Nitric oxide alleviates oxidative damage in the green alga Chlorella pyrenoidosa caused by UV-B radiation
Language English Country United States Media print
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
12879752
DOI
10.1007/bf02931372
Knihovny.cz E-resources
- MeSH
- Acetylcysteine pharmacology MeSH
- Chlorella enzymology metabolism radiation effects MeSH
- Chlorophyll metabolism MeSH
- Dithiothreitol pharmacology MeSH
- Phenylalanine Ammonia-Lyase metabolism MeSH
- Glutathione pharmacology MeSH
- Catalase metabolism MeSH
- Ascorbic Acid pharmacology MeSH
- Nitroprusside pharmacology MeSH
- Nitric Oxide biosynthesis MeSH
- Oxidative Stress drug effects physiology MeSH
- Superoxide Dismutase metabolism MeSH
- Ultraviolet Rays adverse effects MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Acetylcysteine MeSH
- Chlorophyll MeSH
- Dithiothreitol MeSH
- Phenylalanine Ammonia-Lyase MeSH
- Glutathione MeSH
- Catalase MeSH
- Ascorbic Acid MeSH
- Nitroprusside MeSH
- Nitric Oxide MeSH
- Superoxide Dismutase 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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