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Endotoxin treatment protects rats against ozone-induced lung edema: with evidence for the role of manganese superoxide dismutase.
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Ozone is a strong oxidizing agent that can cause lung damage and edema. There is evidence that it does so by causing peroxidation of membrane lipids. However, the elevation in lung activity of copper, zinc superoxide dismutase (Cu, ZnSOD), and manganese superoxide dismutase (MnSOD) during exposure
Suppression of ischemic edema in mice by manganese-hyaluronate conjugate.
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Manganese-hyaluronate conjugate (Mn-HA) was synthesized from a diethylenetriaminepenta-acetic acid derivative of hyaluronic acid and manganese ion. The conjugate markedly scavenged super-oxide anion in vitro and exhibited much higher anti-inflammatory activity than superoxide dismutase in
Pertussis toxin-induced lung edema. Role of manganese superoxide dismutase and protein kinase C.
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The mechanism by which pertussis toxin (Ptx) causes lung edema is not clear. We investigated the role of pulmonary manganese superoxide dismutase (MnSOD) and protein kinase C (PKC) in Ptx-induced lung edema. We demonstrated that intraperitoneal injection of Ptx at a concentration of 5 microg/100 g
Association of manganese superoxide dismutase gene polymorphism (V16A) with diabetic macular edema in Korean type 2 diabetic patients.
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This study was designed to investigate whether V16A polymorphism of the manganese superoxide dismutase (Mn-SOD) gene is associated with the development of type 2 diabetes mellitus and with progression of diabetic retinopathy (DR) and diabetic macular edema (DME). We simultaneously analyzed
Reduced hippocampal manganese-enhanced MRI (MEMRI) signal during pilocarpine-induced status epilepticus: edema or apoptosis?
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Manganese-enhanced MRI (MEMRI) has been considered a surrogate marker of Ca(+2) influx into activated cells and tracer of neuronal active circuits. However, the induction of status epilepticus (SE) by kainic acid does not result in hippocampal MEMRI hypersignal, in spite of its high cell activity.
Anti-inflammatory activity of catalase in carrageenin edema, manganese chloride edema and adjuvant arthritis of rats.
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A novel neurological phenotype in mice lacking mitochondrial manganese superoxide dismutase.
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Reactive oxygen species (ROS) have been implicated in a wide range of degenerative processes including amyotrophic lateral sclerosis, ischemic heart disease, Alzheimer disease, Parkinson disease and aging. ROS are generated by mitochondria as the toxic by-products of oxidative phosphorylation, their
Control of vasogenic edema in a brain tumor model: comparison between dexamethasone and superoxide dismutase.
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OBJECTIVE
The production of prostaglandin (PG) within brain tumors probably generates excessive amounts of oxygen free radicals that may disrupt microvessel permeability within the tumor and in the adjacent brain. We evaluated the effect of systemic therapy with recombinant human
Manganese activates caspase-9-dependent apoptosis in human bronchial epithelial cells.
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Acute inhalation exposure to high levels of manganese (Mn) is associated with pulmonary edema and impaired function. The immune-mediated lung epithelium injury of Mn in vivo and in vitro experiments has been well characterized, whereas its apoptotic effect is not well defined. Our results show that
[Prolidase and manganese deficiency. Apropos of a case: diagnosis and treatment].
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Prolidase deficiency, transmitted on an autosomic recessive mode upsets skin healing and facilitates the occurrence of chronic cutaneous ulcerations. A 36-year-old woman has been followed since the age of 12 for ulcerations and erythematous erysipelatoid plaques of the lower limbs. Two episodes of
The acute toxicity of cyclopentadienyl manganese tricarbonyl in the rat.
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The acute toxicity of cyclopentadienyl manganese tricarbonyl (CMT) was studied in Sprague-Dawley rats. CMT was found to produce convulsions and pulmonary edema. The ED50s for convulsion were 32 mg/kg (95% C.I. 24-42 mg/kg) p.o. and 20 mg/kg (95% C.I. 15-26 mg/kg) i.p. The LD50s for p.o. and i.p.
Magnetic resonance imaging of experimental brain edema in cats.
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The authors observed the natural course of experimental brain edema in vivo using magnetic resonance (MR) imaging. To detect and qualify the edematous lesion, they obtained images by the spin echo technique (repetition time, 2100 ms; echo time, 80 ms). These showed the maximal brain edema on the 1st
Manganese induced brain lesions in Macaca fascicularis as revealed by positron emission tomography and magnetic resonance imaging.
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A series of positron emission tomography scans was made on two monkeys during a 16-month period when they received manganese(IV)oxide by subcutaneous injection. The distribution of [11C]-nomifensine uptake, indicating dopamine terminals, was followed in both monkey brains. The brain distributions of
Manganese-induced neurotoxicity: the role of astroglial-derived nitric oxide in striatal interneuron degeneration.
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Chronic exposure to excessive manganese (Mn) is the cause of a neurodegenerative movement disorder, termed manganism, resulting from degeneration of neurons within the basal ganglia. Pathogenic mechanisms underlying this disorder are not fully understood but involve inflammatory activation of glial
Manganese-Enhanced Magnetic Resonance Imaging of Traumatic Brain Injury.
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Calcium dysfunction is involved in secondary traumatic brain injury (TBI). Manganese-enhanced MRI (MEMRI), in which the manganese ion acts as a calcium analog and a MRI contrast agent, was used to study rats subjected to a controlled cortical impact. Comparisons were made with conventional T2 MRI,
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