zahra zare dorahi

The placenta provides nutrients and oxygen to embryo and removes waste products from embryo’s blood. As far as we know, the effects of exposure to Wi-Fi (2.4 GHz) signals on placenta have not been evaluated. Hence, we examined the effect of prenatal exposure to Wi-Fi signals on anti-oxidant capacity, expressions of CDKNA1, and GADD45a as well as apoptosis in placenta and pregnancy outcome.

Pregnant mice were exposed to Wi-Fi signal (2.4 GHz) for 2 and 4 hr. Placenta tissues were examined to measure the MDA and SOD levels. To measure SOD, CDKNA1, GADD45a, Bax, and Bcl-2 expressions were compared by real-time PCR analysis. TUNEL assay was used to assess apoptosis in placenta tissues. The results were analyzed by one-way analysis of variance (ANOVA) using Prism version 6.0 software.

MDA and SOD levels had significantly increased in exposed Wi-Fi signal groups (P-value< 0.05). Also, quantitative PCR experiment showed that SOD mRNA expression significantly increased in Wi-Fi signal groups. The data showed that CDKN1A and GADD45a genes were increased in Wi-Fi groups (P-value<0.05). The quantitative PCR and the TUNEL assay showed that apoptosis increased in Wi-Fi groups (P-value<0.05).

Our results provide evidence that Wi-Fi signals increase lipid peroxidation, SOD activity (oxidative stres), apoptosis and CDKN1A and GADD45a overexpression in mice placenta tissue. However, further experimental studies are warranted to investigate other genes and aspects of pregnancy to determine the role of Wi-Fi radiation on fertility and pregnancy.

Recently, studies of diketocarotenoids such as astaxanthin (Ax) and canthaxanthin (Cx) with powerful antioxidant have focused on numerous biological mechanisms such as singlet oxygen quenching, radical scavenging, anti-diabetic, anti-carcinogenesis, anti-inflammatory, anti-obesity and anti-melanogenesis activities. There is evidence demonstrating that diketocarotenoid confers neuroprotective effects in experimental models of chronic neurodegenerative disorders and neurological diseases. This study used Ax and Cx to detect its role on senescence of SHSY-5Y Cells. In this study, the sample included the cell control group (SH-SY5Y cell line) that did not receive Ax and Cx, , and the experimental group that received Ax and Cx (20 mM). Ax and Cx were treated with SH-SY5Y cell line at 48 hours. To measure the expression of BAX, Bcl-2 and PPARγ different groups were compared by real‑time PCR analysis. The cell senescence effects of Ax and Cx, a β-galactosidase (SA-β-gal) senescence assay was evaluated. The results were analyzed by the one-way analysis of variance (ANOVA) using Prism version 6.0 software. The results showed that treatment with Ax and Cx (20 mM) for 48h induced apoptosis and senescence. The BAX and Bcl-2 gene expression analysis revealed a significant impact of Ax and Cx in apoptosis induction (P<0.05). The measuring of cell senescence also indicated that Ax and Cx exhibited a senescence inductive activity as determined by an increase in β-galactosidase activity and PPARγ gene expression (P<0.05). It appears that Ax and Cx have therapeutic properties in SH-SY5Y cells and can cause the proliferation of these cells to cease. The results suggest that Ax and Cx treatment may be beneficial for therapy of neuroblastoma and neurodegenerative disorders.