Abstract
Twenty-five 42-days old New Zealand white rabbits were weaned and accustomed to a control ration in the 1st week and randomly allotted to five groups of five rabbits each. They were offered the control ration (G-1), and in other groups a portion of the control ration was replaced by Leucaena leaf meal (LLM) treated with 1.2% FeCl 3 or untreated i.e. 25% LLM (G-2), 50% LLM (G-3), 25% treated LLM (G-4), and 50% treated LLM (G-5) ration in pelleted form in a 8 weeks feeding cum metabolism trial. Average intake of mimosine and 3,4 DHP (dihydroxypyridone) was 304.6 and 129.5; 680.2 and 212.3; 279.6 and 147.6; and 643.1 and 239.9 mg day −1 in G-2–G-5, respectively. Mimosine and 2,3 DHP were not detected in faeces. The faecal excretion of 3,4 DHP (as % intake of mimosine plus 3,4 DHP) in the rabbits of groups G-4 (43.5) and G-5 (40.6) was significantly ( P<0.05) higher due to FeCl 3 treatment as compared to excretion in groups G-2 (30.1) and G-3 (21.4) fed untreated LLM. GOT (Glutamic oxalacetic transaminase), GPT (Glutamic-pyruvic transaminase), T 3 (tri-iodothyronine) and T 4 (thyroxine) levels in blood were within normal physiological range. Mimosine 3,4 DHP and 2,3 DHP, all were excreted through urine. The urinary excretion of 3,4 DHP was significantly lower ( P<0.05) in G-4 and G-5. The overall excretion of DHP (2,3 and 3,4 DHP) was similar in all the groups. Severe hepatic and kidney damage occured in G-2 and G-3, while, in G-4 and G-5 very mild or no damage to liver and kidney was recorded. All tissues were devoid of mimosine, but DHP was present in liver, kidney and lungs. The maximum DHP in liver indicated as the primary site of DHP metabolism. In vitro incubation of LLM with caecal contents revealed 72.68–100% microbial degradation of mimosine. The overall DHP degradation ranged from 7.10% to 37.81% being the highest in G-3. The results indicated that, FeCl 3 treated leucaena could be used in commercial meat rabbit rations.
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