The action of fucoidan (a sulfated polysaccharide) on human serum complement has been under study. Fucoidan inhibited the classical pathway of complement activation up to the complete arrest of the complement-dependent hemolysis achieved at the polysaccharide concentration higher than 200-250 mg per 1 ml of human serum. The classical pathway inhibition by fucoidan seems to be due to the binding to subcomponent C1q. In the alternative pathway, fucoidan also showed an inhibitory effect seen first in dose-dependent elongation of the lag-period preceding complement-dependent hemolysis. Experimental data suggest that fucoidan target is complement factor D, some part of the which (less than 30%) remains stable to the polysaccharide concentration as high as 600 mg/ml. The fucoidan properties described in this study can be used for cell protection against self-activated complement.