Astaxanthin prevents in vitro auto-oxidative injury in human lymphocytes

Author(s)

Bolin, Anaysa P. ^[1] ; Macedo, Rita C. ^[1] ; Marin, Douglas P. ^[1] ; Barros, Marcelo P. ^[2] ; Otton, Rosemari ^{[1, 2]}

Affiliation

^[1] Univ Cruzeiro Sul, Postgrad Program Hlth Sci, Cellular Physiol Lab, CBS, BR-03342000 Sao Paulo - Brazil

^[2] Univ Cruzeiro Sul, Postgrad Program Human Movement Sci, Inst Phys Act & Sport Sci, BR-03342000 Sao Paulo - Brazil

• Document type: Journal article
• Source: CELL BIOLOGY AND TOXICOLOGY; v. 26, n. 5, p. 457-467, OCT 2010.
• Web of Science Citations: 31

Abstract

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 A mu M ASTA showed immediate lower rates of O (2) (aEuro cent a') /H(2)O(2) production whilst NO(aEuro cent) and intracellular Ca(2+) levels were concomitantly enhanced (a parts per thousand currency sign4 h). In long-term treatments (> 24 h), the cytotoxicity test for ASTA showed a sigmoidal dose-response curve (LC50 = 11.67 A +/- 0.42 A mu M), whereas higher activities of superoxide dismutase and catalase in 5 A mu M 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. (AU)