Disease relevance of C01029

• The ratio of N1- to N8-acetylspermidine ranged from 10.3 in the urine of a patient with hepatoma to 1.1 in the urine of a normal subject [1].
• Postoperatively, the excretion of N8-acetylspermidine in patients with multiple trauma without malignancy and in patients with palliative operation was similar, and was higher than in patients with a totally resected malignancy (p less than .01) [2].
• Urinary N1-acetylspermidine and N8-acetylspermidine excretion in normal humans and in patients with colorectal cancer [3].
• N-ethyl-N-nitrosourea-induced rat gliomas showed a stimulation of cytosolic spermidine N-acetyltransferase activity compared with normal brain, with an increased formation of N1 and N8-acetylspermidine, suggesting the activation of two enzymes acetylating the polyamine in N1 and N8 position, respectively [4].

High impact information on C01029

• Animals were sacrificed at each of these time periods and polyamine levels, including N1- and N8-acetylspermidine, as well as the activities of ornithine decarboxylase, spermidine N1-acetyltransferase and polyamine oxidase were measured and compared in rat proximal and distal colonic mucosa of each group [5].
• Circadian rhythm was observed in total polyamine and in N1- and N8-acetylspermidine excretions [6].
• Putrescine (1, 4-diaminobutane) and N8-acetylspermidine were competitive inhibitors of spermidine acetylation by BltD, with Ki values of 0.25 and 5.76 mM, respectively [7].
• Exogenous spermidine, but neither N1- nor N8-acetylspermidine, stimulated cell growth in strains unable to synthesize spermidine [8].
• CHO cells also contained and excreted N8-acetylspermidine, but its synthesis was not increased in cells treated with BENSM, confirming data obtained in vitro that SAT does not produce this derivative [9].

Biological context of C01029

• The effects of deacetylase inhibition were mimicked by addition of N8-acetylspermidine to the culture medium at concentrations greater than 1 mM as indicated by a subsequent increase in rate of cell growth and maximum cell density [10].
• The energy balance and resting energy expenditure could also explain the differences in polyamine excretion between patients with surgically curable and noncurable disease, excluding the increased N8-acetylspermidine [2].
• The ASPD-19 mAb is highly specific for Spd and Spm, almost the same degree to each, and can distinguish alterations in the chemical structure of other polyamine (PA) analogs, showing less than 3.2% cross-reaction with N(1)-acetylspermidine, acetylspermine, or N(8)-acetylspermidine [11].
• Although the ratio of N1-acetylspermidine/N8-acetylspermidine increased somewhat in the urine of animals exposed to UV, the increase was not significant enough to be useful as a marker of enhanced cell proliferation [12].
• Thermal denaturation of mononucleosomes in the presence of spermine, spermidine, N1-acetylspermidine, N8-acetylspermidine or putrescine: implications for chromosome structure [13].

Anatomical context of C01029

• Differentiation of PC12 cells induced by N8-acetylspermidine and by N8-acetylspermidine deacetylase inhibition [14].
• A selective inhibitor of N8-acetylspermidine deacetylation in mice and HeLa cells without effects on histone deacetylation [15].
• Deacetylation of N8-acetylspermidine by subcellular fractions of rat tissue [16].
• The N1-to N8-acetylspermidine ratio in tissues ranged from approx. 5 to 1 in the thymus to 1.5 to 1 in the liver [17].
• From spermidine, more N1-acetylspermidine than N8-acetylspermidine is formed by both the brain and the retinal cytosol [18].

Associations of C01029 with other chemical compounds

• The Ki value for DiAcSpd with the latter competitive ELISA system was 54 nM, and the cross-reactivity with DiAcSpd, N1,N12-diacetylspermine, N8-acetylspermidine, N1-acetylspermidine, and acetylputrescine was 100, 1.2, 0.74, 0.12, and 0.08%, respectively [19].
• Free polyamines and their acetylated derivatives, [putrescine (Put), spermine (Spm), spermidine (Spd), N1-acetylspermidine N1-AcSpd), N8-acetylspermidine N8-AcSpd)], were separated using ion-pair reversed-phase liquid chromatography after pre-column derivatization with dansyl chloride [20].

Gene context of C01029

• In contrast, 24 h exposure to 10 mM sodium butyrate produced no change in N8-acetylspermidine levels and an increase in the acetylation level of histones H4 and H2B [15].
• In these amoeba a considerable polyamine oxidase activity has been found, which acts on N8-acetylspermidine, but not on free polyamines [21].

Analytical, diagnostic and therapeutic context of C01029

• In this study, two different mechanisms were used to produce an elevation in the level of N8-acetylspermidine in PC12 cells: inhibition of N8-acetylspermidine deacetylase and direct addition of N8-acetylspermidine to the cell culture [14].
• Thin layer chromatography (TLC) of the HPLC eluent demonstrated the presence of both radiolabeled N1- and N8-acetylspermidine in the tissues [17].

References