Separation of sulfated, fucose-containing polysaccharides from the brown seaweed Sargassum kjellmanianum and their heterogeneity and antitumor activity.
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Biomedical subjects
Publications and source records attributed to M Fujihara.
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The hypersensitivity of the neuromuscular junctions of diabetic mice to succinylcholine (SuCh), but not to d-tubocurarine (d-TC), was investigated using a cross culture preparation of diabetic skeletal muscle or spinal cord extract with normal tissues. Whether the hypersensitivity is due to the muscle cells themselves was examined using adult muscle of diabetic KK-CAy, prediabetic KK-CAy and normal ddY mice cocultured with embryonic spinal cord of normal ddY mice. The cultured neuromuscular junctions between diabetic KK-CAy muscle and normal ddY spinal cord was hypersensitive to SuCh, but not to d-TC. In contrast, such junctions between prediabetic KK-CAy muscle and normal ddY spinal cord were not hypersensitive to either drug. The involvement of neuronal factors in hypersensitivity to SuCh in diabetic KK-CAy neuromuscular junctions was examined using adult spinal cord extract (SCE) from diabetic KK-CAy and from normal ddY mice. We followed the time course of change in sensitivity of the acetylcholine (ACh) receptors in normal ddY embryonic myotubes to SuCh and d-TC. Both diabetic SCE and normal SCE reduced the sensitivity of myotubes to ACh; the reduction of ACh potential amplitudes by the former was less than that by the latter. Myotubes cultured with diabetic SCE was hypersensitive to both 1.51 microM SuCh and 0.134 microM d-TC. These results suggest that the hypersensitivity of the neuromuscular junctions in diabetic KK-CAy mice to SuCh but not to d-TC is mainly attributable to the diabetic muscle cells themselves.
The neuromuscular junctions of genetically diabetic KK-CAy mice are reported to be hypersensitive to succinylcholine (SuCh) but not to d-tubocurarine (d-TC). Spinal cord-muscle cocultures from normal ddY and diabetic KK-CAy mouse embryos were studied to examine the involvement of genetic factors in this hypersensitivity to SuCh. KK-CAy myotubes were morphologically normal, as determined by light microscopy. KK-CAy myotubes showed a progressive increase in the resting membrane potentials and acetylcholine (ACh) sensitivity with development, but this development was delayed when compared with ddY myotubes. The ACh receptor clusters, fluorescently labeled by fluorescein isothiocyanate conjugated alpha-bungarotoxin (FITC-alpha BuTX), were formed on the surface membrane of KK-CAy myotubes. The developmental increase of the total amount of fluorescence within ACh receptor clusters on KK-CAy myotubes was also slower than that of ddY myotubes. Depolarization by SuCh was sustained at a higher level in KK-CAy myotubes. In regards to the inhibition of ACh potentials, KK-CAy myotubes were not hypersensitive to both SuCh and d-TC when compared with ddY myotubes. These results suggest that the hypersensitivity to SuCh is not dependent on the genetic difference between ddY and KK-CAy mice, and is probably due to the developmentally diabetic state of the neuromuscular junction.
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An almost purified antitumor polysaccharide fraction (SFPP) was obtained by fractional precipitation with ethanol from hot-water extract of Sargassum fulvellum. The fraction showed remarkable tumor-inhibiting effect against sarcoma-180 implanted subcutaneously in mice. The results of chemical and physical analyses suggested that the active substance may be either a sulphated peptidoglycuronoglycan or a sulphated glycuronoglycan.
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