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At least 19 recordsLinked to original sources
PubMed1975

Personal air sampling for vapors of aniline compounds.

A method has been developed for air sampling and laboratory analysis of vapors of seven aniline compounds: aniline, N,N-dimethylaniline, o-toluidine, 2,4-xylidine, panisidine, o-anisidine, and p-nitroaniline. Air is drawn by a personal sampling pump from a worker's breathing zone through a tube containing silica gel to collect any anilines present. In the laboratory each silica gel section is transferred to a glass-stoppered tube and desorbed with ethanol. An aliquot of this is analyzed by gas chromatography to determine the amount of each aniline compound present. The sampling tube can be used for short-term sampling at 1000 cm3/min or for sampling up to eight hours at 200 cm3/min. Maximum interference effects of water vapor have been considered. Results of retention, desorption, storage, accuracy, and precision studies are presented.

Absorption↗
PubMed1977

The nature of the rate-limiting step in aniline hydroxylation involving cytochrome p-450 rat liver microsomes.

The kinetics of aniline hydroxylation was studied with: (1) rat liver microsomes involving NADPH and O2 (system 1), (2) hepatic microsomes and tert-butylhydroperoxide (system 2) and (3) microsomes and cumyl hydroperoxide (system 3) at 15--37 degrees C. The reactions were characterized by the values of the aniline oxidation rate constants, k2 = V/E0, where E0 is the initial concentration of cytochrome P-450: K 1/2 = 1.60 - 10(8) EXP (-13 400/RT) sec-1, k 2/2 = 1.66 - 10(9) exp (-14 500/RT) sec-1, k 3/2 = 6.83 - 10(9) exp (-15 300/RT) sec-1. The values of delta H0 and delta S0, were calculated and compared for the three systems. The evidence suggests that oxygen insertion into the substrate molecule is the rate-limiting step in the reaction of aniline oxidation for the mentioned systems. The nature of aniline binding to cytochrome P-450 and that of the hydroxylating agent have been discussed.

Aniline Compounds↗
PubMed1978

Chromosome banding patterns and breakpoints of three transplantable hepatomas induced in rats by aromatic amines.

The chromosome constitution of transplantable hepatomas H-35tc1, 7316A, and 8994 induced in ACI male, BUF female, and BUF male rats, respectively, by monocyclic or polycyclic aromatic amines was studied by Giemsa banding techniques. Hepatoma H-35tc1 was hyperdiploid, with a dominant stemline of 46 chromosomes. The stemline of the heterogeneous 7316A was in the hypotetraploid region (75-8,). Hepatoma 8994 had a near-triploid complement; most metaphase cells and chromosome numbers from 62 to 68. Thirty marker chromosomes were detected. Nineteen rearanged chromosomes were in hepatoma 8994, whereas only 8-10 markers could be found in the 80 +/- 3 chromosome complement of hepatoma 7316A. Two constant common markers were noted: mar2, a chromosome No. 11 with translocation short arm in H-35tc1 and 8994, and mar10 (mar10a), a chromosome No. 1 with a duplicated segment at breakpoint q54 in hepatomas 7316A and 8994. An analysis of the distribution of 232 breakpoints in the rat karyotype, 26 identified in the hepatomas and 206 collected from the literature, revealed a statistically significant excess of breaks in chromosomes No. 1, 2, 3, and 10 (P less than 0.001). The X- and Y-chromosomes showed a considerably lower number of breaks than anticipated (P less than 0.01). Even after a history of continuous transplantation for 10 years, these 3 hepatomas retained intact sex chromosomes that corresponded to the phenotype of the primary host. Preservation of the sex chromosomes in the hepatomas may be attributed to a lower susceptibility of the sex chromosomes than of the autosomes to breakage.

2-Acetylaminofluorene↗
PubMed1976

Accleration of autooxidation of human oxyhemoglobin by aniline and its relation to hemoglobin-catalyzed aniline hydroxylation.

Changes in the ultraviolet/visible spectrum of human oxyferrohemoglobin upon addition of aniline were indicative of a concentration-dependent interaction of aniline with hemoglobin, resulting in accelerated autooxidation of the hemoprotein. Oxygen was found to markedly inhibit this interaction of aniline with oxyhemoglobin. The dependence of the rate of autooxidation on aniline concentration followed saturation kinetics and showed a half-maximal response at 8 mM aniline. This value is equal to the value of Km for aniline as substrate for the O2-dependent, hemoglobin-catalyzed hydroxylation reaction which yields p-aminophenol (Mieyal, J. J., Ackerman, R.S., Blumer, J.L., and Freeman, L.S. (1976) J. Biol. Chem. 241, 3436-3441). Thus, an aniline-oxyhemoglobin complex is implicated in the overall catalytic reaction. No detectable p-aminophenol was formed when aniline was combined with oxyhemoglobin in the absence of an electron donor, but hydroxylation of aniline does occur when NADPH, NADPH plus P-450 reductase, or Na2S2O4 are also added.

Aniline Compounds↗
PubMed1979

Hypobetalipoproteinemic agents. 2. Compounds related to 4-(1-adamantyloxy)aniline.

While the previously used displacement reaction of sodim 1-adamantyl oxide on 4-fluoronitrobenzene was applicable to the preparation of 4-(1-adamantyloxy)aniline and several related compounds, certain derivatives were not easily accessible by this route. Thus the recently reported ortho alkylation of anilines and the dicyclohexylcarbodiimide-promoted coupling of 1-adamantanol with phenols were useful in the preparation of aromatic-substituted derivatives. Furthermore, addition of phenylmagnesium bromide to 1-cyanoadamantane provided entry to the 4-(1-adamantylmethyl)aniline series. 4-(1-Adamantyloxy)aniline (3) is herein reported to be a more potent hypobetalipoproteinemic agent than the previously reported bicyclooctyloxy analogue. Replacement of the oxygen atom of 3 with sulfur (74) or methylene (62), but not nitrogen (71), results in active compounds. In the oxygen series derived from 3, the widest scope of substitution on nitrogen resulting in activity is found. The N-ethoxycarbonyl (5), acetyl (6), methyl (12), ethyl (13), N-methyl-N-(2-hydroxyethyl) (19), N-methyl-N-formyl (22), N,N-dimethyl (26), pyrrolidine (14), and piperidine (15) derivatives are active. Aromatic ring substitution also provided the active 3-chloro (44b), 2-fluoro (41b, 42, and 43), and 2-methylthiomethyl (48) compounds. Thus these active compounds are identified for further development as hypobetalipoproteinemic agents.

Adamantane↗
PubMed1978

On the mechanisms of induced somatic recombination by certain fungicides in Aspergillus nidulans.

Four fungicides interfered with the segregation of chromosomes at mitosis of Aspergillus nidulans by increasing the somatic recombination, shown as colour sectors in green colonies, in a strain heterozygous for spore colour mutations. In an attempt to discover the mechanisms by which these fungicides increased the somatic recombination, a prototrophic diploid strain, heterozygous for colour and several other appropriate markers in all chromosomes, was used which enabled the detection and classification of all colour recombinants to be made by genetic analysis. The fungicides investigated were: benomyl (methyl-1-(butylcarbamoyl)-2-benzimidazole carbamate) a benzimidazole derivative, botran (2,6-dichloro-4-nitroaniline) and chloroneb (1,4-dichloro-2,5-dimethoxybenzene) of the aromatic hydrocarbon group of fungicides, and the antibiotic actinomycin D. At least three different mechanisms, non-disjunction, mitotic crossing-over and breakage-deletion, were found to be responsible for the recombinogenic activity of the compounds studied.

Aniline Compounds↗
PubMed2026

[Laryngeal squamous cell carcinoma-derived exosomes promote neuronal axonal growth by remodeling the neural microenvironment].

Objective: Perineural invasion (PNI) is a critical determinant of poor prognosis in laryngeal squamous cell carcinoma (LSCC), but its underlying mechanisms remain unclear. This study aimed to investigate whether LSCC-derived exosomes induce axonal growth by delivering neuroactive molecules, thereby contributing to tumor perineural invasion. Methods: Clinical data from the laryngeal cancer cohort of The Cancer Genome Atlas Head and Neck Squamous Cell Carcinoma (TCGA-HNSC) dataset were analyzed. Propensity score matching (PSM) and Cox regression were used to evaluate the prognostic value of nerve density, and these findings were validated using 35 pairs of laryngeal cancer and adjacent normal tissue specimens collected at Yantai Yuhuangding Hospital between 2022 and 2026 to assess neural morphological changes. Exosomes were isolated from the human LSCC cell line AMC-HN-8, characterized by quality-control assays, and co-cultured with PC12 cells. A rescue experiment using GW4869, a specific inhibitor of neutral sphingomyelinase, was performed to confirm the exosome-dependent effect. Neurite outgrowth was evaluated by immunofluorescence, and the expression of axonal growth-related genes was measured by RT-qPCR. Targeted metabolomics was employed for the absolute quantification of neuroactive metabolites within the vesicles and for pathway enrichment analysis. Results: After PSM adjustment, high nerve density was identified as an independent poor prognostic factor in LSCC patients (HR=2.10, P=0.035), with particularly pronounced prognostic value in the early-stage node-negative (N0) subgroup (HR=4.07, P=0.001). Pathological sections showed high expression of the neural markers &#x3b2;III-tubulin and PGP9.5 in LSCC tissues (&#x3b2;III-tubulin: t=2.234, P<0.05; PGP9.5: t=2.575, P<0.05). Exosomes were successfully isolated from AMC-HN-8 cells and passed quality control. In vitro assays showed that LSCC-derived exosomes significantly promoted neurite extension and branching in PC12 cells (t=4.147, P<0.000 1) and upregulated core axonal growth genes, including GAP-43, NEFL, and NEFM (GAP-43: t=3.698, P<0.05; NEFL: t=5.113, P<0.01; NEFM: t=5.263, P<0.01); this effect was completely reversed by the exosome-release inhibitor GW4869 (t=3.535, P<0.001). Targeted metabolomics revealed a specific enrichment of 12 neurotransmitters and metabolites within LSCC exosomes, centered on glutamine (83.411 &#x3bc;mol/L, FC=1.88) and glutamate (18.461 &#x3bc;mol/L, FC=1.21), which were significantly enriched in signaling pathways such as "central carbon metabolism in cancer" and "glutamatergic synapse". Conclusion: Nerve density is a potential adverse prognostic factor in patients with LSCC. LSCC-derived exosomes can directly induce axonal growth in neuron-like cells, suggesting that tumor cells actively remodel the neural microenvironment and drive axonal growth through exosome-mediated long-range signaling.

Exosomes↗
PubMed1976

Spectrophotometric determination of diphenhydramine hydrochloride using dipicrylamine.

A spectrophotometric procedure for the determination of diphenhydramine hydrochloride based on the reaction with dipicrylamine was developed. A yellow complex forms and is easily extractable by chloroform at pH 5. The mole ratio of diphenydramine hydrochloride to dipicrylamine in the complex is 1:3. The absorbance of the complex obeys Beer's law over the concentration range of 3-10 mug of diphenhydramine hydrochloride per ml of chloroform. This procedure can be carried out in the presence of other compounds without interference.

Aniline Compounds↗
PubMed1977

Clinical evaluation of a new anthelmintic - C. 9333 Go./CGP 4540 in human hookworm infection.

A new antihookworm compound, C.9333 Go./CGP 4540, was evaluated clinically in 65 adult patients with hookworm infection. Several dosage schedules were evaluated to determine an effective, well tolerated and convenient regime. The lowest effective dose was 125 mg administered at four-hourly intervals for three doses. The compound was generally well tolerated; mild giddiness was observed in nine patients and severe giddiness was present in one patient. Clinical and biochemical monitoring revealed no other toxicity of the compound.

Ancylostoma↗