|Obeidat, B - NEW MEXICO STATE UNIVERSI|
|Vogt, M - NEW MEXICO STATE UNIVERSI|
|Krehbiel, C - OKLAHOMA STATE UNIVERSITY|
|Remmenga, M - NEW MEXICO STATE UNIVERSI|
|Clayshulte-Ashley, A - NEW MEXICO STATE UNIVERSI|
|Whittet, K - NEW MEXICO STATE UNIVERSI|
|Hallford, D - NEW MEXICO STATE UNIVERSI|
|Hernandez, J - NEW MEXICO STATE UNIVERSI|
Submitted to: Journal of Animal Science
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 7, 2003
Publication Date: January 1, 2005
Citation: Obeidat, B.S., Strickland, J.R., Vogt, M.L., Taylor, J.B., Krehbiel, C.R., Remmenga, M.D., Clayshulte-Ashley, A.K., Whittet, K.M., Hallford, D.M., Hernandez, J.A. 2005. Effects of locoweed on serum swainsonine and selected serum consituents in sheep during acute and subacute oral/intraruminal exposure. Journal of Animal Science. J.Animal Science 2005. 83:466-477. Interpretive Summary: Because certain serum constituents such as alkaline phosphatase change within 22 h following first exposure, and considering that cell death and tissue damage does not occcur until several days ater locoweed ingestion, we speculate that acute changes are the result of altered glycoprotein processing and not cttotoxicity. Therefore, it is plausible that a no-effect level of swainsonine consumption would allow producers to develop a safe management protocol for locoweed-infested areas. If a no-effect level exists, it will be below 0.2 mg swainsonine*kg of BW^-1*d^-1. However until a full accounting of the acute effects of the toxicant are defined, care should be exercised in making recommendations concerning limit grazing.
Technical Abstract: A study was conducted to evaluate the effects of acute and subscute locoweed exposure on serum swainsonine levels and selected serum constituents in sheep. Thirteen mixed breed wethers- Body Weight (BW) =47.5+/- 9.3 kg - were randomly assigned to either 0.2, 0.4, or 0.8 mg swainsonine*kg BW^-1*d^-1 treatment. During acute (24 h) and subacute (19 d) exposure, serum swainsonine was detected in all treatments and was greatest (P<0.03) in the 0.8 mg treatment. Serum alkaline phosphate (ALK-P) activity was increased (P<0.01) for the 0.8 mg treatment compared with baseline (h 0) starting at h 7 and continued to increase (P<0.01) in serum ALK-P activity was noted with the rate being 3.00+/-0.56 U*L^-1*h^-1. Serum ALK-P activity was increased (P<0.05) across treatments on d 7 over d -19, -12, 0, 1, 21, and 26; on d 14 over d -19, -12, 0, and 26; and on d 19 over d -19, -12, 0, 1, 21, and 26. By d 20, approximately 48 h after last exposure to swainsonine, serum ALK-P activities were no longer different (P=0.13) than baseline (d-19, -12, and 0) and by d 26 values had generally returned to baseline. No linear (P=0.98), quadratic (P=0.63) or cubic effects of swainsonine with hour from exposure were noted for serum aspartate aminotransferase (AST). No treatment x time interaction was found for serum activities over the entire course of the study. Similar to serum ALK-P activities, serum AST activities were increased (P<0.05) across the study. Total serum Fe was reduced (P<0.05) within the initial 22 h following the swainsonine mg/L. Concentrations of ceruloplasmin were lower (P<0.06) on d 7, 14, 19, and 30 than d -12 and 0 (baseline values). There was a linear (slope=0.33 mg*dL^*d^-1; P,0.01) effect with time of exposure to locoweed (i.e., swainsonine) on serum triglyceride levels. Triodothyronine was greater (P=0.001) on d 0 22 h after initial exposure to locoweed than all other days during the study. Linear (P<0.06) and quadratic (P=0.0003) effects and Fe levels without parallel changes in other cell damage markers indicate that acute exposure may result in impaired production and health prior to the events of cytoxicity thought to induce clinical manifestation of locoism.