Hippocampal lipidome and transcriptome profile alterations triggered by acute exposure of mice to GSM 1800 MHz mobile phone radiation: An exploratory study.

BACKGROUND: The widespread use of wireless devices during the last decades is raising concerns about adverse health effects of the radiofrequency electromagnetic radiation (RF-EMR) emitted from these devices. Recent research is focusing on unraveling the underlying mechanisms of RF-EMR and potential cellular targets. The "omics" high-throughput approaches are powerful tools to investigate the global effects of RF-EMR on cellular physiology. METHODS: In this work, C57BL/6 adult male mice were whole-body exposed (nExp  = 8) for 2 hr to GSM 1800 MHz mobile phone radiation at an average electric field intensity range of 4.3-17.5 V/m or sham-exposed (nSE  = 8), and the RF-EMR effects on the hippocampal lipidome and transcriptome profiles were assessed 6 hr later. RESULTS: The data analysis of the phospholipid fatty acid residues revealed that the levels of four fatty acids [16:0, 16:1 (6c + 7c), 18:1 9c, eicosapentaenoic acid omega-3 (EPA, 20:5 ω3)] and the two fatty acid sums of saturated and monounsaturated fatty acids (SFA and MUFA) were significantly altered (p < 0.05) in the exposed group. The observed changes indicate a membrane remodeling response of the tissue phospholipids after nonionizing radiation exposure, reducing SFA and EPA, while increasing MUFA residues. The microarray data analysis demonstrated that the expression of 178 genes changed significantly (p < 0.05) between the two groups, revealing an impact on genes involved in critical biological processes, such as cell cycle, DNA replication and repair, cell death, cell signaling, nervous system development and function, immune system response, lipid metabolism, and carcinogenesis. CONCLUSIONS: This study provides preliminary evidence that mobile phone radiation induces hippocampal lipidome and transcriptome changes that may explain the brain proteome changes and memory deficits previously shown by our group.

Mechanisms of enhanced apoptosis in HL-60 cells by UV-irradiated n-3 and n-6 polyunsaturated fatty acids.

We examined the effects of arachidonic acid (AA), eicosapentaenoic acid (EPA), and their ultraviolet (UV)-irradiated products on HL-60 cells and isolated mitochondria to explore the following four obscure points in the mechanism of polyunsaturated fatty acids (PUFAs)-induced apoptosis: (i). the role of reactive oxygen species, (ii). the interaction of PUFAs and their metabolites with mitochondria in situ, (iii). the cyclosporine A (CsA)-sensitivity in PUFA-induced membrane permeability transition, (iv). the specificity of oxidized n-3 PUFAs in the induction of apoptosis in cancer cells. UV-oxidized PUFAs contained conjugated dienes and thiobarbituric acid reactive substances (TBARS). The apoptotic effects of PUFAs on HL-60 cells were increased by UV-irradiation whereas the swelling effect of PUFAs on isolated mitochondria was decreased. Both oxidized n-3 and n-6 PUFAs induced increased depolarization, ferricytochrome c release, the activation of various caspases, and DNA-fragmentation in a CsA-insensitive mechanism concomitant with a slight increase in the value of TBARS in cells. Furthermore, there were no significant differences in the mechanism of apoptosis induced by either oxidized AA or oxidized EPA. On the basis of these results, it was concluded that both oxidized n-3 or n-6 PUFAs induced apoptosis in HL-60 cells by a similar mechanism in a CsA-insensitive manner and also that oxidized products of PUFAs, but not the cellular oxidation process itself, play an important role in the mechanism of apoptosis in HL-60 cells.

Chemical stability of ethyl icosapentate against autoxidation. II. Effect of photoirradiation on oxidation kinetics.

The effect of ultraviolet (UV) or visible light (VIS) irradiation on the chemical stability of ethyl icosapentate [ethyl-(all-cis)-5,8,11,14,17-icosapentaenoate] (EPA) was investigated at 45 degrees C by means of HPLC and by measuring the peroxide value (POV). EPA was oxidized to peroxides after an induction period by photoirradiation, and the peroxide subsequently degraded to secondary products. The autoxidation of EPA followed consecutive reaction kinetics including an induction period, and the kinetic parameters of the oxidation were calculated based upon the consecutive reaction model by computer curve fitting. The results of the degradation rate constant, k, and the induction period obtained by HPLC showed that the radical and the peroxide formation rates are affected by UV, but not by VIS light irradiation. The formation rate constant of peroxide, k1, and its degradation rate constant to secondary products, k2, obtained from the POV under UV light irradiation, increased with irradiation intensity, during which the induction period decreased. On the other hand, k1, k2 and the induction period by VIS light irradiation did not change significantly. The relationship between the induction periods obtained by HPLC and POV and the UV light irradiation energy were superimposed in the plots, indicating that these parameters depended on the UV irradiation energy. The relationship between k1/k2 ratio and the UV irradiation energy suggested that the formation of secondary products was more remarkably accelerated by UV energy than that of peroxide.