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PubMed1997

Cryopreservation of rabbit spermatozoa using acetamide in combination with trehalose and methyl cellulose.

Glycerol is not an effective cryoprotectant for rabbit spermatozoa; therefore, rabbit spermatozoa were used as a model for developing cryopreservation procedures for other cell types which also freeze poorly when glycerol is used as the cryoprotectant. Experiments were conducted to 1) compare several published protocols for cryopreserving rabbit spermatozoa; 2) determine if removal of seminal granules, required for flow cytometry analysis, affects the motility of rabbit spermatozoa; and 3) determine if using a combination of cell permeating cryoprotectants (acetamide) with cell nonpermeating cryoprotectants (trehalose and methyl cellulose; MC), can increase the recovery of viable rabbit spermatozoa after cryopreservation. Media containing acetamide as a cryoprotectant were found to be most effective for rabbit spermatozoa. The cryoprotectants ethylene glycol, dimethylsulfoxide and glycerol were not effective for cryopreserving rabbit spermatozoa. Second, rabbit spermatozoa could be centrifuged through a Percoll gradient composed of equal volumes of Prcoll and a HEPES-buffered sperm medium. This centrifugation removed all seminal granules without affecting the percentage of motile spermatozoa after initial sperm dilution (85 vs 74%) or after cryopreservation (35 vs 30%), when sperm were either centrifuged or not centrifuged, respectively. The substitution of trehalose in the cryopreservation medium for raffinose did not improve recovery of motile cells following cryopreservation (P > 0.05). However, addition of MC resulted in higher percentages of motile sperm after cryopreservation (43 vs 31%; P < 0.05). In addition, sperm viability and acrosomal integrity were simultaneously evaluated using flow cytometry. The addition of both trehalose and MC to media containing acetamide resulted in higher percentages of live acrosome-intact cells than acetamide alone (53 vs 37%; P < 0.05). These results indicate that a combination of permeating and nonpermeating cryoprotectants (acetamide, trehalose and MC) were more effective in preserving rabbit spermatozoa than acetamide alone and that analyzing multiple sperm characteristics, by flow cytometry, can assess sperm damage not detected by analyzing sperm motion characteristics.

Journal Article↗

PubMed2003

Biotransformation of N-(2-alkylamino-4-phenylimidazol-1-yl)-acetamides and kinetic studies by using cells and laccase from Trametes versicolor.

The product pattern of biotransformation of different N-(2-alkylamino-4-phenylimidazol-1-yl)-acetamides were compared. N-(2-alkylamino-4-phenylimidazol-1-yl)-acetamides were transformed by Trametes versicolor into two types of aromatic products identified by chemical structure analysis: 1. Novel heteroaromatic compounds, such as: 2-(alkylamino)-4-phenylimidazoles, N-(2-alkylamino-5-formyl-4-phenylimidazol-1-yl)-acetamides, N-(2-alkylimino-3-hydroxy-4-phenyl-2,3-dihydroimidazol-1-yl)-acetamides and N-(2-alkylimino-5-oxo-4-phenyl-2,5-dihydroimidazol-1-yl)-acetamides, 2. Novel compounds arising from coupling of two molecules of the substrate. These aromatic compounds were produced from the beginning of incubation by cultures of T. versicolor. In addition to these two types of biotransformation products, monoaromatics such as oxophenyl acetic acid, benzoic acid, and benzyl alcohol were formed as degradation products resulting from an extended incubation of the substrates and from the degradation of the first two types of transformation products. Crude preparations of laccase from T. versicolor catalysed only the formation of novel heteroaromatic compounds, though they do so with higher yields and in shorter time than cultures of T. versicolor.

Acetamides↗

PubMed1994

Pharmacological properties of ureido-acetamides, new potent and selective non-peptide CCKB/gastrin receptor antagonists.

We present here the pharmacological properties of 3 ureido-acetamide members of a novel family of non-peptide cholecystokinin-B (CCKB) receptor antagonists. RP 69758 (3-(3-[N-(N-methyl N-phenyl-carbamoylmethyl) N-phenyl-carbamoylmethyl] ureido)phenylacetic acid), RP 71483 ((E)-2-[3-(3-hydroxyiminomethyl phenyl) ureido] N-(8-quinolyl) N-[(1,2,3,4-tetrahydro 1-quinolyl)carbonylmethyl]acetamide) and RP 72540 ((RS)-2-[3-(3-[N-(3-methoxy phenyl) N-(N-methyl N-phenyl-carbamoylmethyl) carbamoylmethyl] ureido) phenyl] propionic acid) displayed nanomolar affinity for guinea-pig, rat and mouse CCKB receptors labelled with [3H]pCCK-8 or with the selective CCKB receptor ligand [3H]pBC264. RP 69758 and RP 72540 showed selectivity factors in express of 200 for CCKB versus CCKA receptors. All three compounds had also high affinity for gastrin binding sites in the stomach. The ureido-acetamides behaved as potent antagonists of CCK-8-induced neuronal firing in rat hippocampal slices in vitro, a functional model of brain CCKB receptor mediated responses. RP 69758 is also a potent gastrin receptor antagonist in vivo that dose dependently inhibits gastric acid secretion induced by i.v. injection of pentagastrin in the rat. None of the three ureido-acetamides, at concentrations up to 1 microM, significantly blocked CCK-8-evoked contractions of the guinea-pig ileum in vitro, a CCKA receptor bioassay. In ex vivo binding studies, i.p. administration of RP 69758 and RP 72540 resulted in a dose-dependent inhibition of [3H]pCCK-8 binding in mouse brain homogenate. However, the relative penetration of these ureido-acetamides into the forebrain after peripheral administration was below 0.01%. RP 71483 did not appear to cross the blood-brain barrier in quantities sufficient to prevent [3H]pCCK-8 binding at low doses, a property that makes it suitable for the exploration of the peripheral versus central origin of the behavioural effects observed following systemic administration of CCK. RP 69758, RP 71483 and RP 72540 are highly potent and selective non-peptide CCKB receptor antagonists which are useful tools to explore the physiological functions of CCKB receptors.

Acetamides↗

PubMed1989

Binding of sulfonamide and acetamide to the active-site Zn2+ in carbonic anhydrase: a theoretical study.

Self-consistent field molecular orbital (SCF MO) calculations at both 4-31G and STO-3G levels have been used to examine the binding conformations of sulfonamide and acetamide compounds to the active site of carbonic anhydrase. The results are as follows: (1) sulfonamide binds to the Zn2+ ion in its deprotonated form through the sulfonamide nitrogen to the fourth coordination site of the metal ion; (2) acetamide as neutral species binds to the basic form of the enzyme through the carbonyl oxygen to the fifth coordination site of the metal ion; and (3) the acetamidate ion binds to the acid form of the enzyme through the amide nitrogen to form a tetracoordinated metal complex with three histidine ligands. Analysis of the effects of individual active-site residues on the binding conformations of these inhibitors suggests that metal alone favors bidentate coordination of sulfonamidate and acetamidate complexes and that electron donation from three histidine ligands to the metal ion determines the formation of a tetracoordinated metal complex, which is further stabilized by the presence of Thr 199, as it receives one hydrogen bond from the sulfonamide NH- or from the acetamide NH- and donates a backbone NH hydrogen bond to a sulfonamide oxygen. The calculated binding conformation of sulfonamide and the hydrogen-bonding interactions between sulfonamide and the enzyme are consistent with the X-ray diffraction study of the AMSulf-HCA II complex. However, no X-ray structures are available for amide-HCA II complexes.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetamides↗

PubMedDate not supplied

Disposition of 14C-acetohydroxamic acid and 14C-acetamide in the rat.

Acetohydroxamic acid (AHA) has been identified as a potential agent for the treatment of infection-induced staghorn renal calculi in patients. The pharmacokinetics and disposition of 14C-acetamide have been evaluated in rats following iv and oral administration. The results of these experiments suggest that, following oral administration to rats, AHA is absorbed very rapidly from the gastrointestinal tract and is metabolized to acetamide and CO2. Approximately 50-56% of the iv dose and 40-49% of the oral dose of 14C-AHA is excreted in the urine, suggesting a significant nonrenal elimination pathway for AHA and metabolite(s). This view is supported by the fact that a significant portion of the administered radioactivity (6-10%) is eliminated by the breath as 14CO2. Administration of 14C-acetamide to rats revealed that the compound is predominantly eliminated via the renal route, accounting for 68% of the administered radioactive dose. However, approximately 30% of the dose in the case of both AHA and acetamide could not be recovered, either in the urine or in the breath, during the 72-hr period of the experiment. This suggests that acetamide, either by direct administration or derived as a metabolite of AHA in the rat, may undergo further metabolism to get incorporated into the acetate pool. This would result in very slow elimination of the remaining activity as 14CO2 or as another unknown metabolite.

Acetamides↗

PubMed1975

[About the decomposition of acetamide as taxonomic marker for some species of the genus pseudomonas (author's transl)].

The comparative examination of the acetamide-decompostition and of the acetamide-utilisation as sole source of carbon demonstrates that various groups of the Pseudomonas species with the same kind of reaction have to be distinguished. The acetamide-decomposition-test according to BUHLMANN et al. and the methylene-blue-reduction-test show homogeneous results. As a positive result of these tests the formation of ammonia has always been shown. An acetamide decomposition of this kind has been demonstrable with P. aeruginosa, P. acidovorans and many P. cepacia strains. On liquid mineral media containing acetamide P. fluorescens, P. putida and P. pseudomallei show growth although ammonia is not produced and the test according to BUHLMANN et al. as well as the methylene-blue-reduction-test result negatively. In all tests P. alcaligenes, P. marginata, P. caryophilli and with certain exceptions P. sutzeri and P. putrefaciens react negatively.

Acetamides↗

PubMed1987

Mutagenicity modulating effect of quercetin on aromatic amines and acetamides.

The effect of quercetin on the mutagenicity of 32 kinds of aromatic amines and their acetamides were investigated using Salmonella typhimurium TA98 with a mammalian metabolic activation system (S9 mix). Quercetin enhanced the mutagenicity of the tricyclic aromatic amines (aminofluorene, aminoanthracene and aminophenanthrene) and their acetamides by 1.2-5.9-fold. Whereas, quercetin depressed the mutagenicity of aniline derivatives, biphenyl derivatives, and bi- and tetra-cyclic amino derivatives. The modulation of mutagenicity of Trp-P-1, Trp-P-2, Glu-P-1 and Glu-P-2 (heterocyclic amines) by quercetin were liable to be affected by the content of S9 in the S9 mix. It seems that quercetin does not have the same effect as norharman, because quercetin did not enhance the mutagenicity of aniline. It is suggested that the modulation of the mutagenicity of aromatic amines and acetamides is caused by the modulation of the balance between the mutagenic activation and inactivation in the metabolism of these amines and acetamides in the presence of quercetin. In this modulation, quercetin may participate through its effects on the promotion of N-hydroxylation and the inhibition of arylhydroxylation and transacylation. The presence of tricyclic aromatic rings of amines and acetamides is a structural requirement for the mutagenicity enhancement by quercetin.

Amides↗

PubMed1978

Effect of p-hydroxyacetanilide, sodium sulfate, and L-methionine on the leukemogenicity of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide.

Dietary administration of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide to mice for 14 weeks followed by 16 weeks of control diet resulted in a high incidence of lymphocytic leukemia and a low incidence of forestomach squamous cell papillomas. The coadministration of p-hydroxyacetanilide at a dose of 1.0% with either 250 or 500 ppm of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide resulted in inhibition of leukemogenesis, whereas when p-hydroxyacetanilide was coadministered with 1000 ppm of N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide the leukemia incidence was not significantly reduced, but the latent period was prolonged. When sodium sulfate was administered with p-hydroxyacetanilide and N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide, leukemogenesis was partially restored. L-Methionine, fed in place of sodium sulfate, unblocked leukemogenicity inhibition by p-hydroxyacetanilide. None of these chemicals, p-hydroxyacetanilide, sodium sulfate, or L-methionine, significantly affected the incidence of forestomach papillomas induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]acetamide, although tumor incidences in all groups were low. p-Hydroxyacetanilide and sodium sulfate had no significant effect on the high incidence of stomach tumors induced by formic acid 2-[4-(5-nitro-2-furyl)-2-thiazolyl]hydrazide or bladder tumors induced by N-[4-(5-nitro-2-furyl)-2-thiazolyl]formamide.

Acetanilides↗

PubMed1999

Synthesis and analgesic activity of 2-methyl-2-[1-(3-benzoyl-4-substituted-1,4-dihydropyridyl)]acetic acid methyl esters, acetic acids, and acetamides.

A group of 2-methyl-2-[1-(3-benzoyl-4-substituted-1,4-dihydropyridyl)]acetic acid methyl esters (7), weak acetic acids (8), and acetamides (9) were designed for evaluation as less acidic non-ulcerogenic non-steroidal antiinflammatory drugs (NSAIDs). In this respect, the model compound 2-methyl-2-[1-(3-benzoyl-4-phenyl-1,4-dihydropyridyl)]acetic acid (8a), unlike traditional arylacetic acid NSAIDs, was shown to be a weak acid with a pKa of 9.17. In contrast to arylacetic acid NSAIDs, the alpha-methylacetic acid sodium salt of 8a, or the methyl alpha-methylacetate ester (7a) did not inhibit cyclooxygenase-1 (COX-1) or -2 (COX-2). In vitro stability studies showed that the methyl alpha-methylacetate ester (7a) acts as a prodrug to the alpha-methylacetic acid derivative (8a), undergoing rapid (< 10 minutes) and quantitative conversion upon incubation with rat plasma, or incubation with rat liver homogenate (t1/2 = 25 min). In contrast, the alpha-methylacetamide (9a) underwent negligible (< 2%) conversion to the alpha-methylacetic acid derivative (8a) upon incubation with either rat plasma, or rat liver homogenate, for incubation times up to 24 h. The effect of a C-3 para-substituted-benzoyl substituent (R1 = H, Cl, Me), a C-4 substituent (R2 = aryl, benzyl, cyclohexyl, alkyl), and the nature of the N1-acetic acid moiety [methyl ester (R3 = OMe), acetic acid (R3 = OH), acetamide (R3 = NH2)] on analgesic activity was determined using the 4% NaCl-induced abdominal constriction (writhing) assay. Compounds 7-9 inhibited writhing 27-95% relative to the reference drug aspirin (58% inhibition). The analgesic potency with respect to the para-benzoyl substituent was H > Cl or Me. Although the effect of the C-4 R2-substituent on analgesic activity was variable within the ester, acid and amide sub-groups of compounds, compounds having a R2-cyclohexyl substituent generally provided superior analgesic activity relative to those having a lipophilic alkyl substituent. The nature of the R3-substituent (OMe, OH, NH2) was a determinant of analgesic activity where the potency order was acetic acid methyl ester > acetic acid or acetamide, except when the C-4 R2-substituent was cyclohexyl or benzyl where the potency order was acetamide > acetic acid methyl ester or acetic acid. Reduction of the 5,6-olefinic bond of the 1,4-dihydropyridyl compound (9a, 94% inhibition) to the corresponding 1,2,3,4-tetrahydropyidyl derivative (10, 69% inhibition) reduced analgesic activity.

Acetamides↗

PubMed1977

Polyamine metabolism II: N-(Monoaminoalkyl)- and N-(polyaminoalkyl)acetamides in human urine.

TLC and high-pressure liquid chromatographic examination of the dansyl derivatives obtained from human urine indicated the presence of N-[3-[4-aminobutyl)amino]propyl]acetamide (N1-acetylspermidine), N-[4-](3-aminopropyl)amino]buryl]acetamide (N8-acetylspermidine), N-(4-aminobutyl)acetamide (N-acetylputrescine), and N-(5-aminopentyl)acetamide (N-acetylcadaverine). 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. The three cancer patients had a considerably higher ratio of N1- to N8-acetylspermidine than did the three normal subjects. These findings indicate the ratio of N1- to N8-acetylspermidine in the 24-hr urine may serve as a biochemical marker for cancer.

Acetamides↗

PubMed2004

Mechanism of metal-mediated DNA damage induced by a metabolite of carcinogenic acetamide.

Acetamide is carcinogenic in rats and mice. To clarify the mechanism of carcinogenesis by acetamide, we investigated DNA damage by and acetamide metabolite, acetohydroxamic acid (AHA), using 32P-5'-end-labeled DNA fragments. AHA treated with amidase induced DNA damage in the presence of Cu(II) and displayed a similar DNA cleavage pattern of hydroxylamine. DNA damage was inhibited by both catalase and bathocuproine, suggesting that H2O2 and Cu(I) are involved. Carboxy-PTIO, a specific scavenger of nitric oxide (NO), partially inhibited DNA damage. The amount of 8-oxo-7,8-dihydro-2'-deoxyguanosine (8-oxodG) by amidase-treated AHA was similar to that by hydroxylamine. ESR spectrometry revealed that amidase-treated AHA as well as hydroxylamine generated NO in the presence of Cu(II). From these results, it has been suggested that AHA might be converted into hydroxylamine by amidase. These results suggest that metal-mediated DNA damage mediated by amidase-catalyzed hydroxylamine generation plays an important role in the carcinogenicity of acetamide.

8-Hydroxy-2'-Deoxyguanosine↗

PubMed2002

Formation and stability of enolates of acetamide and acetate anion: an Eigen plot for proton transfer at alpha-carbonyl carbon.

Second-order rate constants were determined in D(2)O for deprotonation of acetamide, N,N-dimethylacetamide, and acetate anion by deuterioxide ion and for deprotonation of acetamide by quinuclidine. The values of k(B) = 4.8 x 10(-8) M(-1) s(-1) for deprotonation of acetamide by quinuclidine (pK(BH) = 11.5) and k(BH) = 2-5 x 10(9) M(-1) s(-1) for the encounter-limited reverse protonation of the enolate by protonated quinuclidine give pK(a)(C) = 28.4 for ionization of acetamide as a carbon acid. The limiting value of k(HOH) = 1 x 10(11) s(-1) for protonation of the enolate of acetate anion by solvent water and k(HO) = 3.5 x 10(-9) M(-1) s(-1) for deprotonation of acetate anion by HO(-) give pK(a)(C) approximately 33.5 for acetate anion. The change in the rate-limiting step from chemical proton transfer to solvent reorganization results in a downward break in the slope of the plot of log k(HO) against carbon acid pK(a) for deprotonation of a wide range of neutral alpha-carbonyl carbon acids by hydroxide ion, from -0.40 to -1.0. Good estimates are reported for the stabilization of the carbonyl group relative to the enol tautomer by electron donation from alpha-SEt, alpha-OMe, alpha-NH(2), and alpha-O(-) substituents. The alpha-NH(2) and alpha-OMe groups show similar stabilizing interactions with the carbonyl group, while the interaction of alpha-O(-) is only 3.4 kcal/mol more stabilizing than for alpha-OH. We propose that destabilization of the enolate intermediates of enzymatic reactions results in an increasing recruitment of metal ions by the enzyme to provide electrophilic catalysis of enolate formation.

Acetamides↗

PubMed1973

A saturable, vasopressin-sensitive carrier for urea and acetamide in the toad bladder epithelial cell.

The permeability of the toad bladder to a series of isotopically labeled nonelectrolytes was determined in the presence of 150 mM unlabeled acetamide. Under these conditions, overall bladder function was unimpaired, as shown by a normal response to vasopressin of short-circuit current and permeability coefficient of [(3)H]water,[(14)C]ethanol, and [(14)C]propionamide. The permeability of the bladder to isotopic acetamide and urea, however, was significantly depressed by unlabeled acetamide, in both the absence and presence of vasopressin. These experiments indicate a competition between unlabeled and isotopic species for binding sites, and show the existence of a saturable, vasopressin-sensitive carrier for urea and acetamide in the epithelial cell membrane.

Acetamides↗

PubMed1998

A novel histamine 2(H2) receptor antagonist with gastroprotective activity. II. Synthesis and pharmacological evaluation of 2-furfuryl-thio and 2-furfurylsulfinyl acetamide derivatives with heteroaromatic rings.

We recently found that N-[3-[3-(piperidinomethyl)phenoxyl]propyl]acetamide derivatives with a thioether function showed gastric anti-secretory and gastroprotective activities and that the thioether function (particularly furfurylthio or furfurylsulfinyl) was essential for gastroprotection. In the present study, a series of 2-furfurylthio and 2-furfurylsulfinyl acetamide derivatives were synthesized and evaluated for histamine H2 receptor antagonistic activity, gastric anti-secretory activity and gastroprotective action. Based on the structure of N-[3-[3-(piperidinomethyl)phenoxyl]propyl]acetamide, we designed compounds, in which the 3-(piperidinomethyl)phenoxy part is substituted with many types of heteroaromatic ring attached to the tertiary amine and the propyl group is replaced with other carbon linkages. Structure-activity relationships are discussed. 2-Furfurylsulfinyl-N-[4-[4-(piperidinomethyl)-2-pyridylox y]- (Z)-2-butenyl]acetamide was the most potent among the tested compounds and was given the code designation FRG-8813.

Acetamides↗

PubMed2006

Comparison of glycerol, lactamide, acetamide and dimethylsulfoxide as cryoprotectants of Japanese white rabbit spermatozoa.

The rabbit is considered to be a valuable laboratory animal. We compared glycerol, lactamide, acetamide, and dimethylsulfoxide (DMSO) as cryoprotectants in egg-yolk diluent of ejaculated Japanese white rabbit spermatozoa for improvement of sperm cryopreservation methods. Rabbit semen was frozen with 1.0 M glycerol, lactamide, acetamide, or DMSO in plastic straws. Forward progressive motility and plasma membrane integrity of the post-thaw spermatozoa were examined. The rate of forward progressive motile spermatozoa in lactamide (37.8 +/- 3.0%) was significantly (P<0.05) higher than in glycerol (17.0 +/- 3.3%). In addition, the rates of sperm plasma membrane integrity in lactamide and acetamide (35.9 +/- 3.3% and 30.2 +/- 3.0%, respectively) were significantly (P<0.05) higher than in glycerol (17.0 +/- 2.6%). The results indicate that 1.0 M lactamide and acetamide have higher cryoprotective effects than 1.0 M glycerol for cryopreservation of Japanese white rabbit spermatozoa.

Acetamides↗

PubMed1986

Biological effects of acetamide, formamide, and their monomethyl and dimethyl derivatives.

The industrial use of certain acetamides and formamides (particularly DMAC and DMF) for their solvent properties has resulted in rather extensive examination of their biological properties. Both DMAC and DMF are rapidly absorbed through biological membranes and are metabolized by demethylation first to monomethyl derivatives and then to the parent acetamide or formamide. Relatively high single doses to various species following oral, dermal, i.p., i.v., or inhalation exposures generally are required to produce mortality. The liver is the primary target following acute high level exposure, but massive doses can also produce damage to other organs and tissues. Repeated sublethal treatment by various routes also shows the liver to be the target organ with the degree of damage being proportional to the amount absorbed. With MMF, the potential usefulness as a cancer chemotherapeutic agent needs to be measured against the hepatotoxic effects produced in man. Acetamides and formamides are generally inactive in mutagenicity tests. Mammalian test systems do not appear to be genetically sensitive and DMF has been recommended for use as the vehicle in microbial assays designed to test for genetic activity of hard-to-dissolve chemicals. Embryotoxicity can be demonstrated at high doses; doses which generally show toxicity to the maternal animals. Structural abnormalities in sensitive species such as the rabbit are produced following exposure at near-lethal levels. The spectrum of abnormalities seen is broad and fails to show any time or site specificity in terms of developing organs/organ systems. Inhalation exposures to DMAC and DMF at levels producing some maternal toxicity in rats have produced no teratogenic response and only slight evidence of embryotoxicity. Long-term feeding of relatively high levels of acetamide produces liver cancer in rats. DMAC and DMF appear to be noncarcinogenic. The environmental toxicity of these chemicals is low. Liver damage can be produced by overexposure to these chemicals in man. Airborne concentrations need to be controlled and care should be taken to avoid excessive liquid contact as the chemicals are absorbed through the skin. A relationship exists between the amount of DMAC or DMF absorbed and the amount of MMAC or MMF excreted in the urine so that biomonitoring of the urinary metabolites can indicate situations in which total exposures, both dermal and inhalation, are excessive. An interaction between DMF and ethanol occurs such that signs, including severe facial flushing, appear when DMF-exposed individuals consume alcoholic beverages.

Acetamides↗

PubMed2002

Inhibition of human phosphodiesterase 4A expressed in yeast cell GL62 by theophylline, rolipram, and acetamide-45.

AIM: To study the inductive expression of human phosphodiesterase 4A (hPDE4A) in yeast cell GL62 and investigate the inhibitory effects of theophylline, rolipram, and acetamide-45 on PDE4A activity of the expressed product in yeast cell GL62. METHODS: Yeast cell GL62 were transfected with human PDE4A gene cloned in the expression plasmid p138NB. Expression was induced by adding CuSO4 to a final concentration of 150 micromol/L, and the expressed product was extracted. The activity of PDE4A was detected by HPLC. RESULTS: Yeast cell GL62 expressed a certain protein at CuSO4 150 micromol/L, the size of the expressed product was between 62 kDa and 83 kDa, the activity of PDE4A of the expressed product at 3 h was in maximum (188 23) micromol/g/min, and the Km was (17.7 2.6) micromol/L. Theophylline, rolipram, and acetamide-45 could inhibit the activity of PDE4A extracted from yeast cell GL62. The IC50 (95 % confidence limits) of theophylline, rolipram, and acetamide-45 were 1642 (989-2727), 4.58 (3.45-6.08), and 275 (170-444) micromol/L respectively. CONCLUSION: PDE4A expressed in yeast cell GL62 is biologically active. Theophylline, rolipram, and acetamide-45 can inhibit the PDE4A activity. The expressed product in yeast cell GL62 may be used in the research work of PDE4 and its inhibitors.

3',5'-Cyclic-AMP Phosphodiesterases↗

PubMed2002

[Effect of fluoroacetamide on cardiomyocytes of rat and the antidotal effect of acetamide].

OBJECTIVE: To observe the effect of fluoroacetamide on cardiomyocytes of rat and the antidotal effect of acetamide. METHODS: 4 groups of SD rats were treated with various dosages of fluoroacetamid(p.o.) and 2 groups of them were treated with acetamide(i.p.). The changes of cardiomyocytes and serum AST, LDH, CK, CK-MB and HBDH were measured at different intervals after poisoning. RESULTS: In the group treated with fluoroacetamid 8 mg/kg. bw, serum AST[(589.58 +/- 821.72) U/L], CK[(916.78 +/- 343.55) U/L], HBDH[(504.47 +/- 148.88) U/L] raised obviously compared with control[(187.70 +/- 46.87), (755.65 +/- 498.90), (347.25 +/- 228.40) U/L respectively] (P < 0.01), and the pathological findings such as degeneration, liquefactive necrosis and filtration of inflammatory cells in cardiac muscles were observed 24 hours later, while all the male dead within 3 days. In the group treated with fluoroacetamid 4 mg/kg. bw, serum LDH and HBDH rose significantly compared with control(P < 0.01) 5 day later. On the day of 10, myocardial enzymes restored in all experiment groups with some interstitial fibroblastic proliferation. The pathological changes were reduced in the group treated with acetamide synchronously (100 mg/kg. bw). CONCLUSION: Acute intoxication of fluoroacetamide could damage cardiomyocytes while acetamide could reduce the injury of them, but the injury was reversible. The levels of serum myocardial enzymes could be a usable index for early diagnosis.

Acetamides↗