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At least 307 records · Page 17Linked to original sources
PubMed1976

Mutagenic effect of epichlorohydrin. I. Testing on human lymphocytes in vitro in comparison with TEPA.

The mutagenic effect of the monofunctional alkylating agent epichlorohydrin was tested on human lymphocytes in vitro and compared with the mutagenic effect of the polyfunctional alkylating agent TEPA. The same descending concentrations were used for both mutagens: 10(-4), 10(-5), 10(-6), 10(-7), 10(-8), 10(-9), 10(-10) and 10(-11) M. Similar types of chromosomal aberration were found, but the effect of ECHH was 4-5 times lower than that of TEPA. ECHH was found to be a mild mutagen. Different timing of mutagen application was used in the course of 56 h of cultivation of lymphocytes: 1 h before cultivation, one hour between the 24th and 25th h of cultivation and 24 h before the end of cultivation. From the results presented we conclude that the application of the chemical for the last 24 h of human lymphocyte cultivation should be recommended for routine mutagenicity testing.

Azirines↗
PubMed1976

A search for storage effects on chromosome aberrations induced in human normal type- and xeroderma pig-mentosum fibroblasts by tetra-ethylene-imino-1,4-benzochinon and n-acetoxy-n-2-acetylaminofluorene.

Normal human foreskin fibroblasts in stationary phase were treated with tetra-ethylene-imino-1,4-benzochinon. Treated cells were stored for 0, 1, 2 or 3 weeks on special storage medium and then analyzed for induced chromosome aberrations. The results showed that there was a decrease in the frequency of chromosome aberrations with increasing storage times rather than an increase. These observations may indicate that, (1) a storage effect of the type observed in Drosophila, Neurospora and barley (i.e. increase of genetic damage with duration of storage) does not occur in human cells in culture, or (2) the effect is masked by cell selection and/or repair processes. To inquire whether the absence of a storage effect might have been, at least in part, due to the interaction of repair processes and the effect sought, xeroderma pigmentosum cells in stationary phase were treated with N-acetoxy-AAF. This experiment likewise provided no evidence for a storage effect.

Acetoxyacetylaminofluorene↗
PubMed1987

Diaziquone-induced micronuclei in cytochalasin B-blocked mouse peripheral blood lymphocytes.

A mouse peripheral blood lymphocyte (PBL) micronucleus (MN) test was developed using a modification of the technique for assessing MN in human PBLs described by Fenech and Morley (1985). Male C57Bl/6 mice (5/dose) were injected i.p. with either 0, 2.5, 5.0, 7.5, or 10.0 mg diaziquone (AZQ)/kg. After 24 h the mice were bled by cardiac puncture, PBLs were isolated on a Ficoll-density gradient and then cultured in RPMI 1640 medium using 8 micrograms phytohemagglutinin/ml. In some cultures cytochalasin B (CYB) was added at 21 h during the medium change to block cytokinesis. In other cultures, CYB was omitted to compare the sensitivity of analyzing MN in binucleate versus unblocked mononucleate cells. All doses of AZQ yielded significant increases in MN-containing binucleated PBLs. The use of CYB in the mouse PBL MN test increased the sensitivity approximately 3-fold. The MN test in mouse PBLs should be useful in comparative cytogenetic studies of mice and humans.

Animals↗
PubMed1985

Intracerebroventricular administration of ethylcholine mustard aziridinium ion (AF64A) reduces release of acetylcholine from rat hippocampal slices.

Ethylcholine mustard aziridinium ion (AF64A), or vehicle, was infused bilaterally (3 nmol/3 microliter per side) into the lateral ventricles of rats. The effect of such treatment on various cholinergic responses was measured in the hippocampus, cortex and striatum. Potassium-stimulated release of acetylcholine from superfused slices of hippocampus was reduced, 7 and 21 days after treatment with AF64A, to 24 and 35% of control, respectively. The activity of choline acetyltransferase in the hippocampus also decreased, to 42% of control, both 7 and 21 days after treatment with AF64A. Similarly, the activity of acetylcholinesterase and the high affinity transport of choline in the hippocampus were reduced, to 40 and 30% of control; and to 33 and 48% of control, respectively, 7 and 21 days after treatment with AF64A. Synthesis of acetylcholine in slices of hippocampus was also decreased after treatment with AF64A (71 and 51% of control, 7 and 21 days post-AF64A respectively). Only the binding of [3H]QNB in the hippocampus was unchanged at 7 days after treatment with AF64A, although a small reduction (11%) was noted 21 days after treatment with AF64A. The activity of choline acetyltransferase and acetylcholinesterase, the high-affinity transport of choline and the binding of [3H]QNB in cortex and striatum were unaffected by treatment with AF64A under the same experimental conditions. Using a substantially smaller dose than that earlier reported in mice, the earlier finding was thus confirmed, and extended, in rats, of a highly selective effect of AF64A on several components of the cholinergic system. Under the conditions of this study, these effects appeared to be confined to the hippocampus.

Acetylcholine↗
PubMed1987

Time course of ethylcholine aziridinium ion (AF64A)-induced cholinotoxicity in vivo.

The time course of the cholinotoxicity of ethylcholine aziridinium ion (AF64A) has been investigated. Rats were injected with AF64A (3 nmols/3 microliters/side, bilateral, i.c.v.) or with vehicle. One day to one year after treatment, the hippocampus, cortex and striatum were analyzed for the activity of choline acetyltransferase (ChAT) and acetylcholinesterase (AchE) and high-affinity transport of choline (HAChT). In addition, the release of K+-stimulated acetylcholine (ACh) from superfused slices of hippocampus was determined. The first parameter affected was high affinity transport of choline. One day after treatment with AF64A, the high affinity transport of choline in the hippocampus was reduced by 23%. This reduction was maximal one week after treatment (-67%) and persisted for at least 6 months. The high affinity transport of choline in the striatum and cortex was not altered by treatment with AF64A. The activity of ChAT and AChE in the hippocampus was reduced by 2 days after treatment with AF64A. These deficits persisted for at least 6 months (AChE) to 1 year (ChAT). The activity of ChAT and AChE in the cortex and striatum was minimally affected up to 1 year after treatment with AF64A, at which time significant reductions were noted. The release of ACh was affected 3 days after treatment with AF64A, and remained attenuated 6 months later. These data indicate that the cholinergic deficit caused by in vivo treatment with AF64A was first apparent at the level of high affinity uptake of choline in the hippocampus HAChT. Subsequently, the activity of ChAT and AChE and release of ACh in the hippocampus were affected.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholinesterase↗