Electromagnetic fields enhance chemically-induced hyperploidy in mammalian oocytes

Epidemiological studies suggest that exposure to electro-magnetic fields (EMFs) in the environment may be associ-ated with mutagenic changes, but the relation betweenEMF exposure and aneuploidy has not previously beenstudied. Environmental EMFs apparently lack the energynecessary to function as aneugens, but the possibility existsthat EMFs could influence the incidence of aneuploidysynergistically because EMFs can activate the neuroendo-crine system, and ovulation and oocyte meiotic maturationare under neurohormonal control. This hypothesis wastested by examining the effect of EMF exposure on theoccurrence of hyperploidy in mouse oocytes induced byvinblastine sulphate (VBS), which was employed as asurrogate for aneugens in the environment. The incidenceof hyperploidy in metaphase II oocytes of individual micefollowing superovulation was determined, and statisticalmethods were developed to assess whether EMF exposureduring oogenesis in the presence of VBS altered the rateof hyperploidy. A significant effect of EMF exposure onVBS-induced hyperploidy was found {P < 0.05). The datasuggested that the EMF primarily affected the mice thatexhibited a high incidence of VBS-induced hyperploidy.Exposure had no effect on the number of oocytes ovulatednor on the occurrence of hypoploidy. The results supportthe hypothesis that EMF exposure can promote the occur-rence of aneuploidy caused by an aneugen via a mechanisminvolving the neuroendocrine system.IntroductionThe genetic consequences of exposure to electromagnetic fields(EMFs) in the environment are generally unknown, and thereis a consequent need for additional information (Murphy et al,1993). Some epidemiological studies suggested an associationbetween EMFs and cancer, particularly cancer of the blood-forming and nervous systems (Marino, 1993). The possibleteratogenic effects of EMFs have not been examined directlyin epidemiological studies, but an association between theoccurrence of spontaneous abortion and exposure to EMFshas been reported (Wertheimer and Leeper, 1986). Animalstudies showed that EMFs can be teratogenic under certaincircumstances (Juutilainen etai, 1986; Berman etai, 1990).There is apparently no epidemiological evidence concerningthe possibility of a link between EMFs and aneuploidy, exceptfor reports of a possible relationship between Down's syndromeand paternal radar exposure (Cohen and Lilenfeld, 1970;Cohen, 1976).Most attempts to find evidence of direct genetic effects thatcould plausibly serve as a basis for the epidemiologicalassociations have generally been unsuccessful (Reese etai.,1988; Saunders etai., 1988; Frazier etai., 1990; Garcia-Sagredo etai., 1990; Dertinger etai., 1993; McCann etai.,1993; Scarfi et al., 1993). The failure to find direct evidence ofEMF-induced mutagenic effects is consistent with biophysicalmodelling, which does not predict that environmental-strengthEMFs have sufficient energy to break chemical bonds (Adair,1991). It seems unlikely, therefore, that EMFs are mutagensin the sense of initiating mutagenic transformations via a directinteraction with nucleic acids as can occur in the case ofionizing radiation or some chemical agents.Another approach involves consideration of possible modu-latory effects of EMFs on a genetic effect caused by anotherfactor. As examples, EMFs had no effect on UV light-inducedmutations in Saccharomyces cerevisiae (Ager and Radul,1992), but animals treated with 7,12-dimethylbenz[a]anthra-cene (DMBA) and exposed to an EMF exhibited increasedtumour incidence, compared with DMBA-treated non-exposedcontrols (Baum etai., 1995; Mevissen etai, 1995).Since EMFs are probably not mutagenic but can affect thedevelopment of cancer as shown by the DMBA studies, itseemed reasonable to expect that any link with aneuploidywas similarly likely to involve modulation or promotion ratherthan initiation. We therefore considered the question whetherEMFs were capable of modulating the level of aneuploidyinduced in animals by a known aneugen, using an establishedmammalian female germ cell model and vinblastine sulphate(VBS) as the aneugen (Mailhes et al., 1988). It was found thatEMFs significantly enhanced the incidence of hyperploidyinduced by VBS in mouse oocytes.Materials and methods