Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.25 (triphosphatase)
 1,529 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Oxidative stress plays an important role in the pathogenesis of amyotrophic lateral sclerosis (ALS). In the present study, we investigated the expression of two major human enzymes that prevent errors caused by 8-oxoguanine (8-oxoG), a mitochondrial form of 8-oxoG DNA glycosylase (hOGG1) and oxidized purine nucleoside triphosphatase (hMTH1). We also investigated the relationship between their expression and the 8-oxoG accumulation observed in the large motor neurons of the lumbar spinal cord in seven cases of adult onset sporadic ALS, four cases of subarachnoid hemorrhage (SAH) and four control cases. 8-oxoG immunoreactivity increased in most large motor neurons in both the ALS and SAH cases. However, the large motor neurons in the control cases often lacked hOGG1 immunoreactivity, although some neurons expressed hOGG1 in either homogeneous or fine granular patterns. In SAH cases, most large motor neurons showed a fine granular pattern proportional to the increased 8-oxoG immunoreactivity. However, only half of the remaining motor neurons in ALS expressed hOGG1 in the fine granular pattern, and the rest did not show any immunoreactivity. In addition, small aggregates of hMTH1 in the nuclei of the anterior horn cells were present in several ALS cases. Our results indicate that the oxidative damage accumulates in the mitochondria of motor neurons in ALS, and that hOGG1 does not repair the damage efficiently, which may lead to a loss of motor neurons in ALS.
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PMID:Impairment of mitochondrial DNA repair enzymes against accumulation of 8-oxo-guanine in the spinal motor neurons of amyotrophic lateral sclerosis. 1190 61

Astrocytosis is a sequential morphological change of astrocytic reaction to tissue damage, and is associated with regulation of antioxidant defense mechanisms to reduce oxidative damage. The repair enzymes to oxidative DNA damage, oxidized purine-nucleoside triphosphatase (hMTH1) and a mitochondrial type of 8-oxoguanine DNA glycosylase (hOGG1-2a) in brain tumors and neurons of Alzheimer's disease, were previously reported. In the present study, glial expression of these repair enzymes under such pathological conditions as cerebrovascular diseases and metastatic brain tumors, were investigated. Furthermore, an in-vitro experiment using a glioma cell-line under oxidative stress was performed to verify the immunohistochemical results of post-mortem materials. As a result, hOGG1-2a immunoreactivities in reactive astrocytes were more intense than those to hMTH1. Oligodendrocytes of acute or subacute stage of brain infarction were strongly immunoreactive to both repair enzymes. In-vitro study revealed that, hOGG1-2a is constitutively expressed in both untreated glioma cells and the glioma cells under oxidative stress. However, although no immunoreactivity to hMTH1 was found in the control cells, accumulation of hMTH1 was rapidly induced by oxidative stress. These results indicate that the two repair enzymes to oxidative DNA damage are differentially regulated in glial cells, and that there is a difference in the expression of the repair enzymes between reactive astrocytes and oligodendrocytes.
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PMID:Defense mechanism to oxidative DNA damage in glial cells. 1513 89

Oxidative damage can be induced by many environmental stressors. 8-Hydroxydeoxyguanosine (8-OHdG) has been used as a biomarker of oxidative DNA damage in both in vitro and in vivo studies. In the present study, Wistar rats were exposed to radon gas at a concentration of 100,000Bq/m(3) for 12 h/d for 30, 60, and 120 d, equivalent to cumulative doses of 60, 120, and 240 working level months (WLM), respectively. Changes in levels of 8-OHdG, reactive oxygen species (ROS), and total antioxidant (T-AOC), as well as expressions of some DNA repair enzymes such as 8-oxoguanine DNA glycosylase (OGG1) and MutT homolog 1 (oxidized purine nucleoside triphosphatase, MTH1), were determined in rat urine, peripheral blood lymphocytes, and lung after exposure to radon. The results revealed an increase in 8-OHdG and ROS levels, a decrease in T-AOC levels, and reduced OGG1 and MTH1 expression levels. The elevated amount of 8-OHdG in urine or lymphocytes was positively correlated with the cumulative exposure dose, whereas OGG1 and MHT1 expression levels in lung were inversely correlated with cumulative exposure dose. These findings indicate that oxidative damage induced by radon may be involved in radon-induced carcinogenesis.
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PMID:Oxidative damage in various tissues of rats exposed to radon. 2275 73