Nermin Karahan

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.

The effects of subchronic methidathion toxicity on rat liver: role of antioxidant vitamins C and E.

Methidathion (MD) phosphorodithioic acid S-[(5-methoxy-2-oxo-1,3,4-thiadiazol-3(2H)-yl)methyl] O,O-dimethyl ester is the organophosphate insecticide (OPI) most commonly used worldwide in the pest control of crops. Subchronic MD exposure was evaluated for its effects on lipid peroxidation, the serum activities of cholinesterase (ChE), and enzymes concerning liver damage, and the protective effects of combination of vitamins E and C in albino rats. Additionally, the histopathological changes in liver tissue were examined. 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 wight MD plus vitamin E plus vitamin C (MD+AO group). The MD and MD+AO groups were treated orally with MD on five days a week for 4 weeks. The serum activities of cholinesterase (ChE), alanine transferase (ALT), aspartate amiotransferase (AST), lactate dehydrogenase (LDH), γ-glutamyltransferase (GGT), alkaline phosphatase (ALP), and the concentration of malondialdehyde (MDA) and liver histopathology were studied. In serum samples, MD significantly increased MDA concentration and ALP, AST, GGT, LDH activities but decreased the ALT and ChE activities. In the MD+AO group, MDA level and ALP, AST, LDH activities were significantly decreased and ChE activity was increased compared to the MD group. Histopathological changes found in liver tissue of rats treated with MD included were infiltration with mononuclear cells in all portal areas, sinusoidal dilatation, and focal microvesicular steatosis and hydropic degenerations in parenchymal tissue. The severity of these lesions was reduced by administration of vitamins. From these results, it can be concluded that subchronic MD causes liver damage, and lipid peroxidation may be a molecular mechanism involved in MD-induced toxicity. Furthermore, the combination of vitamins E and C can reduce the toxic effects of MD on liver tissue of rats.

Testicular apoptosis and histopathological changes induced by a 2.45 GHz electromagnetic field

There is a growing public concern about the potential human health hazard caused by exposure to electromagnetic radiation (EMR). The objective of this study is to investigate the effects of 2450 mhz electromagnetic field on apoptosis and histopathological changes on rat testis tissue. Twelve-week-old male Wistar Albino rats were used in this study. Eighteen rats equally divided into three different groups which were named group I, II and III. Cage control (group I), sham control (group II) and 2.45 GHz EMR (group III) groups were formed. Group III were exposed to 2.45 GHz EMR, at 3.21 W/kg specific absorption rate for 60 minutes/ day for 28 days. There was no difference among the groups for the diameter of the seminiferous tubules, pyknotic, karyolectic and karyotic cells. However, the number of Leydig cells of testis tissue of the rats in group III was significantly reduced comparing with the group I (p < 0.05). Estimation of spermatogenesis using the Johnsen testicular biopsy score revealed that the difference between groups is statistically significant. The level of TNF-α, Caspase-3 and Bcl-2 were compared, and no significant difference was found between the groups. When Bax apoptosis genes and Caspase-8 apoptosis enzyme were compared, there were significant differences between the groups (p < 0.05). Electromagnetic field affects spermatogenesis and causes to apoptosis due to the heat and other stress-related events in testis tissue.

The protective effect of erythropoietin on renal injury induced by abdominal aortic-ischemia-reperfusion in rats.

BACKGROUND Renal injury induced by aortic ischemia-reperfusion (IR) is an important factor in the development of postoperative acute renal failure following abdominal aortic surgery. The purpose of this study is to examine the effect of erythropoietin on renal injury induced by aortic IR in rats. MATERIAL AND METHODS Twenty-four Wistar-Albino rats were randomized into 3 groups (8 per group). The control group underwent laparotomy and dissection of the infrarenal abdominal aorta without occlusion. The aortic IR group underwent clamping of the infrarenal abdominal aorta for 30 min followed by 60 min of reperfusion. The aortic IR + erythropoietin group underwent the same aortic IR periods and was pretreated with 1000 U/kg subcutaneous erythropoietin 5 min before ischemia. In rat kidney specimens, tissue levels of malondialdehyde (MDA), superoxide dismutase, catalase, and glutathione peroxidase were measured. Histological evaluation of the rat kidney tissues was also done. RESULTS Aortic IR significantly increased the levels of MDA and superoxide dismutase (P < 0.05 versus control). Erythropoietin significantly decreased the levels of MDA, superoxide dismutase, and catalase (P < 0.05 versus aortic IR). Histological evaluation showed that aortic IR significantly increased (P < 0.05 versus control), whereas erythropoietin significantly decreased (P < 0.05 versus aortic IR) the focal glomerular necrosis, dilation of Bowmans capsule, degeneration of tubular epithelium, necrosis in tubular epithelium, interstitial inflammatory infiltration, and congestion of blood vessels. CONCLUSIONS The results indicate that erythropoietin has protective effects on renal injury induced by aortic IR in rats.

Cardiotoxicity in rats induced by methidathion and ameliorating effect of vitamins E and C.

We have examined the effect of subchronic methidathion (MD) administration on heart damage, and have evaluated possible ameliorating effects of a combination of vitamins E and C against MD toxicity. The experimental groups were: control group, rats treated with 5 mg/kg MD and rats treated with 5 mg/kg body weight MD plus vitamin E and vitamin C (MD+Vit). The groups were given MD by gavage 5 days a week for four weeks at a dose level of 5 mg/kg/day (MD and MD+Vit) by using corn oil as the vehicle. Vitamin E and vitamin C were injected at doses of 50 mg/kg i.m. and 20 mg/kg i.p., respectively, after the treatment with MD in the MD+Vit group. The levels of malondialdehyde (MDA) were determined in the heart tissue, and the levels of cardiac troponin I (TnI) in serum. An autoanalyser was used to determine the serum activities of cholinesterase (ChE). Histopathological examination was carried out in the heart tissue. MDA significantly increased in the MD group as compared to controls (P <0.01). When MD was given concurrently with vitamins E and C, the increase in MDA was significantly less (P <0.01). ChE activity significantly decreased in the MD group as compared to controls (P <-0.01). When MD was given concurrently with vitamins E and C, the decrease in ChE activity was significantly higher (P <-0.05). The serum TnI levels significantly increased in the MD group as compared to controls (P <-0.01). When MD was given concurrently with vitamins E and C, the increase in the serum TnI was significantly less (P <-0.01). MD caused the diffuse loss of striation and myocytolysis of the cardiomyocytes, whereas the combination of vitamins E and C caused a significant decrease in these effects of MD. In conclusion, subchronic MD administration caused heart damage and, in addition, treatment with a combination of vitamins E and C after the administration of MD reduced heart damage caused by MD.

Spinal extradural arachnoid cyst

BACKGROUND CONTEXT Spinal extradural arachnoid cysts are uncommon expanding lesions. Idiopathic arachnoid cysts are not associated with trauma or other inflammatory insults. If they enlarge, they usually present with progressive signs and symptoms of neural compression. PURPOSE Total removal of the cyst and repair of the dural defect is the primary treatment for large thoracolumbar spinal extradural arachnoid cysts causing neurogenic claudication. Laminoplasty may prevent spinal deformities in long segmental involvement. STUDY DESIGN A clinical case was performed. PATIENT SAMPLE We report a case of 25-year-old man with 1-year history of progressive back pain radiating to both legs. His diagnosis was dorsal intraspinal extradural cystic lesion longing from the level of T11 to L2 on magnetic resonance imaging. OUTCOME MEASURES The patients pain levels were noted as he reported. Physiologic outcome was assessed on pre- and postoperative motor and sensory examination. METHODS The patient underwent a T11-L2 laminotomy and radical cyst wall resection was performed. A small communication with the subarachnoid space was seen at the level of T12. It was sealed with tissue fibrinogen after repair with primary suture. Titanium miniplates were used for laminoplasty. RESULTS Follow-up magnetic resonance imaging demonstrated cyst resolution, and neurologic examination revealed no sensory and motor deficit. CONCLUSION Extradural arachnoid cysts are primarily treated with total removal of the cyst wall and closure of the dural defect. Surgical treatment is curative for this rare lesion.

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.

Expression of cyclooxygenase-2, matrix metalloproteinase-2 and matrix metalloproteinase-9 in premenopausal and postmenopausal endometrial polyps.

OBJECTIVES Cyclooxygenase-2 (COX-2) and matrix metalloproteinase-2 and -9 (MMP-2 and MMP-9) are influenced by relative levels of estrogen and are involved in promoting cell proliferation and angiogenesis. The present study investigated expression of COX-2, MMP-2 and MMP-9 in endometrial polyps from premenopausal and postmenopausal women. METHODS Premenopausal (n=18) and postmenopausal (n=22) endometrial polyps were included in the study. None of the women were using non-steroid anti-inflammatory drugs, hormone replacement therapy or any other estrogen containing pills. Immunohistochemical analysis for MMP-2, MMP-9 and COX-2 were performed on formalin fixed, paraffin-embedded tissue using the streptavidin-biotin-peroxidase technique. The cut-off value for positiviy was set to 10% and staining more than 50% was regarded as intense staining. Staining of 10-25% and 25-50% were recorded as mild and moderate, respectively. RESULTS COX-2, MMP-2 and MMP-9 were stained in epithelial cells and stroma of premenopausal and postmenopausal endometrial polyps. Stromal expression of COX-2, MMP-2 and MMP-9 were found significantly higher in premenopausal polyps compared to postmenopausal polyps (p<0.05). There were no other significant differences in the immunohistochemical expressions in the epithelium of premenopausal and postmenopausal endometrial polyps except MMP-9. CONCLUSION Polyps from both premenopausal and postmenopausal women express epithelial and stromal COX-2, MMP-2 and MMP-9, however immunohistochemical expression of these markers may be different due to menopausal status. This may suggest a shared pathogenesis for pre- and postmenopausal endometrial polyps.