[Studies on aminoacetonitrile and its related compounds. II. Infiltration of pontamine sky blue into poisoned mouse liver cells, and its protection by aminoacetonitrile].
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Animals↗
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[Studies on aminoacetonitrile and its related compounds. IV. Effect of aminoacetonitrile on experimental fatty liver].
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Animals↗
[Studies on aminoacetonitrile and its related compounds. V. Effects of aminoacetonitrile on hepatic lesions induced by carbon tetrachloride in adrenalectomized rat].
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Adrenalectomy↗
Comparative effects of indole and aminoacetonitrile derivatives on dimethylnitrosamine-demethylase and aryl hydrocarbon hydroxylase activities.
The effect of in vivo administration of indole and five 3-indolyl derivatives including L-tryptophan, as well as of aminoacetonitrile and 3 of its derivatives, were studied on the carcinogen-metabolizing hepatic mixed-function oxidases dimethylnitrosamine (DMN)-demethylase I and II and aryl hydrocarbon hydroxylase (AHH). Indole, 3-indolylmethanol, 3-indolyl-acetonitrile, 3-indolylacetone and L-tryptophan induce AHH activity from 3- to 6-fold of the control level, whereas beta-3-indolylethanol has no effect; the latter compound produces a 21% decrease of the endoplasmic reticulum content in the tissue. Only L-tryptophan induces DMN-demethylase I and only L-tryptophan and 3-indolylmethanol induce DMN-demethylase II, representing a doubling of enzyme activity in all 3 instances. Aminoacetonitrile is a potent repressor of DMN-demethylase I. Substitutions on the amino group bring about strong decrease or abolishment of mixed-function oxidase repressor activity; thus, iminodiacetonitrile has only about 1/5th the repressor activity of the parent compound, whereas nitrilotriacetonitrile and dimethylaminoacetonitrile appear to be inactive. Aminoacetonitrile and its derivatives studied have no effect on DMN-demethylase II and AHH activities. The mixed-function oxidase-modifying effects of the indole compounds and of aminoacetonitrile and its derivatives illustrate the potential complexity of effects of dietary constituents on the carcinogenic responses.
Acetonitriles↗
Inhibition of the alkylation of nucleic acids and of the metabolism of 1,2-dimethylhydrazine by aminoacetonitrile.
Pretreatment of rats with aminoacetonitrile inhibited the metabolism of [14C]1,2-dimethylhydrazine to 14CO2 and increased the expiration of [14C]-azomethane. Alkylation of nucleic acids following administration of 1,2-dimethylhydrazine was reduced by aminoacetonitrile to 5% of control levels in liver, 11% of control levels in kidney and 43% of control levels in colon.
Acetonitriles↗
The effects of aminoacetonitrile and its derivative on components of hepatic connective tissue in rats with chronic hepatic injury.
Aminoacetonitrile (AAN) and its derivative, p-carboxyphenylglycyl-aminoacetonitrile (p-CPGAAN) were given to rats with chronic liver injury induced by carbon tetrachloride and their effects of the components of the hepatic connective tissue were studied. 1. Both AAN and p-CPGAAN markedly inhibited an increase in the amount of collagen in injured liver and in addition these agents interferred with an increase in the amount of hepatic glycosaminoglycans, particularly of the sulfated fraction. 2. In the AAN-treated group, such side effects attributable to AAN as loss of the body weight, depilation and exostosis were observed and an increase in the hepatic collagen solubility was also noted. However, no apparent side effect was found in the p-CPGAAN-treated group, and there was no difference in the solubility profile of hepatic collagen between the p-CPGAAN-treated and control groups. 3. It is assumed that p-CPGAAN has an action to prevent the hepatic fibrosis via a mechanism different from that of the lathyrogenic action.
Acetonitriles↗
[The influencing of blastogenesis and embryogenesis in rats through aminoacetonitrile].
The study was designed to determine the influence of the lathyrogenic substance aminoacetonitrile on blastogenesis and embryogenesis of the Wistar rat. 91 female Wistar rats, weighing from 190 through 380 g, received a single injection of 300 mg aminoacetonitrile (AAN)/kg body weight. Substance was given intraperitoneally on days 5, 7, 9, 11 or 13 of pregnancy. The detection of sperms in the vaginal smears was counted as day 1 post coitum. Animals were sacrificed on day 21 of pregnancy. The following parameters served as a base of interpretation: fetal body weight, numbers of implantations, resorptions, dead and living fetuses. Malformations were detected by outer inspection for gross anomalies, by the razor blade technique for internal malformations, and by skeletal preparations. All results were evaluated by statistical means. AAN influences pregnancy and fetal development. The rates of fetal resorptions are enhanced after application of AAN beyond the 7th day p. c. The maximum of fetal death is reached on day 11 p. c. There is no influence on the mean implantation number. With the exception of the 5th day of development AAN reduces the number of living fetuses. After application of AAN on day 13 p.c. the mean body weight decreases significantly. All over the investigated range malformations can be observed. Abnormalities of internal organs are frequent: Hydrocephalus, hydronephrosis, situs inversus. Malformations of the skeletal system are only observable on days 5, 7 and 9: sternal fissure, supernumerary ribs, destruction of the lumbar spine. AAN does not induce gross anomalies of the fetus.
Abnormalities, Drug-Induced↗
[Aminoacetonitrile and fetogenesis of the rat. II. Malformations of organ systems (author's transl)].
We investigated the action of the lathyrogenic compound aminoacetonitrile (300 mg/kg body weight) on fetogenesis of the Wistar rat. In a 1st section we dealt with influence on the outer body shape and common reproductive parameters (WENDLER and coworkers 1980). This 2nd section describes toxic effects on internal organs and malformations on organ systems detected by free-hand razor blade technique. Especially, we observed cardial ectopia, rupture of the ascendant aorta, situs inversus, hydrocephalia, hydronephroses, and dystopic kidneys. Enlargement of heart atria, and main thoracic veins, dilatations of salivary gland ducts and bronchial tree are considered to be nonspecific toxic effects of aminoacetonitrile.
Abnormalities, Multiple↗
Cellular injury and carcinogenesis. Inhibition of metabolism of dimethylnitrosamine by aminoacetonitrile.
1. Aminoacetonitrile, a lathyrogenic agent known to decrease the hepatotoxic action of dimethylnitrosamine, inhibited the metabolism of this compound by rats in vivo and by rat liver slices in vitro. 2. Methylation of nucleic acids in rat liver and kidney by dimethylnitrosamine in vivo was inhibited by treatment of the animals with aminoacetonitrile. 3. These findings are discussed in relation to the hypothesis that dimethylnitrosamine requires metabolism to exert its hepatotoxic and carcinogenic action.
Animals↗
Effects of aminoacetonitrile on net photosynthesis, ribulose-1,5-bisphosphate levels, and glycolate pathway intermediates.
The effects of aminoacetonitrile (a competitive inhibitor of glycine oxidation) on net photosynthesis, glycolate pathway intermediates, and ribulose-1,5-bisphosphate (RuBP) levels have been investigated at different O(2) and CO(2) concentrations with soybean (Glycine max)[L] Merr. cv Pioneer 1677) leaf discs floated on 25 millimolar aminoacetonitrile (AAN) for 50 minutes prior to assay.At 2% O(2) and 200 or 330 microliters per liter CO(2), the inhibitor had no effect on the rate of net photosynthesis and RuBP levels when compared with the control levels. At 11% to 60% O(2), AAN caused a decrease in net photosynthesis in addition to the inhibition by O(2). This extra inhibition ranged from 22% to 59% depending on the O(2) and CO(2) concentrations. The levels of RuBP, however, were 1.3 to 2.7 times higher than in the control plants at the same O(2) concentrations. At 40% O(2) and 200 microliters per liter CO(2), the inhibitor caused a 6-fold increase in glycine and more than 2-fold increase in glyoxylate levels, whereas those of glycolate decreased by approximately one-half.The decrease in net photosynthesis observed with AAN is not the result of the depletion of the RuBP pool due to the lack of recycling of carbon from the glycolate pathway to the Calvin cycle. The higher levels of RuBP caused by AAN in photorespiratory conditions, suggest that RuBP carboxylase was inhibited. Glyoxylate could be a possible candidate for the inhibition of the enzyme but what is known so far about its inhibitory properties in vitro may not fit the existing in vivo conditions. An alternative explanation for the inhibition is proposed.
Journal Article↗
Effects of Aminooxyacetate and Aminoacetonitrile on Glycolate and Ammonia Release by the Cyanobacterium Anabaena cylindrica.
Aminooxyacetate and aminoacetonitrile cause increased excretion of glycolate by the cyanobacterium Anabaena cylindrica. Both compounds also reduce NH(4)-N release induced by methionine sulfoximine in non-nitrogen-fixing cultures. Changes in amino acid pool sizes together with changes in activities of some enzymes related to glycolate metabolism show that glyoxylate to glycine conversion and glycine to serine conversion are inhibited by aminooxyacetate and aminoacetonitrile, respectively. The results also verify that photorespiratory glycolate metabolism via amination of glyoxylate is operative in A. cylindrica.
Journal Article↗
Protonation thermochemistry of aminoacetonitrile.
The gas-phase basicity (GB) of aminoacetonitrile (NH2CH2CN, 1) has been determined from measurement of proton transfer equilibrium constants in an ion cyclotron resonance mass spectrometer (GB(1) = 789.3 +/- 1.0 kJ x mol(-1)). Molecular orbital calculations up to the G2 level demonstrate that protonation occurs preferentially on the nitrogen atom of the NH2 group, and provide a theoretical proton affinity (PA(1)) of 824.0 kJ x mol(-1). Exact calculation of the entropy associated with hindered rotations and consideration of Boltzman distribution of conformers allow a theoretical estimate of the molar protonation entropy S degrees (1H+) - S degrees (1) = 8.6 J x mol(-1) x K(-1). Combining this value with experimental GB(1) leads to an 'experimental' proton affinity of 819.2 kJ x mol(-1), in close agreement with the G2 expectation.
Algorithms↗
Reversible decrease of collagen crosslinking by protein low diet and aminoacetonitrile--effect of D-penicillamine and prednisolone on the rise of crosslinks.
After ending a 4-week period of low-protein diet with or without aminoacetonitrile (AAN), the tail tendons of rats showed an increase of hydroxylysinonorleucine (HLNL) together with other unidentified reducible crosslinks. The binding of dihydroxylysinonorleucine type (DHLNL) was an exception: its content remained unchanged. It may be, assumed, therefore, that the procedures mentioned above act indiscriminately against all reducible crosslinks with the exception of DHLNL. The rise in crosslinks after the 4-week pretreatment was disturbed, when d-penicillamine was given, because it specifically inhibited the formation of HLNL. The content of other crosslink components was slightly increased above that of controls so that the absolute content of total isolated crosslinks increased in the presence of d-penicillamine. No statistically significant differences could be obtained under prednisolone.
Acetonitriles↗
Inhibition by aminoacetonitrile and propargylamine of glycine cleavage system from rat brain and liver mitochondria.
Glycine degradation in the CNS is catalyzed by the glycine cleavage system (GCS). We have tested several compounds with a structural analogy to glycine for their inhibition of the GCS. Compounds having an inhibitory activity, such as aminoacetonitrile and propargylamine, are characterized by having a primary amine group and a pi-electron system present in the group substituting for the carboxylic function. The inhibition by these compounds of glycine degradation may be of pharmacological interest given the neurotransmitter role of glycine.
Acetonitriles↗
Prevention of thioacetamide-induced liver necrosis by prior aminoacetonitrile or imidazole administration.
Prior administration of aminoacetonitrile (AAN) or imidazole but not isoxazole to rats, was able partially to prevent thioacetamide (TAC)-induced liver necrosis at 24 h. AAN and isoxazole did not prolong the pentobarbital sleeping time of the rats, while imidazole did. These and previous observations suggest a possible participation of non-cytochrome P-450 (P-450)-dependent aminoxidases in TAC activation to a necrogenic metabolite.
Acetamides↗
Inhibition of cytochrome oxidase by aminoacetonitrile.
Aminoacetonitrile (AAN) decomposes with the formation of a substance that is a potent inhibitor of cytochrome oxidase. The inhibitor is probably cyanide. Connective tissue contains cytochrome oxidase that varies in amount with the maturity of the tissue and is also inhibited by the product of AAN decomposition.
Aminoacetonitrile↗
Effect of a lathyrogen (aminoacetonitrile hydrochloride) on aortic physiosclerosis and skeletal mineralization in growing rats of different age.
In one experiment, four groups of six-week-old-male PVG rats were, respectively, given tap water ('control group'), 0.00125M, 0.0025M, and 0.005M lathyrogen (aminoacetonitrile hydrochloride: AAN) solutions ad libitum for a period of 20 weeks. In a second experiment, 12-week-old male rats were similarly treated. It was found that the younger rats were far more susceptible to lathyrogenic influences than the older rats. For example, the rate of aortic physiosclerosis was significantly retarded in the six-week-old rats at dosages of 0.00125M and 0.0025M (the six-week-old rats exposed to 0.005M AAN were eliminated from the experiment before its completion), whilst physiosclerosis was unaffected even in those 12-week-old rats exposed to 0.005M AAN. The degree of mineralization of the femur (as reflected by its ash, Ca, Mg, Na, and K content) was retarded in approximately dose-dependent fashion in the rats of both ages, the effect being somewhat more pronounced in the younger animals. These results were discussed in the context of the known effects of lathyrogenic compounds on the biochemical maturation of connective tissue components, and also in the context of previous attempts to modify the lifespan of laboratory animals by lathyrogen administration.
Acetonitriles↗
The effect of aminoacetonitrile on calcium metabolism and bone in the rat.
1. The effect of the osteolathyrogen aminoacetonitrile (AAN) on plasma calcium, phosphate and alkaline phosphatase, on bone, on growth rates, on absorption of calcium and phosphate in the gut and on their urinary excretion, has been examined in rats. 2. AAN caused a general deterioration in the health of the rat and reduced its rate of growth. 3. AAN reduced plasma calcium and increased plasma alkaline phosphatase but did not affect plasma phosphate. 4. AAN caused obvious deformity of the long bones with large exostoses. The femurs of the lathyritic rats had an increased fat-free weight and increased fat-free weight to ash weight ratio. 5. AAN increased true and apparent absorption of calcium but did not consistently affect urinary excretion of phosphate or apparent absorption of phosphate. 6. AAN did not produce a significant reduction in the plasma calcium of parathyroidectomized or thyroparathyroidectomized rats. 7. Absorption of calcium from ligated jejunal loops was increased in AAN-treated parathyroidectomized rats. 8. In some experiments parathyroidectomy or thyroparathyroidectomy protected the bones from the effect of AAN.
Acetonitriles↗