Avaliação dos efeitos de 5-hidroxitriptofano em-hidroxibenzilhidrazine associados a Lactobacillus spp. na morfometria intestinal e imunomarcação de serotonina em frangos de corte desafiados com Salmonella Enteridis / Assessment of the effects of 5-hydroxytryptophan and m-hydroxybenzyl hydrazine associated with Lactobacillus spp. in intestinal morphology and immunostaining of serotonin in broilers challenged with Salmonella Enteritidis.

As células enterocromafins são um dos componentes da mucosa intestinal que liberam serotonina para o lúmen, promovendo atividades secretórias e crescimento celular de vários tecidos, incluindo vilosidades intestinais. O presente estudo avaliou as influências do 5-hidroxitriptofano (5HTP) e do m-hidroxibenzilhidrazine (NSD1015), associados a Lactobacillus spp., sobre o peso corporal e o desenvolvimento das vilosidades intestinais na porção proximal do duodeno de frangos de corte desafiados com Salmonella Enteritidis. Verificou-se também se a presença de Lactobacillus spp. e Salmonella Enteritidis influenciaram a imunomarcação de serotonina no duodeno e, para isso, o estudo foi dividido em dois experimentos, com e sem desafio por S. Enteritidis. No Experimento 1, em aves sem desafio, os pesos corporais não diferiram significantemente (p>0,05) e, no Experimento 2, aves com desafio, os tratamentos com o precursor isolado e associado a Lactobacillus spp. determinaram maior peso corporal das aves. Nos dois experimentos, as aves tratadas com 5HTP apresentaram aumento na densidade e altura das vilosidades no duodeno, sugerindo a atuação de 5HTP como um agente trófico. A administração de Lactobacillus spp. também determinou altura maior de vilosidades duodenais. Quanto a imunomarcação de serotonina, as aves tratadas com Lactobacillus spp. no Experimento 1 e as aves tratadas com Lactobacillus spp. e desafiadas com S. Enteritidis no Experimento 2, apresentaram valores superiores aos demais tratamentos, sugerindo que a presença destas bactérias promove maior liberação de serotonina para o duodeno, porém o mecanismo exato de como este processo ocorre necessita ser mais elucidado.(AU)

Enterochromaffin cells are components of the intestinal mucosa to release serotonin lumen, promoting cell growth and secretory activity of various tissues, including intestinal villi. This study evaluated the influence of 5-hydroxytryptophan (5HTP) and m-hidroxibenzilhidrazine (NSD1015) associated with Lactobacillus spp. on body weight and development of intestinal villi in the proximal duodenum of broilers challenged with Salmonella Enteritidis. It was found that the presence of Lactobacillus spp. and Salmonella Enteritidis influenced immunostaining of serotonin in the duodenum. The study was divided into two experiments with and without challenge by S. Enteritidis. In Experiment 1, birds without challenge, body weights did not differ significantly (p>0.05), and in Experiment 2, the treatments with precursor and precursor associated with Lactobacillus spp. determined higher body weight of the birds. In both experiments the birds treated with 5HTP showed increased density and villus height in the duodenum, suggesting the presence of 5HTP as a trophic agent. The use of Lactobacillus spp. also determined greater duodenal villus height. The immunostaining of serotonin, birds treated with Lactobacillus spp. in Experiment 1, and the birds treated with Lactobacillus spp. and challenged with S. Enteritidis in Eperiment 2 showed higher values, suggesting that the presence of these bacteria promotes greater release of serotonin into the duodenum. The exact mechanism of how this process occurs needs to be further elucidated.(AU)

Folinic acid therapy in treatment of dihydropteridine reductase deficiency.

We gave folinic acid to three siblings, and to a fourth child, who have or had dihydropteridine reductase (DHPR) deficiency. The youngest began folinic acid therapy in addition to neurotransmitter precursors and a phenylalanine-restricted diet at age 2 months, and at 2 years of age has near normal development without evidence of neurologic impairment. His older brother began similar treatment at 5 1/2 months of age, when early neurologic findings were evident. At age 6 years his mental retardation and neurologic impairment are less severe than reported in most patients with DHPR deficiency. Little improvement occurred in their sister, who first received treatment at 2 years of age, when she already had severe neurologic impairment. An unrelated boy with profound neurologic impairment showed subtle signs of improvement after he began treatment with folinic acid alone at age 9 years. These results provide evidence that folinic acid is important in the treatment of DHPR deficiency and, if begun early in infancy, may prevent irreversible neurologic damage. The mechanism of folinic acid action in DHPR deficiency may be to increase indirectly the synthesis of 5-methyltetrahydrofolate.