Nitric oxide alleviates oxidative damage in the green alga Chlorella pyrenoidosa caused by UV-B radiation
Jazyk angličtina Země Spojené státy americké Médium print
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
12879752
DOI
10.1007/bf02931372
Knihovny.cz E-zdroje
- MeSH
- acetylcystein farmakologie MeSH
- Chlorella enzymologie metabolismus účinky záření MeSH
- chlorofyl metabolismus MeSH
- dithiothreitol farmakologie MeSH
- fenylalaninamoniaklyasa metabolismus MeSH
- glutathion farmakologie MeSH
- katalasa metabolismus MeSH
- kyselina askorbová farmakologie MeSH
- nitroprusid farmakologie MeSH
- oxid dusnatý biosyntéza MeSH
- oxidační stres účinky léků fyziologie MeSH
- superoxiddismutasa metabolismus MeSH
- ultrafialové záření škodlivé účinky MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- acetylcystein MeSH
- chlorofyl MeSH
- dithiothreitol MeSH
- fenylalaninamoniaklyasa MeSH
- glutathion MeSH
- katalasa MeSH
- kyselina askorbová MeSH
- nitroprusid MeSH
- oxid dusnatý MeSH
- superoxiddismutasa MeSH
The effect of ultraviolet-B radiation (UV-B; 280-320 nm) on induction of nitric oxide was estimated in the suspensions of green alga Chlorella pyrenoidosa with or without the NO scavenger N-acetyl-L-cysteine, and reductants such as 1,4-dithiothreitol, glutathione (reduced form), and ascorbic acid. Exogenously added sodium nitroprusside (NO donor), glutathione, 1,4-dithiothreitol, and ascorbic acid were able to prevent chlorophyll loss mediated by UV-B. Addition of NO to algal suspensions irradiated by UV-B increased the activity of catalase and superoxide dismutase but lowered the activity of phenylalanine ammonia-lyase. UV-B thus appears to be a strong inducer of NO production, exogenously added NO and reductants protecting the green alga against UV-B-induced oxidative damage.
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