Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P30044 (antioxidant enzyme)
 8,037 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Microcosm studies were undertaken to relate biomarker responses to the toxicities in soil ecosystems contaminated by phenanthrene (Phe) and pyrene (Pyr), both singly and combined. Growth inhibition, enzyme activity, MDA content, sperm count, neutral-red retention time (NRRT) and annetocin and TCTP gene transcriptions were determined in earthworm Eisenia fetida exposed to Phe and Pyr, both singly and combined pollution in microcosm. Exposure to 0.5 and 2.5 mg kg(-1) Phe or 50 and 100 mg kg(-1) Pyr alone significantly decreased E. fetida growth, NRRT and sperm count. Two-way ANOVA analysis shows that the combination of these two compounds decreased growth, SOD activities, NRRT and sperm count synergistically, but increased the CAT activities and MDA content. The highest suppression rate of growth was 48.12%, the lowest levels of SOD activities and NRRT were 51.66% and 45.57% of the control, respectively. The highest increase in CAT activities and MDA content were 120.05% and 121.03% greater than that of the control when exposed to 0.5 (Phe)+100 (Pyr) mg kg(-1) soils. A clear dose-related response with exposure concentration was established for the NRRT. Real-time PCR shows that Phe and Pyr increased the expression levels of annetocin and TCTP gene synergistically. These results demonstrate that earthworms were under physiological stress at field dose of 0.5 (Phe)+100 (Pyr) mg kg(-1) soils. Phe and Pyr synergistically decreased sperm count and NRRT, but antagonistically caused changes in antioxidant enzyme activities to disrupt the detoxification functions and inhibit earthworm growth.
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PMID:Biomarker responses of earthworms (Eisenia fetida) exposured to phenanthrene and pyrene both singly and combined in microcosms. 2234

Fortilin, a pro-survival molecule, inhibits p53-induced apoptosis by binding to the sequence-specific DNA-binding domain of the tumor suppressor protein and preventing it from transcriptionally activating Bax. Intriguingly, fortilin protects cells against ROS-induced cell death, independent of p53. The signaling pathway through which fortilin protects cells against ROS-induced cell death, however, is unknown. Here we report that fortilin physically interacts with the antioxidant enzyme peroxiredoxin-1 (PRX1), protects it from proteasome-mediated degradation, and keeps it enzymatically active by blocking its deactivating phosphorylation by Mst1, a serine/threonine kinase. At the whole animal level, the liver-specific overexpression of fortilin reduced PRX1 phosphorylation in the liver, enhanced PRX1 activity, and protected the transgenic animals against alcohol-induced, ROS-mediated, liver damage. These data suggest the presence of a novel oxidative-stress-handling pathway where the anti-p53 molecule fortilin augments the peroxidase PRX1 by protecting it against degradation and inactivation of the enzyme. Fortilin-PRX1 interaction in the liver could be clinically exploited further to prevent acute alcohol-induced liver damage in humans.
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PMID:Fortilin potentiates the peroxidase activity of Peroxiredoxin-1 and protects against alcohol-induced liver damage in mice. 2672 32