Oxidative stress, uptake and bioconversion of 5-fluorouracil in algae
Jazyk angličtina Země Velká Británie, Anglie Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
24380438
DOI
10.1016/j.chemosphere.2013.11.074
PII: S0045-6535(13)01679-2
Knihovny.cz E-zdroje
- Klíčová slova
- Bioaccumulation, Confocal microscopy, Immunochemistry, Mass spectrometry, Nitric oxide,
- MeSH
- aminokyseliny metabolismus MeSH
- biologický transport MeSH
- chemické látky znečišťující vodu škodlivé účinky metabolismus MeSH
- ekotoxikologie * MeSH
- fluoruracil škodlivé účinky metabolismus MeSH
- glutathion metabolismus MeSH
- kyselina askorbová metabolismus MeSH
- oxid dusnatý metabolismus MeSH
- oxidační stres účinky léků MeSH
- peroxidace lipidů MeSH
- reaktivní formy kyslíku metabolismus MeSH
- Scenedesmus účinky léků metabolismus MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- aminokyseliny MeSH
- chemické látky znečišťující vodu MeSH
- fluoruracil MeSH
- glutathion MeSH
- kyselina askorbová MeSH
- oxid dusnatý MeSH
- reaktivní formy kyslíku MeSH
Impact of cytostatic drug 5-fluorouracil (FU) and its metabolite 2-fluoro-3-alanine (FA) on green alga Scenedesmus quadricauda was studied. FA elevated fluorescence signal of reactive oxygen species (ROS) more pronouncedly than FU at 1 and 10 μM doses while both ROS and reactive nitrogen species (RNS/NO) increased more expressively in 100 μM FU treatment. Cellular damage staining (Acridine Orange and Calcofluor White) did no reveal substantial difference between FU and FA. Majority of free amino acids including proline was unaffected after 24h of exposure. FA depleted ascorbate peroxidase activity more than FU therefore ascorbate content (AsA) was less affected while FU stimulated glutathione reductase activity less than FA and therefore glutathione (GSH) was more depleted. Both compounds accumulated concentration-dependently with higher absolute FA amounts but FU conversion to FA was also detected. We subsequently influenced 100 μM FU- and FA-induced changes using known ROS (DTT - dithiothreitol) and RNS/NO (SNP - sodium nitroprusside and PTIO - 2-phenyl-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide) modulators and results showed that PTIO depleted NO and elevated ROS while the opposite was found after SNP and DTT addition. Changes of lipid peroxidation (using BODIPY staining) confirmed that FU and FA toxicity is related to alteration of ROS/RNS balance.
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