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For protection against environmental deterioration, pollutants should be reduced as much as possible. Therefore, a sensitive detection method for air pollutants is required, particularly for benzene, a compound with mutagenic, teratogenic, and carcinogenic properties. Some microorganisms have a number of enzymes that degrade organic compounds. The genetic information for many of these enzymes is codified in plasmids that usually comprise some elements such as proteins and RNA for their replication, and proteins for cell division control. Some plasmids have been obtained from Pseudomonas putida, a ubiquitous microorganism that is able to degrade biologic and inorganic compounds. P. putida contains the TOL plasmid, responsible for the degradation of benzene and its derivatives. The TOL plasmid has been fused with the gene for firefly luciferase (pTNS316 plasmid) to produce a luminescent bacterium (Escherichia coli HB101), which can be applied to the environmental monitoring of these chemicals. The recombinant E. coli transformed with the plasmid (E. coli HB101-pTNS316) was applied to the environmental biosensing of benzene and its derivatives. Measurement of bacteria-generated photons was done using a color-coded device to estimate quantitatively the pollutant concentration. The expression of luciferase was induced in the presence of aromatic compounds but the E. coli sensitivity has a detection limit: this bacterium dies if the benzene concentration is higher than 0.5 ppm and at this concentration the luminescence decreases so it is impossible to detect. Another limit for this biodevice is that the microorganism, very likely, accumulates the benzene and its derivatives, and therefore it is very important to consider the time of exposure. This biomonitor potentially offers a rapid, inexpensive, and sensitive technique for environmental detection of aromatic pollutant compounds. [Copyright &y& Elsevier]

Previous works showed that exposure to static and extremely low frequency (ELF) magnetic fields (MF) over 3 mT slows down the growth kinetics of human tumors engrafted s.c. in immunodeficient mice, reducing their metastatizing power and prolonging mouse survival. In the experiments reported here, immunocompetent mice bearing murine Lewis Lung carcinomas (LLCs) or B16 melanotic melanomas were exposed to MF and treated respectively with two commonly used anti-cancer drugs: cis-diamminedichloroplatinum (cis-platin) and N,N-bis (2-chloroethyl)tetra-hydro-2H-1,3,2-oxazaphosphorin-2-amine 2-oxide (cyclophosphamide). The experiment endpoint was survival time. The survival time of mice treated with cis-platin (3 mg/kg i.p.) and exposed to MF was significantly (P<0.01) longer than that of mice treated only with cis-platin or only exposed to MF, superimposing that of mice treated with 10 mg/kg i.p. of the drug, showing that MF act synergically with the pharmacological treatment. On the contrary, when mice treated with cyclophosphamide (50 mg/kg i.p.) were exposed to MF no synergic effects were observed, the survival curve being exactly the same as that of mice treated with the drug alone. No clinical signs or toxicity were seen in any of the mice exposed to MF alone or along with cis-platin or cyclophosphamide treatment, compared to mice given only the two known drugs.A possible explanation for the synergic effect of MF being found in mice treated with cis-platin could be that the platinum ion stimulates radical production and that MF enhance active oxygen production bringing about changes in tumor cell membrane permeability, influencing positively the drug uptake. Alternatively, or in addition to this, it has been demonstrated that the rate of conversion of cis-platin to reactive species able to bind to DNA, is increased by localized production of free radicals by MF. [Copyright &y& Elsevier]