Baha Oral

Endometrial apoptosis induced by a 900-MHz mobile phone: Preventive effects of vitamins E and C

Numerous reports have described the effects induced by an electromagnetic field (EMF) in various cellular systems. The purposes of this study were to examine oxidative stress that promotes production of reactive oxygen species induced by a 900-megahertz (MHz) mobile phone and the possible ameliorating effects of vitamins E and C on endometrial tissue against EMF-induced endometrial impairment and apoptosis in rats. Animals were randomly grouped as follows: (1) sham-operated control group (n=8), (2) 900 MHz EMF-exposed group (n=8; 30 min/d for 30 d), and (3) 900 MHz EMF-exposed group, treated with vitamins E and C (n=8; 50 mg/kg intramuscularly and 20 mg/kg body weight intraperitoneally before daily EMF exposure). Malondialdehyde (an index of lipid peroxidation) was used as a marker of oxidative stress-induced endometrial impairment; Bcl-2, Bax, caspase-3, and caspase-8 were assessed immunohistochemically. In this study, increased malondialdehyde levels in endometrial tissue and apoptosis illustrated the role of the oxidative mechanism induced by exposure to a 900-MHz mobile phone-like device and vitamins E and C; via free radical scavenging and antioxidant properties, oxidative tissue injury and apoptosis were ameliorated in rat endometrium. In conclusion, exposure to 900-MHz radiation emitted by mobile phones may cause endometrial apoptosis and oxidative stress, but treatment with vitamins E and C can diminish these changes and may have a beneficial effect in preventing endometrial changes in rats.

900 MHz radiofrequency-induced histopathologic changes and oxidative stress in rat endometrium: protection by vitamins E and C

There are numerous reports on the effects of electromagnetic radiation (EMR) in various cellular systems. Mechanisms of adverse effects of EMR indicate that reactive oxygen species (ROS) may play a role in the biological effects of this radiation. The aims of this study were to examine 900 MHz mobile phone-induced oxidative stress that promotes production of ROS and to investigate the role of vitamins E and C, which have antioxidant properties, on endometrial tissue against possible 900MHz mobile phone-induced endometrial impairment in rats. The animals were randomly grouped (eight each) as follows: 1) Control group (without stress and EMR, Group I), 2) sham-operated rats stayed without exposure to EMR (exposure device off, Group II), 3) rats exposed to 900MHz EMR (EMR group, Group III) and 4) a 900MHz EMR exposed + vitamin-treated group (EMR + Vit group, Group IV). A 900 MHz EMR was applied to EMR and EMR + Vit group 30min/day, for 30 days using an experimental exposure device. Endometrial levels of nitric oxide (NO, an oxidant product) and malondialdehyde (MDA, an index of lipid peroxidation), increased in EMR exposed rats while the combined vitamins E and C caused a significant reduction in the levels of NO and MDA. Likewise, endometrial superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) activities decreased in EMR exposed animals while vitamins E and C caused a significant increase in the activities of these antioxidant enzymes. In the EMR group histopathologic changes in endometrium, diffuse and severe apoptosis was present in the endometrial surface epithelial and glandular cells and the stromal cells. Diffuse eosinophilic leucocyte and lymphocyte infiltration were observed in the endometrial stroma whereas the combination of vitamins E and C caused a significant decrease in these effects of EMR. It is concluded that oxidative endometrial damage plays an important role in the 900 MHz mobile phone-induced endometrial impairment and the modulation of oxidative stress with vitamins E and C reduces the 900MHz mobile phone-induced endometrial damage both at biochemical and histological levels. Toxicology and Industrial Health 2007; 23: 411—420.

Protective effects of vitamins C and E against endometrial damage and oxidative stress in fluoride intoxication.

1 Fluoride (F) is an essential trace element that has protective effects against bone mineral loss. However, it becomes toxic at higher doses and induces some adverse effects on a number of physiological functions, including reproduction. The aims of this study were to examine F‐induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of vitamins C and E against possible F‐induced endometrial impairment in rats. 2 Rats were divided into three groups: control, F and F plus vitamins. The F group was given 100 mg/L orally for 60 days. Combined vitamins were also administered orally. Fluoride administration to control rats significantly increased endometrial malondialdehyde (MDA) but decreased superoxide dismutase (SOD), glutathione peroxidase (GSH‐Px) and catalase (CAT) activities. Endometrial glandular and stromal apoptosis were investigated by DNA nick end‐labelling (TUNEL) method on each sample and the mean endometrial apoptotic index (AI) was calculated. 3 Vitamin administration with F treatment caused endometrial MDA to decrease, but SOD, GSH‐Px and CAT activities to increase, all to significant levels. Vitamins showed a histopathological protection against F‐induced endometrial damage. There was a significant difference in the AI between the groups. Lymphocyte and eosinophil infiltration in stroma in F‐treated rats were more than those in the control and F + Vit groups. 4 It can be concluded that oxidative endometrial damage plays an important role in F‐induced endometrial toxicity, and the modulation of oxidative stress with vitamins reduces F‐induced endometrial damage both at the biochemical and histological levels.

Neuroprotective effects of tamoxifen on experimental spinal cord injury in rats

The aim of this study was to evaluate the effects of tamoxifen on tumor necrosis factor alpha (TNF-alpha) and interleukin 1beta (IL-1beta) levels and ultrastructural changes in rats with spinal cord injury. Rats were divided into four groups: control group (laminectomy only), trauma group (laminectomy+spinal trauma), tamoxifen group (laminectomy+spinal trauma+tamoxifen), and vehicle group (laminectomy+spinal trauma+vehicle). Spinal cords were extirpated at the T(7)-T(12) level and tissue samples from the spinal cords were gathered for TNF-alpha and IL-1beta measurements at 1 and 6hours. Spinal cords harvested at 6 hours were evaluated for ultrastructural changes. TNF-alpha and IL-1beta levels at 6 hours were significantly lower in the tamoxifen group than in the trauma group. Electron microscopic examination of tissue from the trauma group revealed gross cell deformities with widespread edema of all structures as well as severe edema in the neuropil. At 6 hours after trauma, these ultrastructural changes were less marked in the tamoxifen group. Our findings support a neuroprotective and restorative role for tamoxifen in the context of secondary pathological biochemical events after SCI.

Ovarian toxicity in rats caused by methidathion and ameliorating effect of vitamins E and C

We have investigated the effect of subchronic administration of methidathion (MD) on ovary evaluated ameliorating effects of vitamins E and C against MD toxicity. Experimental groups were as follows: control group; a group treated with 5 mg/kg body weight MD (MD group); and a group treated with 5 mg/kg body weight MD plus vitamin E and vitamin C (MD + Vit group). MD and MD + Vit groups were given MD by gavage five days a week for four weeks at a dose level of 5 mg/kg/day by using corn oil as the vehicle. Serum malondialdehyde (MDA: an indicator of lipid peroxidation) concentration, serum activity of cholinesterase (ChE), and ovary histopathology were studied. The level of MDA increased significantly in the MD group compared with the control (P < 0.005). Serum MDA decreased significantly in the MD + Vit group compared with the MD group (P < 0.05). The activities of ChE decreased significantly both in the MD and MD + Vit groups compared with the controls ( P < 0.05). However, the decrease in the MD + Vit groups was less than in the MD group; the ChE activity in the MD + Vit group was significantly higher compared with MD group (P < 0.05). Number of ovarian follicles were significantly lower in the MD group compared to the controls (P < 0.05). Number of atretic follicles were significantly higher in the MD group than in the controls (P < 0.05). Follicle counts in MD + Vit group showed that all types of ovarian follicles were significantly higher, and a significant decrease in the number of atretic follicles compared with the MD group (P < 0.05). In conclusion, subchronic MD administration caused an ovarian damage, in addition, LPO may be one of the molecular mechanisms involved in MD-induced toxicity. Treatment with vitamins E and C after the administration of MD reduced LPO and ovarian damage. Human & Experimental Toxicology (2007) 26 , 491—498

Effect of caffeic acid phenethyl ester on the regression of endometrial explants in an experimental rat model.

The objective of this study is to determine the effects of antioxidant and anti-inflammatory caffeic acid phenethyl ester (CAPE) on experimental endometriosis, peritoneal superoxide dismutase (SOD) and catalase (CAT) activities, and malondialdehyde (MDA) levels in the rat endometriosis model. Thirty rats with experimentally induced endometriosis were randomly divided into 2 groups and treated for 4 weeks with intraperitoneal CAPE (CAPE-treated group; 10 µmol/kg/d, n = 13) or vehicle (control group; n = 13). The volume and weight changes of the implants were calculated. Immunohistochemical and histologic examinations of endometriotic explants by semiquantitative analysis and measurements of peritoneal SOD, CAT, and MDA levels were made. Following 4 weeks of treatment with CAPE, there were significant differences in posttreatment spherical volumes (37.4 ± 14.7 mm3 vs 147.5 ± 41.2 mm3) and explant weights (49.1 ± 28.5 mg vs 158.9 ± 50.3 mg) between the CAPE-treated groups and controls. The mean evaluation nomogram levels in glandular epithelium for COX-2 positivity by scoring system were 2.1 ± 0.3 in the CAPE-treated group and 3.9 ± 0.3 in the control group. In the CAPE-treated group, peritoneal levels of MDA and activities of SOD and CAT significantly decreased when compared with the control group (P < .01). Histologic analysis of the explants demonstrated mostly atrophy and regression in the treatment group, and semiquantitative analysis showed significantly lower scores in rats treated with CAPE compared with the control group. CAPE appeared to cause regression of experimental endometriosis.

Bone Mineral Density of the Spine and Femur in Early Postmenopausal Turkish Women with Endemic Skeletal Fluorosis

The aim of this prospective, comparative study was to investigate the bone mineral density (BMD) changes in a group of early postmenopausal Turkish women with endemic skeletal fluorosis and to study effects of endemic fluorosis on BMD. Bone mineral density of L2–L4 vertebra, femur neck, femur trochanter, and Ward’s triangle were measured in 45 female patients with endemic skeletal fluorosis and 41 age-matched controls by dual X-ray absorbtiometry (DXA). The BMD of L2–L4 vertebra and Ward’s triangle were higher in the endemic fluorosis group than in the control group (P < 0.001). Patients with endemic fluorosis had higher femur neck and femur trochanter BMDs than did controls (P < 0.01 and P < 0.05, respectively). There was a positive correlation between serum fluoride content and BMD at the spine (r = 0.345, P = 0.001), femoral neck (r = 0.274, P = 0.011), Ward’s triangle (r = 0.295, P = 0.006), and trochanter (r = 0.217, P = 0.045). In conclusion, higher bone mineral density levels were seen in early postmenopausal women with endemic skeletal fluorosis. BMD measurement is a tool in the diagnosis and management of this preventable crippling disease.

Lipid peroxidation in umbilical arterial blood at birth : the effects of breech delivery

Objective To determine oxygen free radical activity in breech presentation at birth and relate it to umbilical cord blood acid‐base status.

Thrombin activatable fibrinolysis inhibitor and other hemostatic parameters in patients with polycystic ovary syndrome

Objectives. To investigate the plasma levels of thrombin-activatable fibrinolysis inhibitor (TAFI) in women with polycystic ovary syndrome (PCOS) and its correlation with various metabolic, hormonal and hemostatic parameters. Methods. Forty-eight women with PCOS and 43 age- and BMI-matched ovulatory controls were recruited during a 20-month study period. Blood samples were drawn for all tests, which included plasma lipids and lipoproteins, reproductive hormones, glucose, insulin, TAFI antigen concentration, plasminogen activator inhibitor-1 (PAI-1) activity, fibrinogen concentration, thrombomodulin, thrombin–antithrombin (TAT) complexes, D-dimer, Protein C Antigen, Protein S Antigen, Antithrombin III (AT III) and activated protein C (APC) resistance. Results. Plasma TAFI levels of PCOS patients were found to be significantly higher than in healthy controls (93.8%±30.6%vs. 79.8% ± 22.4%, p < 0.05). Plasma levels of D-dimer, AT III, PAI-1 and thrombomodulin were also significantly higher in women with PCOS compared with healthy controls. All the other hemostatic parameters (including TAT complexes; Protein C; APC; and Protein S) were comparable between the two study groups. Conclusion. This study showed that plasma levels of TAFI, PAI-1, D-dimer, AT III and thrombomodulin were significantly increased in women with PCOS compared with age- and BMI-matched controls.

Efficacy of intrauterine lidocaine for removal of a "lost" intrauterine device: a randomized, controlled trial.

OBJECTIVE: To evaluate the efficacy of intrauterine lidocaine instillation in reducing patient discomfort during the removal of a “lost” intrauterine device (IUD). METHODS: This double-blinded, randomized, placebo-controlled trial included 68 women who underwent removal procedure for a “lost” IUD. Thirty-four women were allocated to the lidocaine group and 34 to the saline group. The main outcome measure was the intensity of pain during, immediately after, and 20 minutes after the procedure, assessed by a visual analog scale. Statistical analysis was performed using the Friedman test with Bonferroni correction, Student t test, and &khgr;2. RESULTS: There were no statistically significant differences between the study group and the control group in mean age, parity history of chronic pelvic pain and dysmenorrhea, history of curettage, education, socioeconomic status, menopausal status, breastfeeding, type of IUD, and duration of IUD. Pain scores demonstrated a significant difference between groups during the procedure (placebo 6.41 ± 1.15, lidocaine 5.23 ± 0.69, P < .01), immediately after procedure (placebo 6.05 ± 1.01, lidocaine 4.94 ± 0.60, P < .01), and 20 minutes after procedure (placebo 4.32 ± 0.63, lidocaine 4.44 ± 0.66, P < .01). The number needed to treat was 3 (95% confidence interval 2–9). CONCLUSION: Intrauterine lidocaine appears to be effective in decreasing pain in women undergoing the removal procedure of a “lost” IUD. CLINICAL TRIAL REGISTRATION: Clinicaltrials.gov, NCT00308841. LEVEL OF EVIDENCE: I