Gene/Protein Disease Symptom Drug Enzyme Compound
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Indole and 3-methylindole (3MI) are ruminal metabolites of L-tryptophan (TRP) and have similar physical and chemical properties. 3-Methylindole causes acute bovine pulmonary emphysema (ABPE). The effects of indole when administered orally to cows were determined. Four mature Holstein cows were given increasing doses of 0.05, 0.1 and 0.2 g indole per kg body-weight orally at two-week intervals. The animals were killed one week after the last dose. Plasma indole concentrations peaked three house after administration at 4.5, 8.8 and 19.8 microgram per ml after the 0.05, 0.1 and 0.2 doses, respectively. Detectable concentrations of indole (more than 0.02 microgram per ml) persisted in the plasma from three to 25 hours after dosing. Packed cell volume was decreased (P less than 0.01) at 48 and 72 hours after the 0.2 g per kg dose and at 72 hours after the 0.1 g per kg dose. Plasma haemoglobin was increased (P less than 0.05) at 48 hours after the 0.2 and 0.1 g per kg doses. By 72 hours after the 0.2 g per kg dose, all cows had mild diarrhoea and haemolysis and two of the cows had haemoglobinuria. At necropsy, microscopic lesions of haemoglobinuric nephrosis were seen in all four cows. No lesions of ABPE were found in any of the animals.
Vet Rec 1980 Oct 11
PMID:Indole toxicity in cattle. 721 Apr 36

The pathogenesis of acute bovine pulmonary oedema and emphysema (ABPE) is related to the ruminal formation of 3-methylindole (3MI) from L-tryptophan (TRP), a naturally occurring amino acid and constituent of forage. The objectives of the present study were to determine whether monensin and lasalocid, both polyether antibiotics, were effective in reducing ruminal conversion of TRP to 3MI in vivo and to confirm that reduction in ruminal conversion of TRP to 3MI prevented tryptophan induced ABPE. Sixteen mature Hereford cows were assigned to one of four groups and given TRP to induce ABPE. Group 1 was given 100 mg monensin orally twice daily starting one day before and ending four days after TRP dosing. Group 2 was given 200 mg monensin once daily and group 3 was given 100 mg lasalocid twice daily. Group 4, the control, was given only TRP without further treatment. All control cows developed clinical signs of respiratory disease and lesions of ABPE; one control cow died of ABPE. Mean ruminal 3MI concentrations in control cows reached a peak of 36.4 micrograms per ml. Clinical signs of pulmonary disease appeared in two cows treated with lasalocid and one died. Mean ruminal 3MI in these animals peaked at 38.8 micrograms per ml. No clinical signs of respiratory disease were observed in any of the monensin treated cows and at necropsy there were no pulmonary lesions of ABPE. Mean ruminal 3MI concentrations in monensin treated cows did not exceed 8.9 micrograms per ml. In all groups plasma 3MI concentrations generally reflected ruminal 3MI concentrations but at lower concentrations. The results of this experiment demonstrate that reduction in ruminal 3MI formation by monensin prevents tryptophan induced ABPE.
Vet Rec 1980 Oct 04
PMID:Prevention of tryptophan-induced acute bovine pulmonary oedema and emphysema (fog fever). 746 89