Investigation of oxidative damage, antioxidant balance, DNA repair genes, and apoptosis due to radiofrequency-induced adaptive response in mice.

This study aims to determine whether exposure to non-ionizing radiofrequency fields could induce an adaptive response (AR) in adult mice and to reveal potential molecular mechanisms triggered by RF-induced AR. The study was performed on 24 adult male Swiss-Albino mice. The average mass of the mice was 37 g. Four groups of adult mice, each consisting of 6, were formed. The radiofrequency group (R) and the adaptive response group (RB) were exposed to 900 MHz of global system for mobile communications (GSM) signal at 0.339 W/kg (1 g average specific absorption rate) 4 h/day for 7 days, while the control group (C) and the bleomycin group (B) were not exposed. 20 minutes after the last radiofrequency field (RF) exposure, the mice in the B and RB groups were injected intraperitoneal (ip) bleomycin (BLM), 37.5 mg/kg. All the animals were sacrificed 30 minutes after the BLM injection. Oxidative damage and antioxidant mechanism were subsequently investigated in the blood samples. Changes in the expression of the genes involved in DNA repair were detected in the liver tissue. TUNEL method was used to determine the apoptosis developed by DNA fragmentation in the liver tissue. The RB group, which produced an adaptive response, was compared with the control group. According to the results, the increase of reactive oxygen species (ROS) in the RB group may have played an important role in triggering the adaptive response and producing the required minimum stress level. Furthermore, tumor suppressor 53(p53), oxo guanine DNA glycosylase (OGG-1) levels responsible for DNA repair mechanism genes expression were increased in conjunction with the increase in ROS. The change in the poly (ADP-ribose) polymerase 1 (PARP-1) and glutathione peroxidase 1 (GPx-1) gene expression were not statistically significant. The antioxidant enzyme levels of superoxide dismutase (SOD), catalase (CAT), and total antioxidant capacity (TAC) were decreased in the group with adaptive response. According to the data obtained from terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) analysis, apoptosis was decreased in the RB group due to the decrease in cell death, which might have resulted from an increase in gene expression responsible for DNA repair mechanisms. The results of our study show that exposure to RF radiation may create a protective reaction against the bleomycin. The minimal oxidative stress due to the RF exposure leads to an adaptive response in the genes that play a role in the DNA repair mechanism and enzymes, enabling the survival of the cell.

The protective role of melatonin and curcumin in the testis of young and aged rats.

We aimed to investigate the effect of melatonin and curcumin treatment on oxidative stress, apoptosis, and histology of testicular tissue in our study. Four groups were formed using young (4 months old, n = 6) and aged (20-22 months old, n = 18) male Wistar albino rats: (a) Young control (1% ethanol:phosphate-buffered saline [PBS], subcutaneously [s.c.]); (b) Aged control (CTL; n = 6, 1% ethanol:PBS, s.c.); (c) Aged Melatonin (MLT; n = 6, 10 mg/kg, s.c.); (d) Aged Curcumin (CUR; n = 6, 30 mg/kg, i.p.). At the end of 21 days, the rats were sacrificed, and testicular tissues were removed. Malondialdehyde (MDA) in the testicular tissue was determined with thiobarbituric acid reactive substances formation, and glutathione (GSH) was determined with modified Ellman method; testosterone level was determined with chemiluminescence method and histologic changes were determined with Haematoxylin-Eosin and Johnsen's scoring; Apoptotic cell counts were made with TUNEL staining of seminiferous tubule in testis. With ageing, MDA level increased in testicular tissue, but GSH and blood testosterone levels decreased. Melatonin treatment for aged rats significantly decreased Paired total testicular/body weight ratio compared to aged control group (p < 0.05). Curcumin treatment for aged rats significantly increased GSH level compared to the aged control group (p < 0.05). Besides, melatonin and curcumin treatment significantly decreased the number of apoptotic cells and significantly increased Johnsen's score (p < 0.05).

Ellagic acid increases implantation rates with its antifibrotic effect in the rat model of intrauterine adhesion.

Intrauterine adhesions (IUA) are defined as the adhesion of opposing endometrial tissue with dense fibrous adhesive bands within the uterine cavity. With the increase in cesarean sections and endometrial surgical procedures, intrauterine adhesions have become a problem with increasing incidence and decreasing implantation. The purpose of the study was to investigate the effect of ellagic acid (EA), a phenolic compound, on fibrosis in IUA model rats. Another goal of the study was to increase endometrial receptivity with EA. The groups in the study were planned as control, DMSO, EA, IUA, IUA+DMSO, and IUA+EA, with 8 Sprague Dawley rats in each group. EA was administered at a dose of 100 mg/kg/day for 35 days. At the end of the experiment, the uterine tissues of the rats were removed. Histochemical staining was used to validate the IUA model and determine the degree of fibrosis. The levels of some fibrosis-related genes and proteins in the obtained uterine tissues were evaluated. In addition, implantation rates were determined. In our findings, it was observed that the fibrotic structure was decreased in the treated IUA+EA group compared to the IUA group, while fibrotic improvement was supported by down-regulation of TGFß1 activity and up-regulation of BMP7 activity. The increase in the expression of the endometrial marker LIF with EA treatment was consistent with the increase in implantation rates with treatment. As a result of the study, it can be said that EA applied as a treatment against IUA causes healing in uterine tissue by reducing fibrosis and increases implantation rates by increasing endometrial receptivity.