Detail of "56-88-2"

Reference

A preliminary analysis of dietary effects on serum ninhydrin-positive compounds of immature lobsters Homarus americanus (Milne Edwards)

A preliminary analysis of dietary effects on serum ninhydrin-positive compounds of immature lobsters Homarus americanus (Milne Edwards). Carter, John A.; Dunphy, Gary B. (Biol. Dep., Memorial Univ. Newfoundland, St. John's, Newfoundland, Can.). Can. J. Zool., 56(2), 359-63 (English) 1978. CODEN: CJZOAG. ISSN: 0008-4301. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) Thirty-eight ninhydrin-pos. compds. (NPCs) were detected in the serum of wild, controlled-diet and starved lobsters, Homarius americanus. Glycine, proline, alanine, taurine, serine, glutamic acid, ornithine, and glutamine comprised ~82% of the total serum NPC concn. in wild and starved lobsters and 70% in fed lobsters. The urea cycle intermediate arginine, citrulline, ornithine, and urea were detected in many samples. The following NPCs, previously unreported in lobster hemolymph, were detected as well. b-Alanine [107-95-9], a-aminoadipic acid [542-32-5], a-amino-n-butyric acid [80-60-4], g-aminobutyric acid [56-12-2], ammonia, anserine [584-85-0], asparagine [70-47-3], cystathionine [56-88-2], cysteic acid [13100-82-8]-phosphoserine [407-41-0], ethanolamine [141-43-5], glycerophosphoethanolamine [1190-00-7], hydroxyproline [51-35-4], 1- [332-80-9] and 3-methylhistine [368-16-1] were among those detected. Starved lobsters showed pronounced redns. in serum NPC concns. relative to those of fed lobsters. Starvation caused an apparent increase in the serum concns. of the methylhistidine isomers and glycerophosphoethanolamine.

Effect of chronic folate deficiency on the metabolism in nervous tissue of mice

Effect of chronic folate deficiency on the metabolism in nervous tissue of mice. Relation to changes in amyotrophic lateral sclerosis. Wakabayashi, Yukio (Sch. Med., Kyorin Univ., Mitaka 181, Japan). Shinkei Kenkyu no Shinpo, 28(4), 671-80 (Japanese) 1984. CODEN: SKNSAF. ISSN: 0001-8724. DOCUMENT TYPE: Journal CA Section: 18 (Animal Nutrition) The influence of impaired folate [59-30-3] cycle on the level of S-amino acids, esp. taurine [107-35-7], the elevation of which was shown in amyotrophic lateral sclerosis (ALS) was investigated in mice. In the folate-deficient mice, the content of folate was decreased markedly not only in the blood and liver, but also in the brain, spinal cord, and muscle. Among S-amino acids, a pronounced elevation of cystathionine [56-88-2] level was noted in the brain and spinal cord. Although the increase in taurine content was not obsd., this might be due to the large pool size of this amino acid in mouse brain. Presumably, considerable changes in taurine might have been assigned to the normal variation. It is likely that the increase in cystathionine indicates the same derangement in metab. as that in taurine, namely enhanced prodn. of S-amino acids caused by the impairment of the folate cycle. Several amino acids were changed in each tissue, but most changes were diverse, indicating that the influence of folate deficiency on free amino acid metab. is not uniform in different tissues. The exception was glycine [56-40-6] which was increased in the all organs excluding plasma. The elevation of glycine level seems to be a characteristic obsd. metabolically in chronic folate deficiency. Among the folate deriv.-converting enzymes, only the activity of N5-methyltetrahydrofolate homocysteine methyltransferase showed a redn., although this was not significant. As for nucleic acid, the content of RNA was decreased, whereas DNA was not changed in brain. No direct evidence presently exists to implicate damage to the folate cycle as the primary metabolic disturbance in the degenerative process of ALS. However, it should be stressed that there is some similarly in metabolic alterations in nervous tissue between folate deficiency and ALS.