The initiation and promotion of sporocyst propagation and subsequent production of cercariae by intramolluscan larval stages of digenic trematodes are thought to depend on mollusc-derived factors. The ability to investigate this using in vitro cultures of Schistosoma mansoni sporocysts has been impeded by the fact that plasma from the host, Biomphalaria glabrata, becomes toxic to the parasite in long-term cultures. The present study identifies hemoglobin as the plasma component responsible for this toxicity. The addition of the enzyme catalase to sporocyst cultures neutralized the toxic effects of both purified hemoglobin and whole plasma, suggesting that the generation of H2O2 as a consequence of hemoglobin oxidation is the mechanism of plasma toxicity. Furthermore, cultures incubated in unconditioned schistosome medium with plasma plus catalase yielded significantly higher numbers of daughter sporocysts than cultures with media or plasma alone, but not higher than cultures with catalase alone. These latter results suggest that the oxidative environment and the antioxidant capacity of the media are critical factors for in vitro propagation of S. mansoni sporocysts.
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February 2002
Research Article|
February 01 2002
SCHISTOSOMA MANSONI SPOROCYSTS IN CULTURE: HOST PLASMA HEMOGLOBIN CONTRIBUTES TO IN VITRO OXIDATIVE STRESS
Randall C. Bender;
Randall C. Bender
Department of Zoology, Oregon State University, Corvallis, Oregon 97331. benderr@bcc.orst.edu
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Lia M. Bixler;
Lia M. Bixler
Department of Zoology, Oregon State University, Corvallis, Oregon 97331. benderr@bcc.orst.edu
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Jennifer P. Lerner;
Jennifer P. Lerner
Department of Zoology, Oregon State University, Corvallis, Oregon 97331. benderr@bcc.orst.edu
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Christopher J. Bayne
Christopher J. Bayne
Department of Zoology, Oregon State University, Corvallis, Oregon 97331. benderr@bcc.orst.edu
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J Parasitol (2002) 88 (1): 14–18.
Citation
Randall C. Bender, Lia M. Bixler, Jennifer P. Lerner, Christopher J. Bayne; SCHISTOSOMA MANSONI SPOROCYSTS IN CULTURE: HOST PLASMA HEMOGLOBIN CONTRIBUTES TO IN VITRO OXIDATIVE STRESS. J Parasitol 1 February 2002; 88 (1): 14–18. doi: https://doi.org/10.1645/0022-3395(2002)088[0014:SMSICH]2.0.CO;2
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