Stainless Steel-Mediated Hydrogen Generation from Alkanes and Diethyl Ether and Its Application for Arene Reduction.

Hydrogen gas can be generated from simple alkanes (e.g., n-pentane, n-hexane, etc.) and diethyl ether (Et2O) by mechanochemical energy using a planetary ball mill (SUS304, Fritsch Pulverisette 7), and the use of stainless steel balls and vessel is an important factor to generate the hydrogen. The reduction of organic compounds was also accomplished using the in-situ-generated hydrogen. While the use of pentane as the hydrogen source facilitated the reduction of the olefin moieties, the arene reduction could proceed using Et2O. Within the components (Fe, Cr, Ni, etc.) of the stainless steel, Cr was the metal factor for the hydrogen generation from the alkanes and Et2O, and Ni metal played the role of the hydrogenation catalyst.

Stainless-Steel Ball-Milling Method for Hydro-/Deutero-genation using H2O/D2O as a Hydrogen/Deuterium Source.

A one-pot continuous-flow method for hydrogen (deuterium) generation and subsequent hydrogenation (deuterogenation) was developed using a stainless-steel (SUS304)-mediated ball-milling approach. SUS304, especially zero-valent Cr and Ni as constituents of the SUS304, and mechanochemical processing played crucial roles in the development of the reactions.

Practical remediation of the PCB-contaminated soils.

A practical method for the elimination of PCBs from PCB-contaminated soil has been developed by the combination of Soxhlet extraction using a newly-developed modified Soxhlet extractor possessing an outlet valve on the extraction chamber with the chemical degradation. Various types of PCBs contaminated in soils could be completely extracted in refluxing hexane, and the subsequent hydrodechlorination could also be completed within 1 h in a hexane-MeOH (1 : 5) solution in the presence of Pd/C and Et3N under ordinary hydrogen pressure and temperature without the transfer of the extracted PCBs to other reaction container (a complete one-pot procedure). The present system is quite useful as a simple, safe, mild and reliable remediation method of PCB-contaminated soil.

Aspirin intake suppresses MMC-induced genotoxicity in mice.

The genotoxicity induced by mitomycin C (MMC) was found to be decreased by aspirin on alkaline single cell gel electrophoresis (SCG) assay in multiple organs of mice. Aspirin at doses of 0.5, 5 and 50 mg/kg and MMC at 2 mg/kg were administered and then liver, lung, kidney, spleen, colon and bone marrow were sampled after 3 h. Significant protective effects of aspirin against MMC-induced genotoxicity was observed in all but the bone marrow, where no change was evident. The results suggest that the radical scavenging ability of aspirin prevents danage by MMC-induced reactive oxygen species (ROS) in multiple organs.

Effect of aspirin on DNA damage induced by MMC in Drosophila.

In our previous paper, we found that aspirin suppressed the genotoxicity of mitomycin C (MMC) in a somatic mutation and recombination test (SMART) in Drosophila melanogaster. In order to reveal the mechanism of antigenotoxicity of aspirin, we evaluated the protective effects of aspirin against the genotoxicity of MMC with the DNA repair test in Drosophila melanogaster. Three types of treatment of aspirin were performed as co-, post- and pre-treatment. Aspirin co-treatment suppressed effectively the genotoxicity of MMC in a dose-dependent manner and the sex ratio at a dose of aspirin 10mg/bottle elevated from 0.01 (without aspirin) to 0.65 at sc z(1) w(+(TE)) mei-9(a) mei-41(D5)/-C(1)DX, y f [mei-9 mei-41, Rec(-) male.Rec(+) female] consists of DNA repair-deficient (Rec(-)) males and -proficient (Rec(+)) females. The antigenotoxic effect of aspirin on [mei-41, Rec(-) male.Rec(+) female] was similar to that on [mei-9, Rec(-) male.Rec(+) female]. But post- and pre-treatment by aspirin did not affect the genotoxicity of MMC on [mei-9 mei-41, Rec(-) male.Rec(+) female].

Suppressive effect of post- or pre-treatment of aspirin metabolite on mitomycin C-induced genotoxicity using the somatic mutation and recombination test in Drosophila melanogaster.

In our previous paper, we found that aspirin suppressed in a somatic mutation and recombination test (SMART) of mitomycin C (MMC) in Drosophila melanogaster. In order to reveal the mechanism of bio-antimutagenicity and/or preventive effect of aspirin, we evaluated the suppressive ability of each aspirin metabolite, such as salicylic acid (SA), salicyluric acid (SUA), gentisic acid (GA), gentisuric acid (GUA) and 2,3-dihydroxybenzoic acid (DHBA), in SMART in D. melanogaster using post- and pre-treatments. As for the post-treatment, SA reduced the numbers of large single and twin spots. GA reduced the small single and large single spots, and GUA reduced the single spots, large single and twin spots. The inhibition of GUA is slightly stronger than that of any other metabolites; the inhibition percentage is 49 at the dose of 5 mg/bottle. On the other hand, as for the pre-treatment, aspirin, SUA, GA and DHBA reduced the numbers of small single spots. SUA, GE and DHBA reduced the number of large single spots. Aspirin and its metabolites did not reduce the number of twin spots. The results of the present study suggest that SA, GA and GUA repair or replicate DNA-damage by MMC and SUA, GA, GUA and DHBA prevent DNA-damage by MMC. It is suggested that secondary cancer is prevented by aspirin post-treatment without losing the medicinal effectiveness (anti-tumor activity). Therefore, we consider there are effective doses and/or administration timing of aspirin and MMC to prevent secondary cancer.

Effect of cotreatment of aspirin metabolites on mitomycin C-induced genotoxicity using the somatic mutation and recombination test in Drosophila melanogaster.

In our previous reports, aspirin, an antipyretic analgesic, suppressed the genotoxicity of mitomycin C (MMC) in a somatic mutation and recombination test (SMART) in Drosophila melanogaster. In order to reveal the mechanism of the anti-genotoxicity of aspirin, we evaluated the suppressing ability of each aspirin metabolite, such as salicylic acid (SA), salicyluric acid (SUA), gentisic acid (GA), gentisuric acid (GUA), and 2,3-dihydroxybenzoic acid (DHBA), in SMART in Drosophila melanogaster using the cotreatment protocol in this report. SUA, GA, GUA, and DHBA reduced the number of the three types of spot induced by MMC without decrease of survival. These aspirin metabolites decreased the genotoxicity frequency of MMC for total spots in a dose-dependent manner. Furthermore, each metabolite decreased the genotoxicity frequency of MMC by approximately 80% at a dose of 40 mg/bottle, respectively. It is suggested that these metabolites are the main substances of anti-genotoxicity in the aspirin metabolic pathway.