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Formation and loss of methylated purines in DNA of various fetal and maternal tissues were measured up to 7 days following intravenous administration of N-[14C]methyl-N-nitrosourea to rats on the 21st day of gestation. Methylation products were detected in all tissues examined, the level in maternal liver being higher than in other tissues. The concentrations of 7-methylguanine and 3-methyladenine decreased faster in fetal than in corresponding maternal tissues, due to a higher rate of DNA synthesis in fetal tissues, as determined by incorporation of labelled thymidine. Removal of the promutagenic DNA lesion O6-methylguanine was most efficient in maternal and fetal liver; but it was very poorly repaired in kidney and brain. The persistence of O6-methylguanine relative to 7-methylguanine was highest in the DNA of fetal brain. The principal targets for the transplacental carcinogenic effect of N-methyl-N-nitrosourea under these experimental conditions were fetal neurogenic tissue and kidney; and malignant tumors developed at these sites in 31-34% and 15-16% of male and female descendants, respectively. These results support the concept that a complex interaction between DNA alkylation, repair and replication is the molecular basis of initiation of carcinogenesis by alkylating agents.

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Radiation from a personal computer monitor reduces antioxidant activity and the contents of diene conjugates and Schiff bases in rat serum and has no effect on chemiluminescence and the content of carbonyl derivatives. The radiation causes no significant changes in blood contents of nitrites and ceruloplasmin and activity of Cu,Zn-superoxide disnmtase. The results obtained indicate that radiation from a monitor produces potentially hazardous biological effects. Key Words: monitor; lipid peroxidation; antioxidant systemsThe problems associated with biological effects of radiation from a personal computer monitor (PCM) have been discussed in the literature [1,8,13]. A PC user is exposed to electromagnetic field (EMF), visible and ultraviolet light, radio-range waves, and low-frequency fields (50 Hz) and their harmonics [8]. Preliminary experiments showed that EMF of varied frequency and intensity activates some oncogenes, suppresses the immune system, causes neurologic disorders, impairs the function of hypothalamohypophyseal system, and increases the risk of tumorigenesis [7,13]. The incidence of premature births and infants born with pathologies and the risk of brain tumors are higher for PC operators [13]. The PCM radiation stimulates the growth of urethane-induced lung tumors in mice [2]. Modification of free-radical processes in the organism may be a key factor in the mechanism of biological effects of PCM radiation. These processes play an important role in age-related pathologies, atherosclerosis, ilmnunodepression, and tumorigenesis. As we are aware, the effects of PCM radiation on free-radical oxidation and antioxidant systems have not been investigated. The present study is an attempt to examine these effects. MATERIALS AND METHODSExperiments were performed on 40 male 3-monthold LIO rats bred at the N. N. Petrov Institute of Oncology. The rats were maintained in polypropylene cages (55x36x15 cm, 5-6 animals) at 21-23~ and 12:12 h light regime and had free access to standard vivarium chow and water. A Litron Professional Co. PC/AT-286 computer (Singapore) with an EGA color monitor (230 V, 50 Hz, 0.4 A, Taiwan) was used as a source of radiation (Fig. 1). A text file was on the monitor during irradiation (1 h during a 5-day period). Control rats were subjected to the same manipulations without irradiation. The doses of PCM radiation components were measured as previously [2].