title: Effect of 6mT static magnetic field on the bcl-2, bax, p53 and hsp70 expression in freshly isolated and in vitro aged human lymphocytes.
abstract: An increasing number of evidence indicates that static magnetic fields (SMFs) are capable of altering apoptosis, mainly through modulation of Ca(2+) influx. Here we present data that suggest apoptotic-related gene expression as an alternative pathway, through which exposure to 6milliTesla (mT) SMF can interfere with apoptosis. Exposure to 6mT SMF affects the apoptotic rate (spontaneous and drug-induced) and [Ca(2+)](i) in isolated human lymphocytes; the aged cells are more susceptible to exposure than fresh ones. The exposure to 6mT exerted a protective effect on chemical or physical-induced apoptosis, irrespective of the age of the cells. The investigation of the gene expression of bcl-2, bax, p53 and hsp70 in freshly isolated and in culture-aged human lymphocytes indicates that these genes are modulated by SMF exposure in the experimental conditions used, in a gene-, age- and time-dependent manner. The exposure of isolated lymphocytes to SMF for up to 24h modulated increased bax and p53 and decreased hsp70, and bcl-2. The amount of increment and/or decrement of the proteins varied for each gene examined and was independent of the apoptotic inducers. Finally, the same stress applied to freshly isolated or aged lymphocytes resulted in different modulation of bcl-2, bax and hsp70.
authors.affiliation: Department of Biological and Environmental Science and Technology, University of the Salento, 73100 Lecce, Italy.
authors.forename: B
authors.initials: B
authors.lastname: Tenuzzo
authors.forename: C
authors.initials: C
authors.lastname: Vergallo
authors.forename: L
authors.initials: L
authors.lastname: Dini
mesh_terms: D000328:Adult; D017209:Apoptosis / Q000502:physiology / Q000528:radiation effects*; D051017:Apoptosis Regulatory Proteins / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects*; D002470:Cell Survival / Q000235:genetics / Q000528:radiation effects; D002478:Cells, Cultured; D016922:Cellular Senescence / Q000235:genetics / Q000528:radiation effects*; D019610:Cytoprotection / Q000502:physiology / Q000528:radiation effects; D015536:Down-Regulation / Q000235:genetics / Q000528:radiation effects; D004574:Electromagnetic Fields; D005786:Gene Expression Regulation / Q000235:genetics / Q000528:radiation effects; D050884:HSP72 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D006801:Humans; D008214:Lymphocytes / Q000378:metabolism / Q000528:radiation effects*; D008297:Male; D008875:Middle Aged; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D013312:Stress, Physiological / Q000235:genetics; D013997:Time Factors; D016159:Tumor Suppressor Protein p53 / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects; D015854:Up-Regulation / Q000235:genetics / Q000528:radiation effects; D051028:bcl-2-Associated X Protein / Q000235:genetics / Q000378:metabolism / Q000528:radiation effects
chemical_list: D051017:Apoptosis Regulatory Proteins; D050884:HSP72 Heat-Shock Proteins; D019253:Proto-Oncogene Proteins c-bcl-2; D016159:Tumor Suppressor Protein p53; D051028:bcl-2-Associated X Protein