Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0040822 (tremor)
18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ninety preselected children, aged between 8 and 14 years, living in two rural West African (Gambian) villages, were randomly divided into three groups, matched for age and sex. One group received a placebo (lactose) tablet, one received riboflavin (5 mg) on 5 d every week, which was sufficient to correct an endemic riboflavin deficiency, and one received a multivitamin supplement (Protovit; Hoffmann La Roche), on 5 d every week, together with FeSO4 (200 mg) once weekly, and the supplements were given for 1 year. Neuromuscular tests, including arm tremor and manipulative skills, were performed on three occasions: once just before the introduction of the supplements; again 6 weeks after commencing the supplements; and again 1 year later. Venous blood samples were collected at the same time as the first two sets of neuromuscular tests. These samples were used for haematology and nutrient status indices: plasma ferritin, ascorbic acid, cyanocobalamin and pyridoxal phosphate, and erythrocyte tests for folate status, for riboflavin status (erythrocyte glutathione reductase activation coefficient) and thiamine status (erythrocyte transketolase activation coefficient). The riboflavin in both supplements achieved a clear-cut response in biochemical status, which was dose-dependent. The pyridoxine, ascorbic acid and Fe components of the multivitamin also affected the associated biochemical indices. Although overall the arm tremor and related neuromuscular function tests did not respond significantly to the supplements, significant improvement was seen in the boys for the arm-tremor test in both the supplemented groups.
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PMID:Biochemical indices and neuromuscular function tests in rural Gambian schoolchildren given a riboflavin, or multivitamin plus iron, supplement. 798 90

Cu, Zn-superoxide dismutase (Cu,Zn-SOD), Mn-superoxide dismutase (Mn-SOD), catalase (CAT), peroxidase (POX), glutathione peroxidase(GP) and glutathione reductase (GR) activities were assayed in the brains of genetically selected neurological mutant rabbits pt and their controls. Paralytic tremor (pt) is a spontaneous mutation in rabbit that affects irregular and defective myelination of CNS. Antioxidant enzyme levels were different in three brain regions: brain hemispheres, cerebellum, and brain stem. In brain hemisphere and cerebellum of pt rabbits Mn-SOD and Cu, Zn-SOD activities were elevated. Catalase activity in brain hemispheres and peroxidase activity in the brain stem of pt rabbits were reduced. It was also noticed, that in the pt rabbit the ratio CAT/Cu, Zn-SOD was lower by 20% in the brain hemispheres and by 13% in the cerebellum and the ratio POX/Cu, Zn-SOD was lower by 31.8% in the brain stem. These findings indicated that pt mutations are associated with changes in the antioxidant defense system in the rabbit brain.
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PMID:Antioxidant enzyme activities in different brain areas of the neurological mutant--pt rabbit. 870 86

Scrapie, one of the prion diseases, is a transmissible neurodegenerative disease of sheep and other animals. Clinical symptoms of prion diseases are characterized by a long latent period, followed by progressive ataxia, tremor, and death. To study the induction of neurodegeneration during scrapie infection, we have analyzed the activities of various antioxidant enzymes and mitochondrial enzymes in cerebral cortex, brain stem, and cerebellum of scrapie-infected hamsters. The activity of mitochondrial Mn-superoxide dismutase (SOD) was decreased, while the activities of cytosolic Cu/Zn-SOD and catalase were not altered in infected brains. The activities of glutathione peroxidase and glutathione reductase were increased in scrapie-infected hamsters. The decreased activity of Mn-SOD might result in increasing oxidative stress in the mitochondria of infected brain; this concept is supported by our findings of a high level of lipid peroxidation, and low levels of ATPase and cytochrome c oxidase activity in the infected cerebral mitochondria. In addition, structural abnormalities of mitochondria have been observed in the neurons of hippocampus and cerebral cortex of infected brain. These results suggest that mitochondrial dysfunction caused by oxidative stress gives rise to neurodegeneration in prion disease.
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PMID:Mitochondrial dysfunction induced by oxidative stress in the brains of hamsters infected with the 263 K scrapie agent. 975 61

The aim of this study was to determine oxidative stress status as well as blood lead (Pb) and zinc (Zn) levels and clinical markers in workers of a Zn-Pb mine. A comparative cross-sectional analysis was performed in 67 mine workers who have been in contact with Zn and Pb in comparison to a control group containing 67 healthy subjects with the same age and sex. Lipid peroxidation, superoxide dismutase, catalase, glutathione reductase, myleoperoxidase, DNA damage, total antioxidant capacity, Zn, and Pb levels were measured in blood of workers and controls. Clinical examination was accomplished to record any abnormal sign or symptoms. Comparing with controls, the workers showed higher blood levels of superoxide dismutase, myleoperoxidase, glutathione reductase, lipid peroxidation, Pb, and Zn. Workers showed lower DNA-damage as compared with controls. Workers showed clinical symptoms such as memory impairment, less of concentration, insomnia, headache, claudication, epigasteric, inappetence, agitation, tremor, decreasing of reflection of deep tendon, conduction deafness of ear, and fatigue. The workers had extra normal levels of Pb (0.9-3 microg/dL) and showed oxidative stress. Taken together, the results indicate that exposure to combination of Pb and Zn in mine elevates total antioxidant capacity of body in a reflex to overcome to oxidative stress. Especially, in the present case, it seems that toxic effect of Pb has been greater than positive effects of Zn, but the combination exposure has resulted in not such a critical toxicity situation.
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PMID:Study on clinical and biochemical toxicity biomarkers in a zinc-lead mine workers. 2037 35