Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P04040 (Catalase)
 3,577 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

One way to study the effect of radiation on gene expression is to monitor changes in the levels of specific messenger RNAs. We describe the use of reverse transcription-polymerase chain reaction (RT-PCR) analysis, a faster and more sensitive procedure than the traditional techniques to monitor RNA levels. Using RT-PCR, we confirmed previous results showing increased levels of GADD45 transcripts after high dose-rate X-irradiation in normal human fibroblasts. No differences were observed in the transcript levels of beta-ACTIN, beta-MICROGLOBULIN, Cu-Zn SUPEROXIDE DISMUTASE (SOD-1) and CATALASE. In cells exposed to 3-6 Gy low dose-rate gamma-irradiation we observed increased levels of the GADD45 transcript and lower transcript levels of the genes TOPOISOMERASE II alpha, FACC, CYCLIN A and CYCLIN B. No differences were detected in the transcript levels of beta-ACTIN, beta-MICROGLOBULIN, SOD-1, URACYL-DNA GLYCOSYLASE, CYCLIN C, CYCLIN E, CYCLIN D1, CYCLIN D2, CYCLIN D3, TOPOISOMERASE I and TOPOISOMERASE II beta.
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PMID:Use of semiquantitative reverse transcription-polymerase chain reaction to study gene expression in normal human skin fibroblasts following low dose-rate irradiation. 788 81

Steroid hormones have been reported to activate various signal transducers that trigger a variety of cellular responses. Among these hormones, testosterone has been identified as an antioxidant that protects against cellular damage. Therefore, using mouse embryonic stem (ES) cells as a model system, this study evaluated the effects of dihydrotestosterone (DHT), a biologically active testosterone metabolite, on H2O2-induced apoptosis. H2O2 increased the release of lactate dehydrogenase (LDH) and DNA fragmentation but reduced the cell viability in a time-dependent manner (> or =8 h). Moreover, H2O2 decreased the level of DNA synthesis and the levels of the cell cycle regulatory proteins [cyclin D1, cyclin E, cyclin-dependent kinase (CDK) 2, and CDK 4]. These effects of H2O2 were inhibited by a pretreatment with DHT. However, a treatment with flutamide (androgen receptor inhibitor, 10(-3) M) abolished the protective effects of DHT. This result was supported by the presence of the androgen receptor in mouse ES cells. The activity of the antioxidant enzyme, catalase, was increased by the DHT treatment but not by a co-treatment with DHT and flutamide. Using CM-H(2)DCFDA (DCF-DA) for the detection of intracellular H2O2, DHT decreased the intracellular H2O2 levels but flutamide blocked this effect. H2O2 also increased the level of p38 MAPK, JNK/SAPK, and NF-kappaB phosphorylation, which were inhibited by the DHT pretreatment. Catalase inhibited the effect of H2O2 on MAPKs and NF-kappaB. However, the flutamide treatment abolished the inhibitory effects of DHT on the H2O2-induced increase in the levels of p38 MAPK, JNK/SAPK, and NF-kappaB phosphorylation. DHT inhibited the H2O2-induced increase in caspase-3 expression and decreased the level of Bcl-2 and the cellular inhibitor of apoptosis protein (cIAP)-2. These effects were abolished by the flutamide treatment. In conclusion, DHT prevents the H2O2-induced apoptotic cell death of mouse ES cells through the activation of catalase and the downregulation of p38 MAPK, JNK/SAPK, and NF-kappaB via the androgen receptor.
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PMID:Effect of dihydrotestosterone on hydrogen peroxide-induced apoptosis of mouse embryonic stem cells. 1833 Aug 93