ISSN:
1432-069X
Keywords:
UVB irradiation
;
Tanning
;
Reactive oxygen species
;
Lipid peroxides
;
Superoxide dismutase
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Abstract Lipid peroxide levels, the activities of superoxide dismutase (SOD), catalase and glutathione peroxidase (GSH-Px), and the development of tanning in the skin of C57 BL/6 mice were assessed for long periods, from very early to late stages, after acute or chronic UVB irradiation. Acute UVB irradiation produced an increase in lipid peroxide levels that peaked 18 h after irradiation, after which the levels declined to a minimum 2–3 days after irradiation and then gradually rose to baseline. Chronic irradiation caused the lipid peroxide level to fall to a minimum at 0.5–1.0 weeks, after which it gradually returned to baseline by the third week. SOD and GSH-Px activities decreased sharply after acute irradiation, reaching a minimum 18 h after irradiation. Following chronic irradiation, these enzyme levels peaked after 0.5 weeks, and thereafter declined gradually to the original levels 3 weeks after irradiation. In contrast, catalase activity did not change significantly. Tanning began to increase at 1.5 weeks after irradiation, with an accelerated rate of increase from the third week. Although UVB has been reported only to decrease or impair reactive oxygen species (ROS) scavenging enzyme activity, we postulate the following from our results: (1) the increase in lipid peroxide levels observed after irradiation was due to UVB-induced ROS; (2) the parallel decrease in enzyme activities may have been due to inactivation by ROS; (3) the decrease in lipid peroxide levels following the peak at 18-h resulted from the scavenging effect of increasing SOD and GSH-Px activities, and (4) the increase in these two enzyme activities was the result of their induction by the increased lipid peroxides or ROS. In addition, these results seem to suggest a possible correlation of melanogenesis with UVB-induced ROS.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00375843
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