J. Anim Sci.
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J. Anim Sci. 1985. 60:226-231.
© 1985 American Society of Animal Science

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Duration of Inhibition of 3-Methylindole Production by Monensin1,2,3,

D. C. Honeyfield4, J. R. Carlson4, M. R. Nocerini4 and R. G. Breeze5

Washington State University, Pullman 99164-6320

Abstract

A series of in vitro and in vivo trials was conducted to determine if continuous monensin feeding for up to 56 d would reduce ruminal conversion of L-tryptophan (TRP) to 3-methylindole (3MI). Fourteen mature beef cows were adapted to a maintenance diet for 3 wk. In trial I, the sampling time to optimize 3MI production was determined. Trials II through IV were to determine the duration of efficacy of monensin on reducing 3MI concentrations in vitro and in vivo. During trials II, III and IV one-half of the cows were fed 200 mg monensin·head–1·d–1 for 21, 36 and 55 d, respectively, while the remaining cows served as controls. All cows were fed the control diet for 21 d between each trial. Volatile fatty acid (VFA) concentrations and in vitro conversion of TRP to 3 MI were determined in ruminal fluid samples collected during trials I through IV. On d 28 of trial IV, all cows were given an oral dose of .35 g TRP/kg of body weight to induce acute bovine pulmonary edema and emphysema (ABPE). Ruminal concentrations of 3MI and indole were measured at intervals for 96 h. Results of trial I demonstrated that ruminal fluid collected 15 h postfeeding produced the highest in vitro conversion of TRP to 3MI. Therefore, ruminal fluid samples were collected at that time in trials II, III and IV. In vitro conversion of TRP to 3MI was lower (P<.01) in samples from monensin-treated cows (12.1%) compared with controls (25.6%). Monensin reduced 3 MI production for 55 d, the longest time tested in these experiments. Conversion of TRP to indole, a secondary degradation product, also was lower (P<.05) in samples from monensin-treated cows (4.3%) vs controls (5.8%). The addition of 5 µg/ml of monensin to the in vitro incubations further depressed 3MI production, suggesting that ruminal micro- organisms remain sensitive to monensin and amounts of dietary monensin above the 200 mg·head–1·d–1 may be beneficial to further reduce 3MI production. Monensin increased ruminal propionate and decreased acetate in all trials (P<.05). Total VFA production averaged 79 µmol/ml and was not different between groups. Monensin reduced in vivo 3MI production (P<.05) at 12, 18 and 24 h after TRP challenge. Five control cows died from ABPE while only one cow in the monensin-treated group died. These results demonstrate that monensin reduced acute clinical cases of ABPE when prefed for 28 d and was effective in reducing in vitro 3MI formation for 55 d.


Footnotes

1 Scientific Paper No. 6670. College of Agriculture and Home Economics Research Center, Washington State Univ., Pullman. Project 1893.

2 Supported in part by NIH grant HL-13645 and a gift from Elanco Products Co., Greenfield, IN.

3 The authors thank Karen Weller for her technical assistance.

4 Dept. of Anim. Sci.

5 Dept. of Vet. Microbiol. Pathol.







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Copyright © 1985 by the American Society of Animal Science.