Can safe and long-term exposure to extremely low frequency (50 Hz) magnetic fields affect apoptosis,reproduction, and oxidative stress?

Abstract

Purpose: To determine whether 50 Hz extremely low frequency-magnetic fields (ELF-MF) affects apoptotic processes, oxidative damage, and reproductive characteristics such as sperm count and morphology in rat testes.

Materials and methods: Thirty male Sprague-Dawley rats were used in the present study, which were divided into three groups (sham group, n = 10, and two experimental groups, n = 10 for each group). Rats in the experimental group were exposed to 100 and 500 μT ELF-MF (2 h/day, 7 days/week, for 10 months) corresponding to exposure levels that are considered safe for humans. The same experimental procedures were applied to the sham group, but the ELF generator was turned off. Tissues from the testes were immunohistochemically stained for active (cleaved) caspase-3 in order to measure the apoptotic index by a semi-quantitative scoring system. The levels of catalase (CAT), malondialdehyde (MDA), myeloperoxidase (MPO), total antioxidative capacity (TAC), total oxidant status (TOS), and oxidative stress index (OSI) were also measured. Additionally, epididymal sperm count and sperm morphology was evaluated.

Results: There were no significant differences in the reproductive and oxidative stress parameters between the sham group and the exposed groups (p > 0.05). While no difference was observed between the final apoptosis score of the sham and the 100 μT ELF-MF group (p > 0.05), the final apoptosis score was higher in the 500 μT ELF-MF exposure group than in the sham group (p < 0.05).

Conclusion: Long-term exposure to 100 μT and 500 μT ELF-MF did not affect oxidative or antioxidative processes, lipid peroxidation, or reproductive components such as sperm count and morphology in testes tissue of rats. However, long-term exposure to 500 μT ELF-MF did affect active-caspase-3 activity, which is a well-known apoptotic indicator.     

Genetic susceptibility to thymic lymphomas and K‐ras gene mutation in mice after exposure to X‐rays and N‐ethyl‐N‐nitrosourea

Purpose: Ras activation is one of the major mechanisms for the development of murine thymic lymphomas by radiation and chemical carcinogens. To gain insight into the relationship between genetic susceptibility and ras gene mutation, the frequency and spectrum of ras gene mutation was examined in thymic lymphomas from susceptible and resistant mice.

Materials and methods: K‐ and N‐ras mutations in thymic lymphomas that arose in X‐ray‐irradiated and N‐ethyl‐N‐nitrosourea (ENU)‐treated mice of susceptible C57BL/6, rather resistant C3H and their hybrid B6C3F1 were analysed by polymerase chain reaction‐single‐strand conformation polymorphism and subsequent DNA sequencing.

Results: C57BL/6 exhibited a higher incidence of thymic lymphomas after exposure to X‐rays and ENU than C3H, with B6C3F1 being intermediate. K‐ras gene mutations occurred frequently in the pathogenesis of ENU‐induced thymic lymphomas in susceptible C57BL/6 as opposed to resistant C3H. The ras mutations were more frequent in ENU‐induced thymic lymphomas than X‐ray‐induced thymic lymphomas, and with the latter, there was no clear evidence for strain differences, suggesting that the genetic susceptibility to X‐rays was independent of ras activation. The mutations of K‐ras in thymic lymphomas from C57BL/6 were predominantly GGT to GAT in codon 12, whereas this mutation type was never found in those from C3H. No strain difference was observed in the nucleotide sequence or expression levels of O⁶‐alkylguanine alkyltransferase, indicating that this enzyme did not account for the genetic susceptibility to ras activation.

Conclusions: The results indicate that there is a clear strain and carcinogen dependency of K‐ras mutation and that the frequency of ras mutation might determine the genetic susceptibility to ENU‐induced lymphomagenesis, whereas pathways independent of ras activation might determine the susceptibility to X‐ray‐induced lymphomagenesis.