Ultraviolet-B-induced oxidative stress and responses of the ascorbate-glutathione cycle in a marine macroalga Ulva fasciata.
The regulation of the antioxidant defence system by ultraviolet-B (UV-B) was determined in a marine macroalga Ulva fasciata Delile exposed to low (0.5, 1 W m(-2)), medium (2.5, 5 W m(-2)), and high (10, 20 W m(-2)) UV-B irradiance. UV-B > or =2.5 W m(-2) increased H2O2 contents that are positively correlated with lipid peroxidation and total peroxide contents. Inhibition of the UV-B-induced H2O2 increase by a specific O2.- scavenger, 1,2-dihydroxy-benzene-3,5-disulphonic acid, shows that O2.- is the primary source of H2O2. Superoxide dismutase activity was increased by UV-B with a peak at 2.5 W m(-2), which did not match the H2O2 pattern. Alleviation of UV-B-induced oxidative damage by a H2O2 scavenger, dimethylthiourea, and a free radical scavenger, sodium benzoate, which inhibited UV-B-induced H2O2 accumulation, suggests that oxidative damage caused by UV-B > or = 2.5 W m(-2) is ascribed to accumulated H2O2. However, a decrease in growth rate and TTC reduction ability only at high UV-B doses indicates that the defence and repairing systems operate at low and medium UV-B doses. H2O2 not only can be excreted but can also be detoxified via the ascorbate-glutathione cycle. Increases in catalase, peroxidase, ascorbate peroxidase, and glutathione reductase activities and ascorbate (AsA) and glutathione pools, as well as AsA regeneration ability, function to keep the balance of cellular H2O2 under low UV-B doses. Dehydroascorbate reductase and monodehydroascorbate reductase are responsible for AsA regeneration under low and medium UV-B radiation, respectively. The appearance of oxidative damage in medium and high UV-B flux is attributable to a lower induction of the ascorbate-glutathione cycle as an antioxidant defence system. Overall, the availability of antioxidants and the induction of antioxidant enzyme activities for detoxifying reactive oxygen species (ROS) are regulated in U. fasciata against UV-B-induced oxidative stress, and experiments using ROS scavengers demonstrate that the antioxidant defence system is modulated by O2.- or H2O2.
Shiu
Chia-Tai
CT
Institute of Marine Biology, National Sun Yat-sen University, Kaohsiung 80424, Taiwan, Republic of China.
Lee
Tse-Min
TM
D000975:Antioxidants / Q000378:metabolism; D001205:Ascorbic Acid / Q000378:metabolism*; D002338:Carotenoids / Q000378:metabolism; D002734:Chlorophyll / Q000378:metabolism; D000077194:Chlorophyll A; D016166:Free Radical Scavengers / Q000378:metabolism; D018506:Gene Expression Regulation, Plant / Q000528:radiation effects; D005978:Glutathione / Q000378:metabolism*; D006861:Hydrogen Peroxide / Q000378:metabolism; D015227:Lipid Peroxidation / Q000528:radiation effects; D008386:Marine Biology; D018384:Oxidative Stress / Q000528:radiation effects*; D017382:Reactive Oxygen Species / Q000378:metabolism; D014466:Ultraviolet Rays / Q000009:adverse effects*; D044445:Ulva / Q000378:metabolism* / Q000528:radiation effects*
D000975:Antioxidants; D016166:Free Radical Scavengers; D017382:Reactive Oxygen Species; D002734:Chlorophyll; D002338:Carotenoids; D006861:Hydrogen Peroxide; D005978:Glutathione; D001205:Ascorbic Acid; D000077194:Chlorophyll A