Biomedical subjects

Masaru Kato

Publications and source records attributed to Masaru Kato.

39 records · Page 3Linked to original sources

PubMed2002

L-cysteine prevents oxidation-induced block of the cardiac Na+ channel via interaction with heart-specific cysteinyl residues in the P-loop region.

The present study investigated the protective effects of L-cysteine on the oxidation-induced blockade of Na+ channel a-subunits, hH1 (cardiac) and hSkM1 (skeletal), expressed in COS7 cells. Na+ currents were recorded by the whole-cell patch clamp technique (n = 3-7). L-cysteine alone blocked hH1 and hSkM1 in a dose-dependent manner, with saturating L-cysteine block at 3,000 micromol/L. Hg2+, a potent sulfhydryl oxidizing agent, blocked hH1 with a time to 50% inhibition (Time50%) of 20s. Preperfusion of COS7 cells with 100 micromol/L L-cysteine significantly slowed the Hg2+ block of hH1 (Time50% = 179 s). L-cysteine did not prevent Hg2+ block of hSkM1 (Time50% = 37s) or the C373Y hH1 mutant (Time50% = 43s). As for other sulfo-amino acids, homocysteine prevented the Hg2+ block of hH1, with the Time50% (70s) being significantly smaller than that of L-cysteine, whereas methionine did not prevent the Hg2+ block of hH1. L-cysteine did not prevent the Cd2+ block of hH1. These results indicate that L-cysteine selectively acts on heart-specific Cys373 in the P-loop region of hH1 to prevent Cys373 from the oxidation-induced sulfur-Hg-sulfur bridge formation.

Cysteine↗

PubMedDate not supplied

Characterization of labelling and de-labelling reagents for detection and recovery of tyrosine residue in peptide.

This paper characterized the labelling and de-labelling reagents for reversible labelling of tyrosine (Tyr)-containing peptide, which involves detection and recovery. The phenolic hydroxyl group (-OH) in Tyr structure reacted with 4-fluoro-7-nitro-2,1,3-benzoxadiazole (NBD-F), 4-(N,N-dimethylaminosulfonyl)-7-fluoro-2,1,3-benzoxadiazole (DBD-F), and 1-fluoro-2,4-dinitrobenzene (DNFB) under mild conditions at room temperature at pH 9.3. The labels in the resulting derivatives were removed with the treatment of nucleophiles, such as thiols (cysteine, N-acetyl-L-cysteine and dithiothreitol) and amines (dimethylamine, methylamine, diethylamine, ethylamine and pyrrolidine). The de-labelling reactions of NBD-labelled N-acetyl-L-tyrosine (N-AcTyr) with the nucleophiles produced N-AcTyr, accompanied by NBD-nucleophile. Although DBD-F and DNFB also successfully labeled the -OH group in N-AcTyr, the efficiency of Cbond;O bond cleavage and recovery of N-AcTyr by the nucleophiles was relatively low compared with NBD-label. Among the de-labelling reagents, N-acetyl-L-cysteine and dimethylamine were recommended for the elimination of NBD moiety, with respect to the reaction rate, the side reaction, and the yield of recovery. The proposed procedure, which includes the labelling with NBD-F and the removal of NBD moiety by the nucleophiles, was successfully applied to the reversible labelling of N-terminal amine-blocked peptides, i.e. N-AcTyr-Val-Gly, Z-Glu-Tyr, Z-Phe-Tyr, N-Formyl-Met-Leu-Tyr, and N-AcArg-Pro-Pro-Gly-Phe-Ser-Pro-Tyr-Arg.

Chromatography, High Pressure Liquid↗

PubMedDate not supplied

A case of sectorial benign flecked retina.

PURPOSE: A case of sectorial benign flecked retina not associated with an RDH5 gene mutation is reported. METHODS: A 51-year-old woman showed multiple yellow-white flecks in both eyes similar to those of benign flecked retina but in only the upper half of the retina. We carried out clinical, electrophysiological, and molecular genetic examinations of the patient. RESULTS: Visual acuity was 20/20 OD and 20/20 OS. Fluorescein angiography showed diffuse irregular hypofluorescence that did not correspond to the flecked lesions. A Goldmann-Weeker adaptometer test revealed that the visual threshold of the upper retina was approximately 0.6 to 0.8 log units higher than that of the lower retina. No mutations of the RDH5 gene were detected in exons 2-5 or in the flanking intron sequences. CONCLUSIONS: To our knowledge, this is the first report of sectorial benign flecked retina, and the flecks may not be caused by an RDH5 gene mutation.

Alcohol Oxidoreductases↗