Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes

Anaysa P. Bolin, Rita C. Macedo, Douglas P. Marin, Marcelo P. Barros, Rosemari Otton

Upon mitogen sensitization, lymphocytes undergo proliferation by oxyradical-based mechanisms. Through continuous resting-restimulation cycles, lymphocytes accumulate auto-induced oxidative lesions which lead to cell dysfunction and limit their viability. Astaxanthin (ASTA) is a nutritional carotenoid that shows notable antioxidant properties. This study aims to evaluate whether the in vitro ASTA treatment can limit oxyradical production and auto-oxidative injury in human lymphocytes. Activated lymphocytes treated with 5 microM ASTA showed immediate lower rates of O(2)(*-) /H(2)O(2) production whilst NO* and intracellular Ca(2+) levels were concomitantly enhanced (<or=4 h). In long-term treatments (>24 h), the cytotoxicity test for ASTA showed a sigmoidal dose-response curve (LC50 = 11.67 +/- 0.42 microM), whereas higher activities of superoxide dismutase and catalase in 5 microM ASTA-treated lymphocytes were associated to significant lower indexes of oxidative injury. On the other hand, lower proliferative scores of ASTA lymphocytes might be a result of diminished intracellular levels of pivotal redox signaling molecules, such as H(2)O(2). Further studies are necessary to establish the ASTA-dose compensation point between minimizing oxidative damages and allowing efficient redox-mediated immune functions, such as proliferation, adhesion, and oxidative burst.