We designed and manufactured equipment for long-term and low-density (0 to 9 mT) exposures of cultured cells to extremely low frequency magnetic fields (ELF-MF), and examined the effects of ELF-MF on cell growth and c-myc mRNA expression in Chinese hamster ovary (CHO) cells. The ELF-MF equipment consists of a CO2 incubator with a built-in magnet generator using Helmholtz coils being 250 mm in inner diameter, 160 mm in distance and 128 turns, a slide regulator and a thermocontroller. No significant difference in the growth rate and the c-myc expression of CHO cells was observed with 5 mT ELF-MF exposure, sham-exposure and incubation in a conventional incubator.
The A1235 and T98 cell lines derived from human gliomas have homozygous deletions in their p16 genes and are radiosensitive and radioresistant, respectively, with respect to other established glioma cell lines. These differences in radiosensitivity may be due to variations to some extent among cell lines, rather than genetically defined resistance or sensitivity. We examined the effect on radiation sensitivity of introducing a wild‐type p16 gene into both p16‐deficient glioma cell lines. The plasmid pOPMTS containing human wild‐type plfi cDNA and a neomycin resistance gene, or the control plasmid pOPRSV1, were transfected into these cells. Clones from both cell lines, which expressed wild‐type p16 mRNA constitutively after transfection with pOPMTS, were more radiosensitive than the parental cells and clones obtained after transfection with the negative control plasmid.
Human osteosarcoma SAOS‐2 cells, which have a deletion in p53 gene, were transfected with plasmid pMSVneop53 containing human p53 cDNA and neomycin‐resistance gene. Three clones (SAOS‐MC10, SAOS‐MC11 and SAOS‐MC43) among 60 clones expressed p53 mRNA. No p53 protein was observed in SAOS‐MC10, while SAOS‐MC11 and SAOS‐MC43 produced p53 protein. The molecular weight of p53 protein in SAOS‐MC43 was lower than that in SAOS‐MC11. SAOS‐MC11 and SAOS‐MC43 were more sensitive and more resistant, respectively, to ionizing radiation than the parental SAOS‐2. We suggest that exogenous p53 protein might be one of the factors determining cellular radiosensitivity.
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