Statistical trends of wearers of contact lenses.
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Biomedical subjects
S Kojima
Publications and source records attributed to S Kojima.
Antioxidative activity of benzylideneascorbate and its effect on adriamycin-induced cardiotoxicity.
The in vitro antioxidative activity of benzylideneascorbate (SBA) and the in vivo effect on adriamycin (ADR)-induced cardiotoxicity in a mouse model were investigated. The radical-scavenging activity of SBA was assayed in terms of reduction of chemiluminescence induced by O2-, generated in xanthine/xanthine oxidase and macrophage/phorbol myristate acetate reaction systems. SBA showed a strong antioxidative activity (IC50 = 3 to 4 microM) in both assay systems, though its activity was weaker than that of ascorbic acid (Asc). In the assay of the antioxidative activity against auto-oxidation of linolenic acid, SBA was stable and retained its potency for a long period of time in comparison with Asc, 6-palmitoylascorbic acid (6-P-Asc) and cysteamine (CysNH2). Electron spin resonance examination indicated that SBA strongly scavenged both superoxide anion and hydroxy radical. The in vivo protective effect of SBA against ADR-induced cardiotoxicity, in which active oxygen radicals play a role, was examined. The serum creatine phosphokinase activity, a parameter of cardiotoxicity, was remarkably increased from the 3rd day until the 4th day after ADR treatment. This elevation was significantly suppressed by SBA treatment, whereas Asc, 6-P-Asc and CysNH2 were ineffective. SBA could have clinical potential for the treatment of diabetes and other disorders in which active oxygen species play a pathogenic role.
Animals↗
Enhancing potency of neopterin toward B-16 melanoma cell damage induced by UV-A irradiation and its possible application for skin tumor treatment.
The enhancing potency of the oxidized form of neopterin (NP) towards long-wavelength ultraviolet light (UV-A) induced cytotoxicity was examined in vitro using mouse melanoma (B-16) cells. A sufficient dose of UV-A irradiation was used to cause damage (measured in terms of reduced DNA synthesis) to about 30% of the irradiated cells. NP drastically enhanced the UV-A-induced cell damage, whereas the reduced form of neopterin (NPH4), which possesses a strong antioxidative activity, abolished the UV-A-induced cell damage in a dose-dependent manner. These data suggest that radical oxygen species (ROS) may be involved in UV-Ainduced B-16 cell damage. Among various radical scavengers examined, only catalase protected B-16 cells from UV-A-induced cell damage and also abolished the enhancing potency of NP, suggesting that hydrogen peroxide may mediate the cell damage. We obtained similar results in another experiment on B-16 cell damage induced by hydrogen peroxide instead of UV-A. In an in vitro analysis of the chemilumi-nescence induced by hydrogen peroxide, NP remarkedly enhanced the signal intensity at a high concentration, while NPH4 reduced the intensity in a dose-dependent manner. These results suggest that elevation of the hydrogen peroxide-mediated cytotoxicity by NP may be involved in its enhancing potency toward UVA-induced B-16 cell damage, and may also indicate the possible utility of the oxidized form of neopterin as an enhancer for UV-A-irradiation treatment of tumors.
Animals↗
Enhancement of UV-A-induced cytotoxicity to cancer cell lines by camptothecin.
The exposure of cultured mouse melanoma (B-16) cells, to camptothecin (CAM) after irradiation of the cells with UV-A synergistically enhanced cytotoxicity. CAM treatment prior to irradiation had the same effect. Similar results were also obtained with the combination of gamma-ray irradiation and CAM in this model. Thus, the sensitivity of the cells to UV-A and gamma-ray irradiation was significantly elevated by CAM. These findings have potential clinical utility.
Animals↗
Modulation of S-nitroso-N-acetyl-D,L-penicillamine (SNAP) induced HL-60 cell death by tetrahydrobiopterin.
The effect of 5,6,7,8-tetrahydrobiopterin (BPH4) on HL-60 cell damage induced by a nitric oxide (NO) donor, S-nitroso-N-acetyl-penicillamine (SNAP), was investigated. The activity of lactate dehydrogenase (LDH), a marker of cell damage, was elevated dose- and time-dependently after treatment with SNAP. The cells underwent apoptosis, as judged from the characteristic morphological findings and the electrophoretic ladder pattern of DNA fragments. Apoptosis observed at an early time, 5 hours post-treatment with SNAP, was inhibited by BPH4. However, BPH4 significantly increased cell death observed at a later time, 20 hours after the treatment. These results suggest that BPH4 may be involved in modulating the cytotoxicity, including cell death, mediated by NO.
Apoptosis↗
Elevation of mouse liver glutathione level by low-dose gamma-ray irradiation and its effect on CCl4-induced liver damage.
We examined the elevation of glutathione (GSH) levels in the liver of C57BL/6 female mice after low-dose r-ray irradiation and its inhibitory effect on CClI4-induced liver damage. The liver GSH level increased soon after irradiation with 50 cGy of gamma-rays, reached a maximum at around 12 post-treatment, and returned almost to the control level by 24 h. The activities of glutathione reductase, and glutathione peroxidase also showed the same pattern of change, while the activity of gamma-glutamylcysteine synthetase showed a gradual increase up to 24 h. The effect of pre-irradiation on CCl4-induced liver damage was also investigated. The activities of glutamic oxaloacetic transaminase and glutamic pyruvic transaminase in serum were markedly increased 12 h post-treatment with CCl4. Both increases were significantly suppressed by a single low-dose pre-irradiation. Malondialdehyde, a marker of lipidperoxidation, was also greatly elevated after CCl4 treatment, and its increase was suppressed by irradiation. These results suggest low-dose gamma-ray irradiation might be effective for the prevention of and/or therapy of various reactive oxygen species-related diseases including cancer.
Animals↗
Fluoride release from a light-cured bonding material in openbite orthodontic patients.
This study was undertaken to clarify whether the salivary fluoride concentration on the anterior and premolar teeth, released from an orthodontic bonding material, differed between openbite and non-openbite patients. Using fluoride-releasing bonding materials, brackets were bonded to the teeth in openbite and in non-openbite patients. Saliva films on the tooth surfaces near the brackets were collected with filter paper and fluoride concentrations in the saliva were determined by using a fluoride electrode technique. Saliva was collected and analyzed at different periods after the bonding. Fluoride concentrations in the saliva increased sharply immediately after bonding, decreased gradually thereafter, then leveled off. Fluoride concentrations in the saliva on the tooth surfaces were higher in openbite patients for one day to as long as one week. The results of the two-way analysis (ANOVA) showed that the differences in the overbite factor (openbite, non-openbite) contributed to the variances the most (p < 0.001; contribution, 59.50 percent after one day and p < 0.01; contribution, 49.63 percent after 3 days). In conclusion, the fluoride released from the bonding materials on the tooth surfaces was retained more in openbite than in non-openbite patients, suggesting their lower flow rate of saliva.
Adhesives↗