange Mono Q fast protein liquid chromatography column, and by the enzyme digestion study of the antigens and sodium dodecyl sulfate-polyacrylamide gel electrophoresis [39].

References