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A device consisting of Si microwells and microplasma sources has been fabricated for plasma treatment of individual cells cultured in media. We named the device plasma-on-chip. The microwells have through-holes at the bottom where gas–liquid interfaces form when they are filled with media containing biological samples. The microplasma sources, which supply reactive species, are located on the back of each microwell. Through the gas–liquid interface, the reactive species are supplied to the cells. Chlorella cells were used to demonstrate the feasibility of the device and after three minutes of plasma treatment, the fluorescence intensity of Chlorella cells appeared to be decreased. Optical emission spectroscopy identified O and OH radicals in the plasma, which can affect the cells. In the analysis of biological samples such as human cells or tissues, this device raises the possibility of revealing the mechanisms of plasma medicine in more detail.

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The molecular nature of lead‐induced mutations was examined in this study to more thoroughly understand lead mutagenesis. Chinese hamster ovary K1 cells were exposed to 0.5–3 mM lead acetate for 24 h. The median lethal dose (LD,) value was 1.5 mM, and the hypoxanthine guanine phosphoribosyltransferase (HPRT) mutant frequency increased linearly as lead concentrations were raised from 0.5 to 1.5 mM. We also amplified the HPRTcDNAs of 56 independent lead‐induced mutants by reverse transcriptase‐polymerase chain reaction (PCR). Forty‐two mutant cDNAs were successfully amplified: 36 mutants had transcripts of normal or slightly smaller than normal size, and six mutants had large deletions. The other 14 mutants whose HPRTcDNA could not be amplified were subjected to genomic‐DNA PCR analysis. All of those mutants had one or more exons missing from their genomic HPRT DNA. DNA sequencing of mutant cDNAs showed that 22 had single‐base substitutions, four had small alterations, 10 had single‐exon deletions, and six were missing two or three exons. Furthermore, DNA sequencing of the HPRT intron‐exon boundaries in eight splice mutants revealed that all of them had single‐base substitutions in their genomic DNA. G.C base substitutions occurred 3.3‐fold more frequently than A.T base substitutions. Similar frequencies were observed for G.C → A.T, G.C → T.A, and GC → C.G mutations. These results suggest that GC base pairs may be the primary target sites for lead mutagenesis. © 1996 Wiley‐Liss, Inc.

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