The research, published in a recent edition of Experimental Dermatology, compares the protection provided by astaxanthin (AX) to that of canthaxanthin (CX) and beta carotene.
Out of the three it was astaxanthin that provided the most effective protection when human dermal fibroblasts underwent UV radiation, concluded the scientists led by Emanuela Camera from San Gallicano Dermatology Institute in Rome.
UVA damages antioxidant defence system
UVA radiation is known to both trigger the creation of reactive oxygen species (ROS) and deplete the antioxidant defence system of the fibroblasts by affecting antioxidant enzymes such as catalase and superoxide dismutase.
For this reason supplementing the system with antioxidants can help protect against UV damage, explained the authors.
The researchers treated human dermal fibroblasts with AX, CX or beta carotene, 24 hours prior to exposing the cells to UVA radiation.
They found that AX prevented the UVA-induced inhibition of catalase, whereas beta carotene only showed a slight protective effect and CX had no discernable effect.
Similarly the UVA-induced inhibition of superoxide dismutase was also counteracted by AX and beta carotene, but not by CX.
Astaxanthin protects against cell death
The scientists also looked at the effect of the carotenoids on the apoptotic process (programmed cell death), which is linked to the activity of the enzyme caspase-3.
According to the study, the increased levels of caspase-3 that usually result from UVA radiation were successfully decreased in the AX treated fibroblasts.
In contrast, CX had no significant effects, and beta carotene actually up regulated caspase-3 activity, aggravating cell apoptosis.
The scientists suggested this enhanced apoptotic effect of beta carotene may be related to the compounds pro-oxidant effects under UVA exposure.
AX may prevent ROS production
In order to attempt to understand the protective effect of AX in more detail the scientists looked at the compounds effect in the expressions of HO-1, a marker of oxidative stress and a regulatory mechanism involved in the inflammatory response against oxidative damage.
Interestingly, they found that AX prevented the upregulation of HO-1 by UVA, whereas CX and beta carotene markedly enhanced the UV-induced upregulation.
This is particularly important, the scientists explained, as it suggests that AX plays a role in inhibiting the synthesis of ROS rather than just helping to mop them up once they have been created.
Therefore, the team conclude, AX offers a safe measure for the prevention of a variety of UVA-induced skin damage, mainly mediated by reactive oxygen species.