Cone-beam CT versus Multidetector CT in Postoperative Cochlear Implant Imaging: Evaluation of Image Quality and Radiation Dose.

BACKGROUND AND PURPOSE: Cone-beam CT is being increasingly used in head and neck imaging. We compared cone-beam CT with multidetector CT to assess postoperative implant placement and delineate finer anatomic structures, image quality, and radiation dose used. MATERIALS AND METHODS: This retrospective multicenter study included 51 patients with cochlear implants and postoperative imaging via temporal bone cone-beam CT (n = 32 ears) or multidetector CT (n = 19 ears) between 2012 and 2017. We evaluated the visualization quality of single electrode contacts, the scalar position of the electrodes, cochlear walls, mastoid facial canal, metallic artifacts (using a 4-level visual score), and the ability to measure the insertion angle of the electrodes. The signal-to-noise ratio and radiation dose were also evaluated. RESULTS: Cone-beam CT was more sensitive for visualizing the scalar position of the electrodes (P = .046), cochlear outer wall (P = .001), single electrode contacts (P < .001), and osseous spiral lamina (P = .004) and had fewer metallic artifacts (P < .001). However, there were no significant differences between both methods in visualization of the modiolus (P = .37), cochlear inner wall (P > .99), and mastoid facial canal wall (P = .07) and the ability to measure the insertion angle of the electrodes (P > .99). The conebeam CT group had significantly lower dose-length product (P < .001), but multidetector CT showed a higher signal-to-noise ratio in both bone and air (P = .22 and P = .001). CONCLUSIONS: Cone-beam CT in patients with cochlear implants provides images with higher spatial resolution and fewer metallic artifacts than multidetector CT at a relatively lower radiation dose.

Ottelione A inhibited proliferation of Ehrlich ascites carcinoma cells in mice.

While the main target of chemotherapy in cancer treatment is the induction of apoptosis and cell death, natural products provide a wealth to medicine and are considered great sources of new drugs for cancer treatment. We aimed to determine the antitumor effect of ottelione A (OTTE) on the growth and proliferation of Ehrlich ascites carcinoma cells (EACs) implanted i.p. in female mice. Animals were inoculated with EAC cells to serve as the control group. In the OTTE group, animals were implanted with EAC followed by i.p. administration of OTTE. Antitumor activity was evaluated 15days after tumor implantation. The administration of OTTE significantly reduced ascetic volume, viability of EAC cells and increased the survival of tumor-bearing animals. Flow cytometric analysis indicated that OTTE induced G(0)/G(1) cell cycle arrest and apoptosis. These findings were associated with an alteration of redox state of EAC cells, which might impact cascade effects leading to cell cycle arrest at G(0)/G(1) phase. These effects include a decreased expression of cyclin D1, increased p53 expression and down-regulation of rRNA level, stimulation of CD8+ infiltrating T-lymphocytes. In addition, OTTE normalized oxidative stress in the liver of mice-bearing EAC cells evidenced by increased the levels of glutathione, superoxide dismutase, and catalase. In conclusion, the differential expression of p53, cyclin D1, and rRNA in EAC cells as well as the infiltration of CD8+ after OTTE treatment may play critical roles in the G(0)/G(1) cell cycle arrest that blocks cell proliferation and induce apoptosis of cancer cells. The potent antitumor property of the ottelione A can be exploited further to develop therapeutic protocols for treatment of cancer.

Role of melatonin in ameliorating lead induced haematotoxicity.

Owing to the risks of heavy metals-induced severe haematopoietic disorders, it is important to investigate these chemicals for their haematotoxicity and the possible ways to ameliorate their toxicity. The effects of melatonin on lead-induced haematotoxicity have, therefore, been examined in rat blood and bone marrow. When adult male rats were injected intramuscularly with lead acetate (10 mg kg(-1)) daily for 7 days, the erthrocytic count, haematocrite value and haemoglobin content were significantly decreased. The counts of platelets, total leucocytes and lymphocytes in the peripheral blood were also significantly lower in lead-treated rats than in control animals. The total granulocyte count was significantly elevated in the peripheral blood of the same lead-treated rats. Significant decreases in polychromatic and pyknotic erythroid series as well as lymphocytes in bone marrow of the lead-intoxicated rats were also demonstrated. Meanwhile, the neutrophiles were increased in the same treated rats. The erythropoietin level was significantly decreased and the lead concentration was increased in the plasma of the lead-treated rats compared with the control rats. Bone marrow examination of the rats treated with lead for 7 days showed erythroid hyperplasia with a sign of dyserythropoiesis and demonstrated ringed sideroblasts in varying proportions. Daily pretreatment with melatonin (30 mg kg(-1)) intragastricaly, concurrently with lead injection for 7 days significantly prevented the changes recorded in the peripheral blood parameters. The changes observed in the bone marrow polychromatic erythroid, lymphocytes and the neutrophiles were significantly ameliorated by coadministration of melatonin and lead compared with lead-treated rats, while the pyknotic erythroid series was still significantly low. The levels of erythropoietin and lead in plasma were not changed in melatonin+lead-treated group compared with lead only treated rats. In addition, melatonin administration ameliorated the decrease in erythroid cell count in bone marrow. Less dyserythropoiesis and megaloblastic changes were observed in bone marrow film when melatonin was concurrently administered with lead. In the same animals, iron staining of the bone marrow cells showed absence of ringed sideroblasts. In conclusion, the present results indicate that melatonin has the ability to protect the haematopoietic cells from the damaging effects of exposure to lead. This protection might be attributed to the antioxidative power of melatonin.

L-Arginine ameliorates oxidative stress in alloxan-induced experimental diabetes mellitus.

Oxidative stress occurs in diabetic patients and experimental models of diabetes. The ability of l-arginine to ameliorate the oxidative stress and metabolic changes after treatment with alloxan was investigated in rats. Adult male rats were injected intraperitoneally with 100 mg kg(-1) of alloxan to produce experimental oxidative stress characteristic of diabetes mellitus. Hyperglycaemia and hypercholesterolaemia were observed in serum after 7 days of alloxan treatment. This was associated with a depression of glutathione (GSH) concentration as well as superoxide dismutase (SOD) and catalase (CAT) activities in the liver and brain. In addition, the thiobarbituric acid-reactive substances (TBARS) were significantly elevated, indicating increased lipid peroxidation and oxidative stress in the same tissues. Administration of 100 mg kg(-1) l-arginine for 7 days either before or after alloxan injection significantly ameliorated the oxidative stress evidenced by a lower TBARS and a higher level of the endogenous GSH concentration and SOD and CAT activities than alloxan-treated rats. These effects were paralleled by marked protection and partial prophylaxis against alloxan-induced hyperglycaemia and cholesterolaemia. Thus, these results showed that exogenously administered l-arginine might improve the clinical manifestation of diabetes mellitus and decrease the oxidative stress in the liver and brain. In addition, the study supports the beneficial effect of l-arginine, which might be attributed to its direct, NO-dependent antioxidant capacity and/or NO-independent pathways.

Protection by metal complexes with SOD-mimetic activity against oxidative gastric injury induced by indomethacin and ethanol in rats.

We have investigated the protective effect of oral administration of copper and manganese complexes with superoxide dismutase (SOD)-mimetic activity against oxidative gastric mucosal injury induced by the non-steroidal anti-inflammatory drug indometacin with ethanol in the rat. The total area of the gastric lesions and lipid peroxidation were significantly increased 1 h after oral administration of indometacin (15 mg/kg) and ethanol, indicating an acute oxidative injury. The activities of SOD, catalase (CAT), glutathione-S-transferase (GST) and glutathione content were significantly decreased in the gastric mucosa by indometacin plus ethanol. Manganese or copper complexes showed SOD-mimetic activity. Pretreatment with these complexes protected against gastric mucosal lesions and decreased lipid peroxides, as well as attenuating the decrease in the activities of SOD, CAT and GST in gastric mucosa. These findings suggest that active oxygen species and lipid peroxidation play an important role in the pathogenesis of gastric mucosal injury induced by indometacin. In addition, we have shown that Mn and Cu complexes have gastroprotective properties against ulceration induced by indometacin plus ethanol. The present results suggest that appropriate copper or manganese complex supplementation may potentially provide prophylaxis or therapy for some pathologies associated with excessive free radical production and inhibited SOD activity.

Potential protective role of angiotensin-converting enzyme inhibitors captopril and enalapril against adriamycin-induced acute cardiac and hepatic toxicity in rats.

Captopril and enalapril-angiotensin-converting enzyme (ACE) inhibitors-were evaluated for their antioxidative protective action against adriamycin-induced cardiac and hepatic toxicity. Rats were treated with either captopril (10 mg kg(-1)) or enalapril (2 mg kg(-1)) intragastrically (i.g.) daily for 7 days before single intraperitoneal (i.p.) injection with adriamycin (15 mg kg(-1)). The animals were killed 30 h after adriamycin administration. Adriamycin produced significant elevation in thiobarbituric acid reactive substances (TBARS), which is an indicator of lipid peroxidation, and significantly inhibited the activity of superoxide dismutase (SOD) in heart and liver tissues, with a significant rise in the serum levels of glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase isoenzyme (CK-MB) and lactic dehydrogenase (LDH), indicating acute cardiac toxicity. A single injection of adriamycin did not affect the cardiac or hepatic glutathione (GSH) content or cardiac catalase (CAT) activity, but hepatic CAT activity was elevated. Pretreatment with ACE inhibitors significantly reduced the TBARS concentration in both heart and liver and ameliorated the inhibition of cardiac and hepatic SOD activity. In addition, the ACE inhibitors significantly improved the serum levels of GOT, GPT, CK-MB and LDH in adriamycin-treated rats. Thus, these results suggest that captopril and enalapril possess antioxidative potential that may protect the heart against adriamycin-induced acute oxidative toxicity. This protective effect might be mediated, at least in part, by the limitation of culprit free radicals and the amelioration of oxidative stress.

The protective action of melatonin on indomethacin-induced gastric and testicular oxidative stress in rats.

Reactive oxygen species and lipid peroxidation play a role in the pathogenesis induced by the non-steroidal anti-inflammatory drug indomethacin. Melatonin (MLT) protection against indomethacin-induced oxidative tissue injury was investigated in gastric mucosa and testis of rats. MLT was administered intragastrically (i.g.) 30 min before the administration to fasted rats of 20 mg indomethacin/kg rat given i.g.. The area of gastric lesion as well as thiobarbituric acid reactive substances (TBARS) and lactate dehydrogenase (LDH) activity were found to be significantly increased 4 h after administration of indomethacin in rat gastric mucosa and testis indicating acute oxidative injury. MLT pretreatment reduced gastric lesion area to 80% of the indomethacin-treated rats and reduced the rise in TBARS concentration. MLT treatment reduced the LDH activity increase in testis but not in gastric mucosa. In indomethacin-treated rats, both the cytosolic Cu,Zn superoxide dismutase (Cu,Zn-SOD) and mitochondrial Mn-SOD activities were significantly diminished in gastric mucosa as well as the total SOD activity in testis. In addition, glutathione (GSH) content in both tissues was markedly decreased following indomethacin treatment. Pretreatment with MLT significantly ameliorated both the inhibition of SOD activity and the decreased GSH content in both tissues. Thus, these results show the effective antiperoxidative and preventive actions of MLT against indomethacin-induced gastric mucosal damage and testicular oxidative injury and we propose that this action might be relevant for its use with other free radical generating drugs.

Attenuation of the acute adriamycin-induced cardiac and hepatic oxidative toxicity by N-(2-mercaptopropionyl) glycine in rats.

The protective effect of the synthetic aminothiol, N-(2-mercaptopropionyl) glycine (MPG) on adriamycin (ADR) induced acute cardiac and hepatic oxidative toxicity was evaluated in rats. ADR toxicity, induced by a single intraperitoneal injection (15 mg/kg), was indicated by an elevation in the level of serum glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase isoenzyme (CK-MB), and lactic dehydrogenase (LDH). ADR produced significant elevation in thiobarbituric acid reactive substances (TBARS), indicating lipid peroxidation, and significantly inhibited the activity of superoxide dismutase (SOD) in heart and liver tissues. In contrast, a single injection of ADR did not affect the cardiac or hepatic glutathione (GSH) content and cardiac catalase (CAT) activity but elevated hepatic CAT. Pretreatment with MPG, (2.5 mg/kg) intragastrically, significantly reduced TBARS concentration in both heart and liver and ameliorated the inhibition of cardiac and hepatic SOD activity. In addition, MPG significantly decreased the serum level of GOT, GPT, CK-MB, and LDH of ADR treated rats. These results suggest that MPG exhibited antioxidative potentials that may protect heart and liver against ADR-induced acute oxidative toxicity. This protective effect might be mediated, at least in part, by the high redox potential of sulfhydryl groups that limit the activity of free radicals generated by ADR.

Role of selenium against lead toxicity in male rats.

Male albino rats were intramuscularly administered a single dose of lead acetate (100 micromol/kg b.wt). Another group of rats were injected with sodium selenite (10 micromol/kg b.wt) before lead intoxication. After 3 and 24 hours, lead treatment resulted in significant increases in acid and alkaline phosphatases, GOT and GPT, total proteins, and cholesterol in serum. The total triglycerides in serum was decreased after 24 hours of intoxication. Lead treatment also produced significant elevation of lipid peroxidation in liver and kidney. The antioxidant capacity of hepatic and renal cells in terms of the activities of superoxide dismutase, glutathione reductase, and glutathione content was diminished. It appears from these results that lead may exert its toxic effect via peroxidative damage to renal and hepatic cell membranes after 24 hours. Selenium administration prior to lead injection produced pronounced prophylactic action against lead effects, and it is observed that selenium enhances the endogenous antioxidant capacity of the cells by increasing the activities of the superoxide dismutase and glutathione reductase and the glutathione content. As a result, the lipid peroxidation was decreased in both liver and kidney.