An oxidative fumigant is potent to kill insect pests infesting stored grains. Its oxidative activity generates reactive oxygen species (ROS), which has been considered to be a main insecticidal factor. Furthermore, the oxidative fumigant has cytotoxic effect to insect cell lines, but the cytotoxicity is abrogated by antioxidant treatment. This study aimed to extend the usefulness of the oxidative fumigant in terms of medical purpose against cancer cells. Five cancer cell lines HCT 116 (human colorectal), Lovo (human colorectal), SW480 (human colorectal), MDA-MB-231 (human breast), and MCF-7 (human breast) were tested to determine their susceptibility to the oxidative fumigant with reference to two insect cell lines (Sf9 and Hi-Five). All cancer cell lines were highly susceptible to the oxidative fumigant, compared to the insect cell lines. Interestingly, basal ROS levels of the cancer cell lines were much higher than the insect cell lines. Furthermore, the oxidative fumigant significantly increased the ROS levels in the cancer cells. Treatment of vitamin E as an antioxidant mitigated the cytotoxicity of the oxidative fumigant. Thus, the high susceptibility of cancer cells to the oxidative fumigant may be induced by their high inducible ROS production. This study also investigated the antiviral activity of the oxidative fumigant against insect and plant viruses. The oxidative fumigant significantly inactivated a baculovirus (dsDNA virus) by inhibiting polyhedral production in Sf9 cells. It also inactivated tobacco mosaic virus (ssRNA virus) by suppressing phytopathogenicity. These results support a broad effect of the oxidative fumigant, which can be applied to agricultural and medical purposes.

Selenium (Se) is known to prevent from several cancers, while iron (Fe) is known to be associated with high risk of cancers. The role of Se on colon carcinogenesis was investigated in an animal model induced by azoxymethane (AOM) and dextran sodium sulfate (DSS) in low Fe mice. Six-week old ICR mice fed on a low Fe diet (4.5 ppm Fe; generally 10 times lower than normal Fe) with three different Se (0.02, 0.1 or 0.5 ppm) levels for 24weeks. The animals received weekly three (0~2nd weeks) i.p. injections of AOM (10 mg/kg B.W), followed by 2%DSS with drinking water for 1 week to induce the colon cancer. There were five experimental groups including vehicle,positive control (normal Fe level, AOM/DSS), Low Fe (LFe) + AOM/DSS+Low Se (LSe), LFe + AOM/DSS + medium Se (MSe) and LFe + AOM/DSS + high Se (HSe) groups. HSe group showed a 66.7% colonic tumor incidence, MSe group showed a 69.2% tumor incidence, and LSe group showed a 80.0% tumor incidence. The tumor incidence was negatively associated with Se levels of diets. Tumor multiplicity in Hse group was significantly low compared to the other groups (p < 0.05). With increasing Se levels of diets, the primary anti-proliferating cell nuclear antigen (PCNA)-positive cells were decreased and apoptotic bodies were increased in a dose-dependent manner. Sedependent glutathione peroxidase activity and its protein level were dependent on the levels of Se of diets. Malondialdehyde level in liver was lowest in Hse group among experimental groups. These findings indicate that dietary Se is chemopreventive for colon cancer by increasing antioxidant activity and decreasing cell proliferation in Fe-deficient mice.