Previous studies have shown that the feeding of putrescine, a biogenic amine and the precursor of the mammalian polyamines, can promote whole-body growth of chicks. The current study was undertaken to determine the effect of spermine, also a biogenic amine and the most cationic of the polyamines, under similar conditions. In Exp. 1, 120 week-old chicks were fed purified crystalline amino acid-based diets containing 0, .2, .4, .6, .8, or 1.0% spermine for 14 d. Spermine proved highly toxic and growth rates were reduced compared with controls when even .2% was fed. In Exp. 2, chicks were fed 0, .0375, .0750, or .1000% spermine. These concentrations proved less toxic than those used in Exp. 1. Supplemental dietary cysteine was then provided at 0, .3, .6, and .9% together with 0, .025, .050, or .400% spermine (Exp. 3) because depletion of cellular glutathione has been suggested as contributing to spermine's toxicity. Even high levels of cysteine supplementation did not overcome spermine's toxicity. Subsequent dietary provision of L-2-oxothiazolidine-4-carboxylic acid (OTC, Exp. 4), a cysteine prodrug, showed that depletion of cellular glutathione was not likely a cause of spermine toxicosis. A trend toward increased weight gain and feed efficiency was observed when low concentrations of spermine were fed. It was concluded, however, that dietary spermine was more toxic to chicks than was previously seen for putrescine, that any growth-promoting effects of dietary spermine are small, and that supplements of dietary cysteine or OTC are unlikely to increase these effects by overcoming spermine toxicosis.

Experiments were conducted to determine the relative growth-promoting potential and toxicity of dietary spermidine, a biogenic amine and polyamine. Week-old chicks were fed purified diets containing 0.0, 0.2, 0.4, 0.6, 0.8, or 1.0% supplemental spermidine for 2 weeks. As little as 0.4% supplemental spermidine depressed growth and hepatic ornithine decarboxylase activity, while hepatic concentrations of putrescine, spermidine, and N 1-acetylspermidine increased. In a second experiment, 0.00, 0.05, 0.10, 0.20, and 0.60% supplemental spermidine were fed. Low levels of supplemental spermidine tended to increase relative weights of the duodenum and pancreas. The temporal response to 0.00, 0.05, and 0.60% supplemental spermidine was determined in a third experiment when measurements were taken following 1, 2, 4, and 8 days of feeding. Chicks fed diets containing 0.05% supplemental spermidine had increased growth after only 1 day of feeding. Enlargement of the duodenum and pancreas was subsequently seen, although these changes became less obvious with time. It was concluded that the toxicity of polyamines increases with molecular weight and charge and, although some growth promotion is possible, the biogenic amine content of suspect feedstuffs should be determined before feeding with caution. Keywords: Spermidine; polyamine; growth; toxicity

The inclusion of isolated soy protein in milk replacer diets for calves and neonatal pigs inhibits development of intestinal mucosal cells. Simultaneous administration of putrescine partially overcomes this effect. We therefore conducted experiments to determine the potential for dietary putrescine to overcome the toxicity of raw soybeans in chicks. In the first experiment, week-old chicks were fed either an isolated soy protein-based control diet or an isoenergetic and isonitrogenous diet containing 52% raw, ground soybeans for 14 d. The feeding of raw soybeans depressed (P < .001) growth and feed consumption, caused enlargement (P < .001) of the duodenum and pancreas, depressed (P < .001) activities of polyamine synthetic enzymes in the duodenum, and reduced (P < .01) duodenal tissue concentrations of putrescine. In the second experiment, the diet containing raw soybeans was fed with and without .2, .3, and .4% supplemental putrescine. The feeding of supplemental putrescine largely overcame the inhibition of growth due to the feeding of raw soybeans and increased intestinal putrescine concentrations. Putrescine supplementation had no effect, however, on pancreatic and intestinal enlargement in birds fed raw soybeans and tended to depress the activity of polyamine synthetic enzymes. The beneficial effects of putrescine supplementation were confirmed in the third experiment when up to 1.0% supplemental putrescine was fed. We conclude that the toxicity of raw soybeans to chicks can be overcome by feeding putrescine. These effects are likely due to improved nutrient uptake by overcoming the adverse effects of lectins in the intestinal tract and are not likely due to alleviation of the pancreatic enlargement caused by protease inhibitors.