Acetylcholine Chloride High quality with wholesale price CAS NO.60-31-1

Inhibition of p53 Mutant Peptide Aggregation In Vitro by Cationic Osmolyte Acetylcholine Chloride.[Pubmed: 28117010]

Protein Pept Lett. 2017;24(4):353-357.

Mutations of tumor suppressor protein p53 are present in almost about 50% of all cancers. It has been reported that the p53 mutations cause aggregation and subsequent loss of p53 function, leading to cancer progression.
METHODS AND RESULTS:
Here in this study we focus on the inhibitory effects of cationic osmolyte molecules Acetylcholine chloride, and choline on an aggregation prone 10 amino acid p53 mutant peptide WRPILTIITL, and the corresponding wildtype peptide RRPILTIITL in vitro. The characterization tools used for this study include Thioflavin- T (ThT) induced fluorescence, transmission electron microscopy (TEM), congo red binding, turbidity, dynamic light scattering (DLS), and cell viability assays.
CONCLUSIONS:
The results show that Acetylcholine chloride in micromolar concentrations significantly inhibit p53 mutant peptide aggregation in vitro, and could be promising candidate for p53 mutant/ misfolded protein aggregation inhibition.

Acetylcholine chloride as a potential source of variability in the study of cutaneous vascular function in man.[Pubmed: 21601579]

Microvasc Res. 2011 Sep;82(2):190-7.

Laser-Doppler flowmetry (LDF) coupled with Acetylcholine chloride (ACh) iontophoresis is increasingly recognized as a reliable non-invasive method to study the endothelial function. However, Acetylcholine chloride-vasodilation measurement appears highly variable possibly due to the Acetylcholine chloride pharmacological properties itself. These problems may be partially overcome by using methacholine chloride (MCh), a more stable synthetic agonist of muscarinic receptors, instead of Acetylcholine chloride. Therefore, we first studied the correlation between the two drugs and then the effects of (1) spatial variability (inter-site measurements), (2) temporal variability (inter-day measurements), (3) intra-day variability (morning versus evening), and (4) age on the variability of both Acetylcholine chloride-vasodilation and MCh-vasodilation.
METHODS AND RESULTS:
The endothelium-dependent vasodilation response to simultaneous iontophoretic applications (4 doses of 10s at 0.1mA with 2min of current-free interval) of Acetylcholine chloride(11mM) or MCh (10mM) was studied on the forearm of 40 healthy subjects (36 males, median 28yr, range 21-59yr). The percent change in perfusion (CVCpeak) from baseline and the area under the curve (CVC(AUC)) during iontophoresis were assessed. Inter-site, inter-day and intra-day coefficients of variation (CV) were studied for each drug as well as correlations between drugs and age. A linear relationship was found between ACh- and MCh-CVCpeak (r²=0.75, p=0.01) and between ACh- and MCh-CVC(AUC) (r²=0.55, p=0.02). MCh inter-site CV for both CVCpeak (12.2%) and CVC(AUC) (13.8%) was significantly lower than ACh inter-site CV for CVCpeak (15.5%) and CVC(AUC) (15.3%), respectively. MCh inter-day CV for CVCpeak (17.2%) and CVC(AUC) (14.6%) was significantly lower than ACh inter-day CV for CVCpeak (19.7%) and ACh CVC(AUC) (21.2%). For ACh and MCh, the CVCpeak and CVC(AUC) were higher at 16:00pm than at 11:00am (p<0.05 for all). Finally, both ACh- and MCh-CVCpeak exhibited a logarithmic decrease with age (r²=0.61, p<0.01 and r²=0.58, p<0.01).
CONCLUSIONS:
Although both drugs exhibited circadian and age variability, MCh exhibited less inter-site and interday variabilities than did Acetylcholine chloride for the evaluation of cutaneous endothelium-dependent vasodilation. These findings should be taken into account in studies of cutaneous vascular function by iontophoresis coupled with laser Doppler flowmetry.