Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.3.1.28 (chloramphenicol acetyltransferase)
 5,100 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ascorbate is an important cofactor in many cellular metabolic reactions and is intimately linked to iron homeostasis. Continuously cultured cells are ascorbate deficient due to the lability of the vitamin in solution and to the fact that daily supplementation of media with ascorbate is unusual. We found that ascorbate repletion alone did not alter ferritin synthesis. However, ascorbate-replete human hepatoma cells, Hep3B and HepG2, as well as K562 human leukemia cells achieved a substantially higher cellular ferritin content in response to a challenge with iron than did their ascorbate-deficient counterparts grown under standard culture conditions. Most of the elevation in ferritin content was due to an increase in de novo ferritin synthesis of greater than 50-fold, as shown by in vivo labeling with [35S]methionine and immunoprecipitation. RNA-blot analysis showed only minor changes in steady state levels of ferritin mRNA, suggesting that ascorbate enhances iron-induced ferritin synthesis primarily by post-transcriptional events. Transient gene expression experiments using chloramphenicol acetyltransferase reporter gene constructs showed that the ascorbate effect on ferritin translation is not mediated through the stem-loop near the translational start site that transduces ferritin synthesis in response to cytokines. The data suggest that ascorbate possibly modifies the action of the iron-responsive element on ferritin translation, although more precise structure-function studies are needed to clarify this issue. These data demonstrate a novel role of ascorbate as a signaling molecule in post-transcriptional gene regulation. The mechanism by which ascorbate modulates cellular iron metabolism is complex and requires additional detailed investigation.
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PMID:Ascorbic acid enhances iron-induced ferritin translation in human leukemia and hepatoma cells. 785 59

The response of the antioxidant defense system of an intertidal macroalgae Corallina officinalis L. to different dosages of UV-B irradiation was investigated. Results showed that superoxide dimutase (SOD) and peroxidase (POX) increased and then maintained at a relatively stable level when subjected to UV-B irradiation. Catalase (CAT) activity under medium dosage of UV-B irradiation (Muv) and high dosage of UV-B irradiation (Huv) treatments were significantly decreased. Ascorbate peroxidase (APX) activity first remained unaltered and then increased in Huv treatment. In addition, the assay on isozymes was carried out using non-denaturing polyacrylamide gel electrophoresis (PAGE). The activities of some SOD isoforms were altered by UV-B. Two new bands (POX V and POX VII) appeared upon exposure to all three UV-B dosages. CAT III activity was increased by low dosage of UV-B irradiation (Luv), whereas CAT III and CAT IV disappeared when the alga was exposed to Muv and Huv. Two bands of APX (APX VI and APX VII) were increased and a new band (APX X) was observed under Huv exposure. H2O2 and thiobarbituric acid reacting substance (TBARS) increased under Muv and Huv treatments. Overall, UV-B protection mechanisms are partly inducible and to a certain extent sufficient to prevent the accumulation of damage in C. officinalis.
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PMID:Ultraviolet irradiation induced oxidative stress and response of antioxidant system in an intertidal macroalgae Corallina officinalis L. 2060 8