H. Iyehara Ogawa's research while affiliated with Kyushu Institute of Technology and other places
What is this page?
This page lists the scientific contributions of an author, who either does not have a ResearchGate profile, or has not yet added these contributions to their profile.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
It was automatically created by ResearchGate to create a record of this author's body of work. We create such pages to advance our goal of creating and maintaining the most comprehensive scientific repository possible. In doing so, we process publicly available (personal) data relating to the author as a member of the scientific community.
If you're a ResearchGate member, you can follow this page to keep up with this author's work.
If you are this author, and you don't want us to display this page anymore, please let us know.
Publications (11)
Aflatoxin M1 (AFM1), a metabolic hydroxylation product of aflatoxin B1 (AFB1), and the parent compound were comparatively assayed for DNA-damaging potency and genotoxicity in vivo in Drosophila melanogaster using, respectively, the mei-9a mei-41D5 DNA repair test and the mwh/flr3 wing spot test. In the repair test, larval stock, consisting of meiot...
A series of metal chlorides were subjected to the wing spot test of Drosophila melanogaster. In the test, larvae trans-heterozygous for the wing-hair mutations mwh and flr were orally treated at the third instar stage with a test compound and the wings were inspected at the adult stage for spots expressing phenotypes of the markers. CoCl2, MnCl2, M...
Employing a suspension culture of FM3A cells, we examined the cytotoxic and mutagenic effects of various chemical compounds. Mutagenicity of various types of mutagens (MNNG, ENNG, sterigmatocystin, mitomycin C, Trp-P-1, and X-rays) was sensitively detected by this assay. Mutagenicity of Trp-P-2 was detected in the presence of an activating enzyme s...
The reaction of 5, 14-dihydro-7, 16-diethyl-(E)-or-(Z)-di-pyrido[b,i][1,4,8,11]tetraazacyclotetradecine with bis(2,4-pen-tanedionato)aquazinc(II) led to the corresponding zinc(II) mono-hydrate complexes, while the reaction with sodium tetrachloro-palladate(II) yielded the corresponding palladium(II) complexes. Judging from the behavior of electroni...
The mixture of 6,15-diethyl-4,13-dihydro-(E)-dipyrido [b,i] [1,4,8,11] tetraazacyclotetradecine (2-E) and 6,15-diethyl-4,13-dihydro-(Z)-dipyrido [b,i][1,4,8,11] tetraazacyclotetradecine (2-Z) was prepared by cyclization of 3,4-diaminopyridine and 2-ethyl-3-ethoxyacrolein. Two kinds of isomers were separated by repeated recrystallization from chloro...
Cobalt(II) chloride (CoCl2), non-mutagenic by itself, has been tested for mutagenic activity in the presence of 4-substituted pyridines in the test strains of Salmonella typhimurium. CoCl2 was found to be mutagenic in strains TA1537 and TA2637, when combined pyridine, with methyl isonicotinate, 4-methyl-pyridine, 4-ethylpyridine, 4-chloropyridine o...
The mutagenic activity of cobalt (II) chloride (CoCl2) was examined using the Salmonella test system in the presence of quinoline compounds. CoCl2, which itself is non-mutagenic, exhibited mutagenicity when combined with quinoline, 2-methylquinoline, 3-methylquinoline, 4-methylquinoline, 6-methylquinoline, 7-methylquinoline, 2-aminoquinoline, 4-ami...
Twenty one different metal chlorides have been tested for mutagenicity in the presence of 9-aminoacridine in strains of Salmonella typhimurium. BeCl2, FeCl2, MnCl2, NiCl2, SnCl4, ZnCl2, and ZrCl4, each of which was not mutagenic alone, exhibited mutagenicity when combined with 9-aminoacridine in strains TA1537 and TA2637.
Mutagenic activities of 4-aminopyridine (4AP), 4-aminoquinoline (4AQ), 9-aminoacridine (9AA) and harman (HM) were examined by the Salmonella test system in the presence of cobalt(II) chloride (CoCl2), which itself is non-mutagenic in this system. Mutagenic activity of the mixture of 9AA and CoCl2 was found to be much higher than that of 9AA alone i...
Citations
... Some of these metallic complexes are efficient redox catalysts [8]. For example, CoTAA catalyses 1,2-diphenylhydrazine, hydroquinone and thiol oxidation [10,11]. As an electrode modifier, this complex is also efficient for SO 2 oxidation at gas electrodes [12] Scheme 1. Co(II)-dibenzotetraaza [14]annulene complexes. ...
![[object Object]](https://i1.rgstatic.net/ii/profile.image/847092062908416-1578973894725_Q64/Kazunori-Sakata.jpg)
... In a previous paper, we found for the first time that CoC12 was mutagenic in the Salmonella test system when combined with heteroaromatic compounds such as 4aminoquinoline (4AQ), 9-aminoacridine (9AA) and harman ( Ogawa et al. 1986). It has also been reported that the combined mutagenic activity is presumably the result of an equimolar complex forming between Co(II) cation and heteroaromatic bases ( Ogawa et al. 1986Ogawa et al. , 1987Ogawa et al. , 1988. Of these, the combined mutagenicity for mixtures of CoC12 and heteroaromatic compounds showed an inverse correlation with the strength of their coordinate bonds judging from the spectral data. ...
... In the Salmonella typhimurium mutagenesis test, beryllium chloride produced conflicting results in strains TA1537 and TA2637 in the absence of metabolic activation. It did not produce mutations in strains TA98, TA100, TA102 and TA1535 in the absence of metabolic activation (Ogawa et al., 1987). It did not produce mutations in TA98 in the presence of metabolic activation (Kuroda et al., 1991). ...
Reference: Beryllium and Beryllium Compounds
... Extensive in vitro studies on the genotoxicity of sterigmatocystin are available, and almost all tests give positive results. Sterigmatocystin is mutagenic in vitro in bacterial cells after metabolic activation (48)(49)(50)(51)(52)(53)(54)(55)(56) and in mammalian cells (57)(58)(59)(60). It induces chromosomal aberrations, micronuclei and chromosome damage (sister chromatid exchange, unscheduled DNA synthesis, comet assay) in vitro in mammalian cells, including human cells (54,57,(61)(62)(63)(64)(65)(66)(67)(68)(69)(70)(71)(72). ...
Reference: Sterigmatocystin
... In addition, we newly identified 4-(dimethylamino)-pyridine (4-DMAP) co-varying with the mutagenic activity of the samples. 4-DMAP is produced by the chemical industry discharging via the WWTP, is used as nucleophilic catalyst in industrial processes (Grondal, 2003), but was reported as not mutagenic (Ogawa et al., 1988). An ethoxy(pyrrolidinyl)benzaldehyde and 2-ethoxy-N-(1methyl-3-phenylpropyl)-acetamide were tentatively identified based on matching predicted and experimental retention times and HRMS/MS information. ...
... In vitro studies have suggested that the two major mechanisms involved in the genotoxic and carcinogenic potential of Co are (i) the generation of reactive oxygen species through a Fenton-like mechanism; and (ii) the inhibition of DNA repair mechanisms (Beyersmann & Hartwig, 2008). Co compounds were reported to be mostly non-mutagenic in bacterial test systems, with few exceptions in some tester strains (NTP, 1991;Ogawa et al., 1986). In contrast to the results seen in bacteria, soluble Co compounds were found to be genotoxic in certain mammalian assay systems. ...
... The wing spots were observed in the wing after treatment with CoCl 2 . CoCl 2 can induce both small and large spots in the wings (Ogawa et al., 1994). In mwh/TM3 flies, CoCl 2 could not induce large spots in the wings due to suppressed mitotic crossing-over. ...
... The human health implication of AFs is that AFM1 is converted into a reactive electrophilic epoxide (AFM1-8,9-epoxide) that can covalently bind to both DNA and proteins (Shibahara et al., 1995). The newly formed adducts (instable AF-N7-Gua, Aflatoxin-Guanin N7 group) and the highly instable AF-FAPY (formamidopyrimidine) deriving from that cause DNA mutation by guanin-timin transversion which could eventually could lead to hepatocarcinogenesis (Ismail et al., 2016;Rushing and Selim, 2019). ...
