Skip to main content
ARS Home » Pacific West Area » Logan, Utah » Poisonous Plant Research » Research » Publications at this Location » Publication #268412
Title: Selenium reverses Pteridium aquilinum-induced immunotoxic effects

Author
item LATORRE, A - Universidad De Sao Paulo
item CANICEIRO, B - Universidad De Sao Paulo
item WYSOCKI, H - Biological Institute, Brazil
item HARAGUCHI, M - Biological Institute, Brazil
item Gardner, Dale
item GORNIAK, S - Universidad De Sao Paulo

Submitted to: Food and Chemical Toxicology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 11/20/2010
Publication Date: 2/1/2011
Citation: Latorre, A.O., Caniceiro, B.D., Wysocki, H.L., Haraguchi, M., Gardner, D.R., Gorniak, S.L. 2011. Selenium reverses Pteridium aquilinum-induced immunotoxic effects. Food and Chemical Toxicology. 49(2):464-70.

Interpretive Summary: Pteridium aquilinum, also known as bracken fern, is one of the most common plants in the world and can be poisonous to livestock and humans. The toxic compound in bracken fern is considered to be the terpene glycoside known as ptaquiloside. Most recently bracken fern was shown to be immunotoxic in a mouse model system. It is also known that selenium is not only essential to the normal function of immune cells but also improves immune response. The objective of this study was to verify if the toxic compound ptaquiloside, found in bracken fern, is responsible for the immunotoxic effects of the plant and whether the effects can be reversed by selenium supplementation. Using a mouse model assay system, animals were treated with either bracken fern extract, purified ptaquiloside and with and without co-administration of selenium. The results from the study clearly show that the ptaquiloside had the same immunotoxic effects as bracken fern and that selenium supplementation can prevent as well as reverse these effects.

Technical Abstract: We have previously shown that bracken fern (Pteridium aquilinum) has immunomodulatory effects on mouse natural killer (NK) cells by reducing cytotoxicity. Alternatively, it has been demonstrated that selenium can enhance NK cell activity. Therefore, the aims of the present study were to evaluate if ptaquiloside, the main toxic component found in P. aquilinum, is responsible for the immunotoxic effects observed in mice, and if selenium supplementation could prevent or even reverse these effects. Male C57BL/6 mice were administered the P. aquilinum extract by daily gavage for 30 days, and histological analyses revealed a significant reduction in splenic white pulp area that was fully reversed by selenium treatment. In addition, mice administered ptaquiloside by daily gavage for 14 days demonstrated the same reduction of NK cell activity as the P. aquilinum extract, and this reduction was prevented by selenium co-administration. Lastly, non-adherent splenic cells treated in vitro with an RPMI extract of P. aquilinum also showed diminished NK cell activity that was not only prevented by selenium co-treatment but also fully reversed by selenium post-treatment. The results of this study clearly show that the immunosuppressive effects of P. aquilinum are induced by ptaquiloside and that selenium supplementation can prevent as well as reverse these effects.