The growing public concerns about the possible health effects of exposure to radio frequency (RF) fields from mobile telephones have arisen in many countries because of the increased use of mobile telecommunication devices. This in turn has led to an increase in cognate epidemiological and experimental investigations. However, the results of these studies are conflicting. Some have implicated an increased health risk 1, but most studies have shown no effects 2. The lens epithelial cells (LECs) are a single layer of cuboidal cells at the anterior surface of the lens, which retain the proliferative capacity and are important for maintaining the metabolic homeostasis and transparency of the lens. Damage to LECs has been found to be associated with cataractogenesis. To investigate whether exposure to 1.8 GHz RF can influence the cellular physiology of the LECs, the expression of heat shock proteins (Hsps) and the activation of mitogen-activated protein kinases (MAPKs) in human LECs after exposure to the 1.8 GHz RF of a global system for mobile communications (GSM) were evaluated. The average specific absorption rate (SAR) level of 2 W/kg is the safety limit for mobile phone microwave radiation emission as defined by the ICNIRP (International Commission on Non-Ionizing Radiation Protection). Furthermore, as per the guidelines of the ICNIRP in 1998, the available experimental evidence indicated that the threshold for irreversible effects in even the most sensitive tissues was greater than 4 W/kg, which is recommended as the occupational whole-body exposure restriction with a traditional safety factor of ten, which translates to 0.4 W/kg. On the other hand, we intended to obtain obvious bio-effects of microwave radiation so as to investigate the potential mechanism of microwave-induced cataract. Therefore, we chose the SARs of 1, 2, 3, and 4 W/kg in our study. During the entire course of exposure, the temperature never fluctuated over the range of 37±0.108 °C; all data and experimental settings were stored by the computer every 10 s. The temperature difference between sham and exposure never exceeded 0.108 °C.

The MAPKs comprise three major types, extracellular signal-regulated kinases (ERKs), c-Jun N-terminal kinases (JNKs), and p38, which are involved in the signal transduction pathways in all eukaryotes and mediate the effects of various stimuli to regulate essentially all stimulated processes, including proliferation, differentiation, metabolism, and the stress response 9. It has been proposed that activation of JNKs and p38 MAP kinases contributes to cell death, whereas activation of ERKs contributes to protection against cell injury in multiple organs 10. There is evidence that induction of the MAPK pathway plays significant roles in the activation of specific Hsps 11. We thus examined the activation of MAPKs after exposure to RF at SARs of 2, 3, and 4 W/kg for 0, 5, 15, 30, 60, and 120 min. The results showed that ERK1/2 was markedly activated as early as 5 min after RF exposure; the activation peaked at 30 min and lasted up to 2 h after exposure (Figure 1C). Phosphorylation of JNK1/2 was detected at 2 h after exposure (Figure 1D), while p38 activation was not detected (Figure 1E). Recently, it was reported that ERK was activated within 5 min of the radiation, with the peak activity occurring within 10-15 min, whereas no phosphorylation of JNKs or p38 was detected within a short time of exposure 12. Our results with human LECs are consistent with that study. These results indicate that mobile phone radiation can induce an immediate effect in the cytoplasm that activates ERK signaling so as to further induce transcription of a variety of genes 13, and that long exposure can activate JNK. However, we did not find the activation of p38 after RF exposure. The appearance of p-ERK1/2 and p-JNK1/2, together with Hsp up-regulation, suggests that non-thermal RF exposure can induce the stress response in human LECs.

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