The protective effect of erythropoietin on ischemia- reperfusion injury caused by ovarian torsion-detorsion in the experimental rat model.

Ovarian torsion is one of the most dangerous gynecological emergencies requiring surgery. A total of 50%-90% ovarian torsion cases are caused by physiological cysts, endometriosis, and other benign or malignant ovarian neoplasms. The aim of the study was to investigate the effects of erythropoietin (EPO) treatment on ischemia/reperfusion (IR) injury caused by ovarian torsion/detorsion (T/D) injury. Thirty female Wistar albino rats were divided into five groups as follows: Group I: Control; Group II: Torsion (T); Group III: Torsion/Detorsion(T/D); Group IV: Torsion/Detorsion (T/D) + EPO; Group V: EPO. Sections of the ovaries were evaluated for histopathological changes with hematoxylin and eosin stain, a immunohistochemical assay for caspase 3 expression, and the TUNEL assay for apoptosis. Ovarian sections from torsion/detorsion and torsion groups showed more hemorrhage, vascular congestion, edema, degenerative granulosa, and stromal cells. Fewer histopathological changes were found in EPO and T/D + EPO groups. Caspase 3 and TUNEL positive cells were significantly increased in the torsion/detorsion group as compared with the other groups (p < 0.05). Treatment with erythropoietin decreased the number of caspase 3 and TUNEL positive cells. The results of the study showed that erythropoietin administration is effective for recovery from degenerative changes in the ovary induced by the torsion-detorsion injury.

Protective effect of dipeptidyl peptidase-4 inhibitors in testicular torsion/detorsion in rats: a possible role of HIF-1α and nitric oxide.

Spermatic cord torsion is a serious and common urologic emergency. It requires early diagnosis for prevention of subfertility and testicular necrosis. Vildagliptin and sitagliptin are anti-diabetic drugs of the dipeptidyl peptidase-4 (DPP-4) inhibitors that have a protective role against cerebral ischemic stroke and cardiac ischemia reperfusion. This study aimed to investigate the role and mechanism of action of vildagliptin and sitagliptin in a model of testicular ischemia/reperfusion injury by testicular torsion/detorsion (T/D). Testicular T/D was done and vildagliptin and sitagliptin were administered either alone or in combination with nitric oxide synthase (NOS) inhibitor. Serum total cholesterol and testosterone were measured, while in testicular tissue testosterone, malondialdehyde (MDA) level, total antioxidant capacity (TAC), nitric oxide level, caspase-3, superoxide dismutase (SOD), hypoxia-inducible factor-1α (HIF-1α), tumor necrosis factor-α (TNF-α) and endothelial NOS (eNOS), and inducible NOS (iNOS) and neuronal NOS (nNOS) were measured. Histopathology of testicular tissue was done. Vildagliptin and sitagliptin increased serum testosterone, expression, and activity of SOD and testicular TAC. It also reduced total serum cholesterol, testicular MDA, caspase-3, HIF-1α, TNF-α, and expression of eNOS, iNOS, and nNOS. Vildagliptin and sitagliptin also improved histopathological picture of testicular tissue. NOS inhibitor produced similar result to DDP-4 inhibitors; however, its co-administration augmented the effect of vildagliptin and sitagliptin on these parameters. DPP-4 inhibitors, vildagliptin, and sitagliptin were protective against testicular T/D-induced injury mostly by anti-oxidative stress, and anti-apoptotic and anti-inflammatory actions that was augmented by NOS inhibition with a possible role for HIF-1α expression.

Left Ventricular Twist Is Augmented in Hypoxia by ß1-Adrenergic-Dependent and ß1-Adrenergic-Independent Factors, Without Evidence of Endocardial Dysfunction.

BACKGROUND: Left ventricular (LV) twist mechanics are augmented with both acute and chronic hypoxemia. Although the underlying mechanisms remain unknown, sympathetic activation and a direct effect of hypoxemia on the myocardium have been proposed, the latter of which may produce subendocardial dysfunction that is masked by larger subepicardial torque. This study therefore sought to (1) determine the individual and combined influences of ß1-AR (ß1-adrenergic receptor) stimulation and peripheral O2 saturation (Spo2) on LV twist in acute and chronic hypoxia and (2) elucidate whether endocardial versus epicardial mechanics respond differently to hypoxia. METHODS: Twelve males (27±4 years) were tested near sea level in acute hypoxia (Spo2=82±4%) and following 3 to 6 days at 5050 m (high altitude; Spo2=83±3%). In both settings, participants received infusions of ß1-AR blocker esmolol and volume-matched saline (double-blind, randomized). LV mechanics were assessed with 2-dimensional speckle-tracking echocardiography, and region-specific analysis to compare subendocardial and subepicardial mechanics. RESULTS: At sea level, compared with baseline (14.8±3.0°) LV twist was reduced with esmolol (11.2±3.3°; P=0.007) and augmented during hypoxia (19.6±4.9°; P<0.001), whereas esmolol+hypoxia augmented twist compared with esmolol alone (16.5±3.3°; P<0.001). At 5050 m, LV twist was increased compared with sea level (19.5±5.4°; P=0.004), and reduced with esmolol (13.0±3.8°; P<0.001) and Spo2 normalization (12.8±3.4°; P<0.001). Moreover, esmolol+normalized Spo2 lowered twist further than esmolol alone (10.5±3.1°; P=0.036). There was no mechanics-derived evidence of endocardial dysfunction with hypoxia at sea level or high altitude. CONCLUSIONS: These findings suggest LV twist is augmented in hypoxia via ß1-AR-dependent and ß1-AR-independent mechanisms (eg, α1-AR stimulation), but does not appear to reflect endocardial dysfunction.

The Protective Effects of Pulsed Magnetic Field and Melatonin on Testis Torsion and Detorsion Induced Rats Indicated by Scintigraphy, Positron Emission Tomography/Computed Tomography and Histopathological Methods.

PURPOSE: The aim of the present study was to show the protective effect of pulsed magnetic field (PMF) application and melatonin administration on damage in testis in a one-sided torsion detorsion induced rat model using testicular scintigraphy with 99mTc pertechnetate, PET/CT with 18F-FDG and histopathological methods. MATERIALS AND METHODS: Sixty male rats were used in the study; 30 rats were randomly divided into five groups for one day applications of sham control, torsion, melatonin, pulsed magnetic field (PMF) and melatonin plus PMF. Similarly, for one week group, the other 30 rats were divided into the same five group (n=6), but the animals were sacrificed after one week. Rats were exposed to 50 Hz, 1 mT PMF for two hours. PET/CT with 37 MBq 18F-FDG and testicular scintigraphy with and 37 MBq 99mTc pertechnetate examinations were carried out, and testicular tissue was examined using histopathological methods.  Results: In one day treatment, melatonin administration significantly increased perfusion and glucose metabolism compared to torsion group (p<0.01). Perfusion and glucose metabolism was also higher in the PMF and melatonin plus PMF groups than torsion group (p<0.01). In one week treatment, melatonin administration resulted in a significant higher perfusion rate and glucose metabolism rate compared to torsion group (p<0.01 and p<0.001, respectively). In addition, perfusion and glucose metabolism significantly increased in PMF and melatonin plus PMF groups compared to torsion group (p<0.01 and p<0.001, respectively). Furthermore, caspase-3 immunoreactivity and pathological changes increased in the torsion group (p<0.05). Melatonin and melatonin plus PMF treatment reduced the rate of immunoreactivity and pathological findings compared to the torsion group (p<0.05). CONCLUSION: According to these results it can be concluded that PMF application had a therapeutic benefit as effective as melatonin administering. In addition, it was indicated that PET/CT with 18F-FDG and testicular scintigraphy with 99mTc pertechnetate could be efficiently used in determining the treatment efficiency in testicular torsion.

Effects of Carnosine and Vitamin E on Nucleobindin 2 (NUCB2)/nesfatin-1, Ghrelin, Adropin, and Irisin in Experimentally Induced Ovarian Torsion.

INTRODUCTION: Delay in the diagnosis of ovarian torsion leads to serious histopathological changes and many problems, including infertility. Various agents have been investigated to minimize detorsion-associated potential injury. This study was performed to study the effects of carnosine and vitamin E on tissue and serum expression of Nucleobindin 2 (NUCB2)/nesfatin-1, ghrelin, adropin, and irisin to determine whether they have protective effects in cases of ovarian torsion. MATERIAL AND METHOD: Seventy-eight rats were allocated evenly into 13 groups. All rats, excluding those in the control and sham groups and Groups (G) III, IV, and V, were subjected to ovarian torsion for 12 hours. The groups were designated as follows: G-I (control), G-II (sham), G-III (vitamin E), G-IV (carnosine), G-V (carnosine + vitamin E), G-VI (torsion), G-VII (torsion + detorsion), G-VIII (torsion + vitamin E), G-IX (torsion + carnosine), G-X (torsion + carnosine + vitamin E), G-XI (torsion + detorsion + vitamin E), G-XII (torsion + detorsion + carnosine), and G-XIII (torsion + detorsion + carnosine + vitamin E). Serum levels of NUCB2/nesfatin-1, ghrelin, adropin, and irisin were measured by ELISA. Immunohistochemical methods were used to measure the expression of these hormones in ovarian tissue. RESULTS: The levels of NUCB2/nesfatin-1 immunoreactivity were increased in G-VII, G-XI, and G-XII (p<0.05). The immunoreactivity of ghrelin was significantly decreased in G-VI, G-IX, G-XI, and G-XII. However, adropin immunoreactivity did not differ significantly between the groups (p>0.05). The level of irisin immunoreactivity was decreased in G-VI, G-VII, and G-VIII (p<0.05). The serum levels of NUCB2/nesfatin-1, ghrelin, adropin, and irisin paralleled the tissue immunohistochemical results. CONCLUSION: Carnosine and vitamin E protected the ovaries from ischemia-reperfusion injury in ovarian torsion. These antioxidants, especially carnosine, may be useful for the treatment of ovarian torsion.

Protective effect of hydrogen rich saline solution on experimental ovarian ischemia reperfusion model in rats.

BACKGROUND: The present study aimed to investigate the effects of hydrogen rich saline solution (HRSS) in a rat model of ovarian ischemia-reperfusion injury. METHODS: Thirty-six female Wistar-albino rats were grouped randomly, into six groups of six rats. The groups were classified as: sham (S), hydrogen (H), torsion (T), torsion/detorsion (TD), hydrogen-torsion (HT), and hydrogen-torsion/detorsion (HTD). Bilateral adnexal torsion was performed for 3h in all torsion groups. HRSS was given 5ml/kg in hydrogen groups intraperitoneally. Malondialdehyde (MDA) and glutathione-S-transferase (GST) levels were measured in both the plasma and tissue samples. Tissue sections were evaluated histopathologically, and the apoptotic index was detected by TUNEL assay. The results were analyzed by Kruskal-Wallis and Pearson chi-square tests using computer software, SPSS Version 20.0 for Windows. RESULTS: The MDA levels were higher and GST levels were lower in the torsion and detorsion groups when compared to other groups, but the differences were insignificant (P>0.05). The MDA levels were lower and GST levels were higher in the HT and HTD groups compared with the T and TD groups (P>0.05). Follicular injury, edema, vascular congestion, loss of cohesion and apoptotic index were higher in the torsion groups but decreased in the groups that received HRSS. CONCLUSIONS: According to histopathological and biochemical examinations, HRSS is effective in attenuating ischemia-reperfusion induced ovary injury.

Protective effects of ellagic acid and ozone on rat ovaries with an ischemia/reperfusion injury.

AIM: This study investigated the effects of the antioxidant agents, ozone (O) and ellagic acid (EA), on ischemia/reperfusion (I/R) injuries developed from an ovarian torsion-detorsion model. MATERIALS AND METHODS: Arteries in the left ovaries of rats were clamped for two hours to achieve torsion, and then the clamps were removed for a two-hour detorsion period. Thirty-five female Sprague-Dawley rats were randomly divided into five groups: control: administered only with anesthesia, rats were not subjected to torsion-detorsion; I/R: subjected to torsion and subsequent detorsion, without administering any treatment agent; and I/R + EA, I/R + O and I/R + O + EA: subjected to torsion and detorsion processes and administered with EA, O or EA + O at the 75th minute of torsion. The rats were then sacrificed under general anesthesia and the ovarian tissues were excised. The tissues were homogenized and levels of glutathione reductase, catalase, superoxide dismutase and malondialdehyde (MDA) were analyzed. Tissue damage was evaluated in terms of histopathological parameters, such as hemorrhage, congestion, edema and inflammation. RESULTS: Antioxidant enzyme activity and MDA levels in the ovary tissue increased in the I/R group and decreased in the O, EA and O + EA groups (P < 0.05). Histopathological examination revealed that tissue damage in the O, EA and O + EA groups decreased in comparison with the I/R group (P < 0.05). CONCLUSIONS: These biochemical and histopathological findings suggest that EA and O are effective against ovarian I/R injury.

Protective effect of colchicine on ovarian ischemia-reperfusion injury: an experimental study.

OBJECTIVE: The aim of the present study is to investigate the efficiency of colchicine in the experimental rat ovarian torsion model in the light of histological and biochemical data. STUDY DESIGN: A total of 35 Wistar albino female rats were randomly divided into 5 groups, group 1: (control-sham operated, n = 7); group 2: (torsion/detorsion, n = 7) 2 hours of ischemia and 2 hours of reperfusion; group 3: (torsion/detorsion, n = 7), 2 hours of ischemia and 5 days of reperfusion; group 4: (torsion/detorsion, n = 7) 2 hours of ischemia and 2 hours of reperfusion and a signal dose of oral 1 mL/kg colchicine; and group 5: (torsion/detorsion, n = 7), 2 hours of ischemia and 5 days of reperfusion and 5 days of oral 1 mg/kg colchicine. Histopathologic evaluation was performed by a scoring that assesses congestion, bleeding, edema, and cellular degeneration in the ovarian tissue. Catalase, tissue malondialdehyde (MDA), and protein carbonyl levels were calculated. RESULTS: The histopathologic scores, MDA, and protein carbonyl levels in the control and colchicine groups were significantly lower than groups 2 and 3 (P < .001). Catalase activities were significantly higher in the control and colchicine groups than in groups 2 and 3 (P < .001). The results of the histopathologic parameters and biochemical markers showed that protective effects of colchicine treatment persisted up to 5 days. CONCLUSION: Our study results revealed that colchicine reduced ovarian ischemia-reperfusion injury in experimental rat ovarian torsion model. As the ovarian detorsion is the first choice of the treatment modality in the early phase, antioxidant and anti-inflammatory treatment modalities like colchicine might be used to reduce ovarian ischemia-reperfusion injury.

Vitamin E modulates apoptosis and c-jun N-terminal kinase activation in ovarian torsion-detorsion injury.

The aim of this study was to evaluate the role of vitamin E in follicular degeneration and to assess histopathological and biochemical changes following ischemia-reperfusion (IR) injury in rat ovaries. Twenty-eight Wistar albino rats were randomly divided into four groups: sham, 4h torsion, 24h detorsion, and a vitamin E group. Thirty minutes before detorsion, a single dose of 200mg/kg vitamin E was administered intraperitoneally. The ovarian histology score was determined, serum levels of malondialdehyde (MDA) and myeloperoxidase (MPO) were measured. The apoptosis of granulosa cells and the phospho-c-jun N-terminal kinase (p-JNK) and phospho-p38 (p-p38) immunoreactivities of these cells were determined. MDA and MPO levels were significantly increased in the torsion and detorsion groups. Hemorrhage, edema, and congestion were also apparent in these groups. In addition, the apoptotic index and the immunoreactivity of p-JNK were highest in the detorsion group, which also showed marked follicular degeneration. However, p-p38 activity was not affected by torsion-detorsion (TD) induction. Vitamin E ameliorated TD-induced histological alterations. It also decreased serum levels of MDA and MPO, reduced the activity of p-JNK in the ovaries, and reduced numbers of apoptotic follicular cells. In conclusion, these data indicate that vitamin E attenuated ovarian follicular degeneration by inhibiting the immunoreactivity of p-JNK and reducing the apoptosis of granulosa cells.

Expression of anti-Mullerian hormone receptor on the appendix testis in connection with urological disorders.

The female internal sex organs develop from the paramesonephric (Mullerian) duct. In male embryos, the regression of the Mullerian duct is caused by the anti-Mullerian hormone (AMH), which plays an important role in the process of testicular descent. The physiological remnant of the Mullerian duct in males is the appendix testis (AT). In our previous study, we presented evidence for the decreased incidence of AT in cryptorchidism with intraoperative surgery. In this report, the expression of the anti-Mullerian hormone receptor type 2 (AMHR2), the specific receptor of AMH, on the AT was investigated in connection with different urological disorders, such as hernia inguinalis, torsion of AT, cysta epididymis, varicocele, hydrocele testis and various forms of undescended testis. The correlation between the age of the patients and the expression of the AMHR2 was also examined. Reverse transcriptase-polymerase chain reaction (RT-PCR) and immunohistochemistry were used to detect the receptor's mRNA and protein levels, respectively. We demonstrate that AMHR2 is expressed in the ATs. Additionally, the presence of this receptor was proven at the mRNA and protein levels. The expression pattern of the receptor correlated with neither the examined urological disorders nor the age of the patients; therefore, the function of the AT remains obscure.

Ovarian cystic tumor composed of Brenner tumor and struma ovarii.

Ovarian tumor composed only of Brenner tumor and struma ovarii is very rare; only 6 cases have been reported in the English literature, to the best of the author's knowledge. A 66-year-old woman underwent right oophorectomy because of torsion of right ovarian cyst. Macroscopically, the ovarian cyst was hemorrhagic and red. Cystic content was hemorrhagic fluid. Microscopically, the cyst walls were composed only of Brenner tumor (50% in area) and struma ovarii (50% in area). Hemorrhage and ischemic changes were seen. Other elements were not recognized. No malignant transformation was noted. These two elements were separately present, and no mergers between them were recognized. Immunohistochemically, the Brenner tumor element was positive for cytokeratins (AE1/3 and CAM5.2) and Ki67 (labeling=3%), but negative for thyroglobulin, TTF-1, p53, CA125, and vimentin. The struma ovarii element was positive for cytokeratins (AE1/3 and CAM5.2), thyroglobulin, TTF-1 and Ki67 (labeling=5%), but negative for p53, CA125 and vimentin. The findings suggests that there were cases of ovarian cyst composed only of Brenner tumor and struma ovarii, that such a case may be monodermal mature cystic teratoma or the Brenner tumor element was derived from surface epithelium in the preexisting struma ovarii, and that such a tumor manifest as cystic torsion.

Clinical, hematological, and biochemical findings of uterine torsion in buffaloes (Bubalus bubalis).

The aim of this study was to investigate uterine torsion in buffaloes, examine factors influencing the outcome of the disease, and to characterize the related alterations in blood constituents. A total of 126 buffaloes with uterine torsion were examined for stage of gestation, duration, degree, site and direction of torsion, as well as the location of the pregnant horn. Methods of correction were documented along with dam and calf survival. Blood samples were obtained from 20 buffaloes with uterine torsion and 10 healthy buffaloes for hematological and biochemical comparisons. Results showed that uterine torsion in buffaloes occurred in multi- (81.7%) and primiparous (18.3%), during late pregnancy (58.4%) and at full term (41.6%), clockwise (96%) and counter- clockwise (4%), at post- (98.4%) and precervical (1.6%), and was of high (52.3%), moderate (31%) and mild (16.7%) degrees. Torsion was predominantly (P=0.01) on same direction of the pregnant horn. Fetal and maternal mortalities occurred in 78.6% and 23.8% of the cases, respectively. The stage of pregnancy, and degree and duration of uterine torsion were major risk factors for fetal mortality (P=0.0001), while the stage of pregnancy and fetal viability were important risk factors for maternal mortality (P<0.05). There were significant (P<0.05) increases in monocytes, albumin, aspartate aminotransferase, creatine phosphokinase, blood urea nitrogen, and phosphorus and decreases in mean corpuscular hemoglobin concentration and globulin in the affected buffaloes. Time of occurrence and duration of torsion affected some of these parameters. Uterine torsion appears to be a serious problem in buffaloes that has certain peculiarities including time of occurrence, site and direction of torsion, and the high mortality rates. Uterine torsion adversely affects liver and kidney functions. Multiparous might be at greater risk of uterine torsion. The stage of pregnancy, as well as degree and duration of uterine torsion are risk factors for fetal and maternal mortalities.

Chymase inhibition prevents fibronectin and myofibrillar loss and improves cardiomyocyte function and LV torsion angle in dogs with isolated mitral regurgitation.

BACKGROUND: The left ventricular (LV) dilatation of isolated mitral regurgitation (MR) is associated with an increase in chymase and a decrease in interstitial collagen and extracellular matrix. In addition to profibrotic effects, chymase has significant antifibrotic actions because it activates matrix metalloproteinases and kallikrein and degrades fibronectin. Thus, we hypothesize that chymase inhibitor (CI) will attenuate extracellular matrix loss and LV remodeling in MR. METHODS AND RESULTS: We studied dogs with 4 months of untreated MR (MR; n=9) or MR treated with CI (MR+CI; n=8). Cine MRI demonstrated a >40% increase in LV end-diastolic volume in both groups, consistent with a failure of CI to improve a 25% decrease in interstitial collagen in MR. However, LV cardiomyocyte fractional shortening was decreased in MR versus normal dogs (3.71±0.24% versus 4.81±0.31%; P<0.05) and normalized in MR+CI dogs (4.85±0.44%). MRI with tissue tagging demonstrated an increase in LV torsion angle in MR+CI versus MR dogs. CI normalized the significant decrease in fibronectin and FAK phosphorylation and prevented cardiomyocyte myofibrillar degeneration in MR dogs. In addition, total titin and its stiffer isoform were increased in the LV epicardium and paralleled the changes in fibronectin and FAK phosphorylation in MR+CI dogs. CONCLUSIONS: These results suggest that chymase disrupts cell surface-fibronectin connections and FAK phosphorylation that can adversely affect cardiomyocyte myofibrillar structure and function. The greater effect of CI on epicardial versus endocardial titin and noncollagen cell surface proteins may be responsible for the increase in torsion angle in chronic MR.

Attenuation of ischemia-reperfusion injury with Marrubium cordatum treatment in ovarian torsion-detorsion model in rabbits.

OBJECTIVE: To investigate protective effects of Marrubium cordatum extract on ovary torsion-detorsion. DESIGN: Controlled research study. SETTING: Marrubium cordatum extract was obtained by methanol extraction. ANIMAL(S): Six-month-old female New Zealand rabbits. INTERVENTION(S): In the first phase, antioxidant activity of M. cordatum extract was evaluated. In the second phase, M. cordatum extract at doses of 0, 250, 500, and 1,000 mg/kg was studied for dose determination. In the third phase, the protective role of M. cordatum on ovarian torsion-detorsion injury was evaluated in sham control, torsion-detorsion, torsion-detorsion +M. cordatum (1,000 mg/kg). MAIN OUTCOME MEASURE(S): 1,1-Diphenyl-2-picrylhydrazyl, nitric oxide radical scavenging activity, reducing power capacity, and total phenolic compounds were assayed. Glutathione, malondialdehyde, catalase, and glutathione peroxidase were measured. Histopathological examination was also conducted. RESULT(S): Marrubium cordatum significantly inhibited 1,1-diphenyl-2-picrylhydrazyl, nitric oxide radicals, and showed a powerful reducing activity. Marrubium cordatum did not adversely affect biochemical and histopathological parameters at all doses. Malondialdehyde level and catalase activity in the torsion-detorsion group were significantly increased compared with those of the sham group, whereas the glutathione level and glutathione peroxidase activity were significantly decreased compared with those of the sham group. Marrubium cordatum treatment significantly lowered the malondialdehyde level and catalase activity but increased the glutathione level in torsion-detorsion injury. Histopathologically, severe congestion, hemorrhage, edema, and leukocyte infiltration were observed in the torsion-detorsion group. Marrubium cordatum treatment ameliorated these alterations. CONCLUSION(S): Marrubium cordatum attenuates ischemia-reperfusion-induced biochemical and histopathological alterations.

Protective effect of erythropoietin on torsion/detorsion injury in rat model.

PURPOSE: The aim of the study is to investigate the effects of erythropoietin on torsion/detorsion injury in rats. METHODS: Forty rats were divided randomly into 5 groups: group I (sham, S), sham operation; group II (torsion/detorsion 1, T/D(1)), 3 hours ischemia and 1 hour reperfusion; group III (torsion/detorsion 2, T/D(2)), 3 hours ischemia and 48 hours reperfusion; group IV (erythropoietin 1, EPO(1)), 3 hours ischemia, 1 hour reperfusion, and a single dose of EPO; and group V (erythropoietin 2, EPO(2)), 3 hours ischemia, 48 hours reperfusion, and 2 doses of EPO. Malondialdehyde (MDA) and nitric oxide (NO) levels and activities of superoxide dismutase and catalase were measured. Tissue damage to ovarian tissue was scored by histologic examination. Data were compared among groups with parametric tests. RESULTS: The MDA levels in the S and EPO groups were significantly lower than the T/D groups (P < .001). Catalase and superoxide dismutase activities, and NO levels in the S and EPO groups were significantly higher than in the T/D groups (P < .05). Ovarian tissue damage in the S and EPO groups was significantly less than in the T/D groups (P < .05). Levels of all biochemical markers and ovarian tissue damage scores were similar among the S, EPO(1), and EPO(2) groups (P > .05). CONCLUSION: Erythropoietin attenuates ischemia-reperfusion injury when given during the acute phase of ovarian torsion-detorsion in a rat model.

Protective effects of amlodipine on ischemia-reperfusion injury of rat ovary: biochemical and histopathologic evaluation.

OBJECTIVE: To evaluate the effects of amlodipine as an antioxidant and analyze the histopathologic changes in experimental ischemic and ischemic-reperfusion (I/R) injury in rat ovaries. DESIGN: Experimental study. SETTING: Experimental surgery laboratory. ANIMAL(S): Forty-two rats with experimentally induced ovarian torsion. INTERVENTION(S): Group 1: sham operation; group 2: bilateral ovarian ischemia; group 3: 3-hour period of ischemia plus 3 hours of reperfusion; groups 4 and 5: amlodipine administration at 3 and 5 mg/kg respectively before one half hour of ischemia, and then bilateral ovarian ischemia. The ovaries were removed at the third hour of ischemia. Groups 6 and 7: 3-hour period of bilateral ovarian ischemia. Two and a half hours after the induction of ischemia, the rats received amlodipine. At the end of a 3-hour period of ischemia, 3 hours of reperfusion was continued; then the ovaries were removed. MAIN OUTCOME MEASURE(S): Ovarian tissue superoxide dismutase and nitric oxide activity; histopathologic examination of all ovarian rat tissue. RESULT(S): Ischemia and I/R increased the inducible nitric oxide synthase activity while decreasing the superoxide dismutase activity significantly in comparison with the sham group. Both doses of amlodipine before ischemia and I/R reversed the trend in nitric oxide synthase activities and reversed the trend in the rat's ovary. CONCLUSION(S): Conservative treatment with amlodipine is effective in reducing tissue damage induced by ischemia, I/R, or both in ovaries.

Intense FDG uptake in the ovary with painless torsion.

We report a case demonstrating intense FDG uptake in the ovary, which was diagnosed to be a hemorrhage and congestion due to painless torsion. An asymptomatic retropelvic mass was detected in a 51-year-old female by echography. FDG-PET demonstrated intense uptake in the mass, thus suggesting an ovarian tumor. A resection of the tumor was performed, and histopathological examination revealed hemorrhage and congestion in the ovary due to ovarian torsion. An ovarian hemorrhage due to painless torsion should be considered in the differential diagnosis of intrapelvic masses demonstrating high FDG uptake, even in asymptomatic patients.

Psoralen cross-linking as probe of torsional tension and topological domain size in vivo.

DNA within a cell is organized with unrestrained torsional tension, and each molecule is divided into multiple individual topological domains. Psoralen photobinding can be used as an assay for supercoiling and topological domain size in living cells. Psoralen photobinds to DNA at a rate nearly linearly proportional to superhelical density. Comparison of the rate of photobinding to supercoiled and relaxed DNA in cells provides a measure of superhelical density. For this, in vivo superhelical tension is relaxed by the introduction of nicks by either ionizing radiation or photolysis of bromodeoxyuridine in the DNA. Since nicks are introduced in a random fashion, the distribution of nicks is described by a Poisson distribution. Thus, after nicking, the fraction of topological domains containing no nicks is described by the zero term of the Poisson distribution. From measurement of the number of nicks introduced in the DNA and the fraction of torsional tension remaining, an average topological domain size can be estimated. Using this logic, procedures were designed and described for measuring supercoiling and domain size at specific sites in eukaryotic genomes.