Asojo Oluwatoyin A, Schott Eric J, Vasta Gerardo R, Silva Abelardo M
Pathology and Microbiology Department, University of Nebraska Medical Center, 986495 Nebraska Med Center, Omaha, NE 68198-6495, USA.
Acta Crystallogr Sect F Struct Biol Cryst Commun. 2006 Nov 1;62(Pt 11):1072-5. doi: 10.1107/S1744309106040425. Epub 2006 Oct 25.
Perkinsus marinus, a facultative intracellular parasite of the eastern oyster Crassostrea virginica, is responsible for mass mortalities of oyster populations. P. marinus trophozoites survive and proliferate within oyster hemocytes, invading most tissues and fluids, thus causing a systemic infection that eventually kills the host. The phagocytosis of P. marinus trophozoites lacks a respiratory burst, suggesting that the parasite has mechanisms that actively abrogate the host's oxidative defense responses. One mechanism and the first line of defense against oxidative damage is the dismutation of superoxide radical to molecular oxygen and hydrogen peroxide by superoxide dismutases (SODs). P. marinus possesses two iron-cofactored SODs, PmSOD1 and PmSOD2. Here, the crystallization and X-ray structures of both PmSOD1 and PmSOD2 are presented.
海派金藻（Perkinsus marinus）是美国东海岸牡蛎（Crassostrea virginica）的一种兼性细胞内寄生虫，它会导致牡蛎种群大量死亡。海派金藻滋养体在牡蛎血细胞内存活并增殖，侵入大多数组织和体液，从而引发全身性感染，最终杀死宿主。海派金藻滋养体的吞噬作用缺乏呼吸爆发，这表明该寄生虫具有主动消除宿主氧化防御反应的机制。对抗氧化损伤的一种机制及第一道防线是超氧化物歧化酶（SODs）将超氧自由基歧化为分子氧和过氧化氢。海派金藻拥有两种铁辅助因子的SOD，即PmSOD1和PmSOD2。本文展示了PmSOD1和PmSOD2的晶体结构及X射线结构。
