Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0086543 (cataract)
 29,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Reactive oxygen species, such as superoxide radicals, are thought to underlie the pathogenesis of various diseases. Almost 3 to 10% of the oxygen utilized by tissues is converted to its reactive intermediates, which impair the functioning of cells and tissues. Superoxide dismutase (SOD) catalyzes the conversion of single electron reduced species of molecular oxygen to hydrogen peroxide and oxygen. There are several classes of SOD that differ in their metal binding ability, distribution in different cell compartments, and sensitivity to various reagents. Among these, Cu, Zn superoxide dismutase (SOD1) is widely distributed and comprises 90% of the total SOD. This ubiquitous enzyme, which requires Cu and Zn for its activity, has great physiological significance and therapeutic potential. The present review describes the role of SODs, especially Cu, Zn SOD, in several diseases, such as familial amyotrophic lateral sclerosis (FALS), Parkinson's disease, Alzheimer's disease, dengue fever, cancer, Down's syndrome, cataract, and several neurological disorders. Mutations in the SOD1 gene cause a familial form of amyotrophic lateral sclerosis. The mechanism by which mutant SOD1 causes the degeneration of motor neurons is not well understood. Transgenic mice expressing multiple copies of FALS-mutant SOD1s develop an ALS-like motor neuron disease. Vacuolar degeneration of mitochondria has been identified as the main pathological feature associated with motor neuron death and paralysis in several lines of FALS-SOD1 mice. Various observations and conclusions linking mutant SOD1 and FALS are discussed in this review in detail.
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PMID:Superoxide dismutase--applications and relevance to human diseases. 1221 58

As a delayed neurologic complication following a high-voltage electrical injury, motor neuron disease-like spinal cord injury has often been reported. However, epileptic seizure as a delayed complication of electrical brain injury has not been reported. We report a 32-year-old man, who developed epilepsy 8 years after electrical brain injury. His electroencephalogram (EEG) recordings showed focus on the right side, in which the electrical current passed during the accident eight years earlier. He experienced cataract during these 8 years. On examination, the right side of his tongue was found to be atrophic, and he was unaware when it had started. Systemic EMG examination revealed neuropathic changes in both (interossei dorsalis) IODs, the right biceps, right tongue, and right masseter muscles.
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PMID:Epileptic seizure, cataract, and tongue atrophy during the 8 years after electrical brain injury. 1957 55