Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:1.6.5.2 (NQO1)
 6,196 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Southern armyworm, Spodoptera eridania, larvae were provided ad libitum 0.002-0.25% w/w dichlone, 2,3-dichloro-1,4-naphthoquinone (CNQ). Larval mortality occurred in a time-and-dose dependent manner, with an LC17 of 0.01% and an LC50 of 0.26% CNQ at day-5. Extracts of larvae fed control, 0.01, and 0.25% CNQ diets for 5 days were assayed for antioxidant enzymes. While 0.01% CNQ had a mild effect, 0.25% CNQ profoundly increased levels of all antioxidant enzymes that were examined. The increases as compared to control were: 5.3-, 1.9-, 3.2-, 2.6-, 2.8-, and 3.5-fold higher for superoxide dismutase, catalase, glutathione transferase and its peroxidase activity, glutathione reductase and DT-diaphorase, respectively. At 0.01% CNQ, the thiobarbituric acid reactive substances (TBARS) were similar to the control group. However, despite the induction from 0.25% CNQ of all enzymes examined, the lipid peroxidation was not attenuated; the TBARS were 29.7% over the control value. High mortalities and CNQ-induced pathologies reflected in retarded growth, wasting syndrome, and diuresis clearly indicated that the insect sustained severe oxidant-induced injuries before appropriate defenses were fully mobilized. Thus, this quinone causes an oxidative stress in a model insect species analogous to that observed in mammalian species.
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PMID:Dichlone-induced oxidative stress in a model insect species, Spodoptera eridania. 757 83

Bluegill sunfish BF-2 fibroblasts were used to evaluate the in vitro cytotoxicities of 1,4-naphthoquinone (NQ), 5,8-dihydroxy-1,4-NQ, and 2,3-dichloro-1, 4-NQ (dichlone); comparisons were made with previously obtained data on the response of human hepatoma HepG2 cells. For both cell types, the sequence of potency was 5,8-dihydroxy-1,4-NQ > 1,4-NQ > dichlone. Dichlone, and, although to a lesser extent, 1,4-NQ and 5,8-dihydroxy-1-4-NQ, induced endoreduplication in the BF-2 cells; for the HepG2 cells, endoreduplication was induced only with dichlone. Exposures to the three NQs reduced intracellular glutathione levels in both cell types. For the BF-2 and HepG2 cells, pretreatments with buthionine sulfoximine (BSO), a glutathione-depleting agent, potentiated the cytotoxicity of 5,8-hydroxy-1,4-NQ and dichlone; pretreatment with dicoumarol, an inhibitor of DT-diaphorase, had no effect on toxicity of these two NQs. Apparently, for these two quinones the predominant metabolic pathway in both the BF-2 and HepG2 cells involved redox cycling via a one-electron reduction reaction, generating reactive oxygen intermediates that consumed intracellular glutathione. Pretreatment of the BF-2 cells with BSO, but not with dicoumarol, potentiated the toxicity of 1,4-NQ, again indicating that metabolism occurred via one electron reduction. However, for the HepG2 cells, pretreatment with dicoumarol, but not with BSO, potentiated the cytotoxicity of 1,4-NQ. Apparently, in the HepG2, as compared to the BF-2, cells, 1,4-NQ was metabolized by DT-diaphorase in a reaction involving a two electron reduction.
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PMID:Naphthoquinone cytotoxicity to bluegill sunfish BF-2 cells. 802 24