Effect of dietary protein on zinc phosphide toxicity in albino rats (Rattus norvegicus).

Adult male and female albino rats (R. norvegicus) were administered rodenticide, zinc phosphide ranging from 4, 2, 1, 0.5, 0.25 and 0.125% in the diet containing 10(A), 17(B) and 24%(C) protein. Zinc phosphide induced 100% mortality at 4, 2, 1, 0.5% in diet A; 4 and 2% in diet B; and 4% in diet C. The results reveal influence of dietary protein in modulating the toxicity of zinc phosphide, suggesting that greater caution should be exercised while formulating its baits for effectiveness. The results also suggest that baits having 10% protein are more suitable to carry the rodenticide from view point of acceptability and efficacy towards the target species.

Efficacy of zinc therapy in prevention of crisis in sickle cell anemia: a double blind, randomized controlled clinical trial.

145 patients were recruited in the trial while 130 completed it. Patients were randomized to receive zinc sulphate capsules. 220 mgm three times a day or identical placebo. Major outcome variable was 'Sickle cell crisis'. After a follow up of 1.5 years, the mean number of episodes of crisis was 2.46 +/- 1.04 in the intervention group and 5.29 +/- 2.58 in the control group (p < 0.025; 95% CI for difference between groups: 1.98, 3.42). Mean duration of hospital stay was 4.3 +/- 2.2 days in the intervention group and 3.9 +/- 1.6 days in the control group. The difference was not significant (p > 0.05). There was a significant reduction of the mean number of infective episodes and associated morbidity in patients with sickle cell anaemia.

Cómo estar seguro de que el anciano toma suficiente zinc? / How is secure of that the old man to ingest sufficient zinc?

La mayoría de los ancianos prefieren como fuente de zinc los alimentos más que los suplementos (que además pueden alterar el metabolismo del cobre y del hierro). La inclusión en su dieta diaria de una cantidad moderada de carne, ave y pescado aumentará los aportes de zinc y, junto con los restantes nutrientes esenciales, contribuirá a mejorar su situación nutricional general

Changes induced by zinc on thyroxine deiodination by rat liver in vivo and in vitro

Se estudió el efecto de la administración in vivo o del agregado in vitro de zinc sobre la deiodinación 5'de la tiroxina (T4) por el hígado de rata y sobre la concentración hepática de grupos sulfhidrilos libres (NPSH). Se usaron ratas Wistar macho de 200-240g de peso corporal. A un grupo de 12 ratas se les inyectó i.p. sulfato de zinc 2mg/Kg de peso, 24h antes de iniciar el estudio. Se sacrificaron los animales por dislocación cervical y el hígado fue inmediatamente homogeneizado. Se agregó a los homogenatos dithithreitol (DTT) (0,2.5,5 o 10mM concentración final) y 1µCi de 125I-T4. Para los estudios in vitro en animales sin tratar, se agregó al homogenato de hígado sulfato de zinc o cloruro de cadmio (2.5 o 5mM) más DTT y T4 marcada. Todos los homogenatos fueron incubados durante 90 min a 37ºC y luego cromatografiados en papel Whatman 1. Las ratas inyectadas con zinc tuvieron una disminución significativa (p<0.01) de la deiodinación de T4, de la producción de 125 iodo (P<0.02) y de triiodotironina (T3) (P<0.05). En los estudios in vitro, el agregado de zinc o cadmio disminuyó significativamente la degradación de T4 (P<0.02) y la producción de iodo (P<0.02 para el zinc y P<0.05 para el cadmio) y de T3 (P<0.05). La concentración hepática de NPSH en los animales inyectados con zinc fue normal. La concentración sérica de T4 y T3 en los animales inyectados con zinc fue normal pero en los inyectados con cadmio se redujo significativamente (P<0.01 para T4 y P<0.02 para T3). Los resultados indican que el zinc inhibe la actividad de la 5'-deioidnasa hepática, por um mecanismo probablemente relacionado con la unión del metal a los grupos sulfhidrilos de la enzima

A study of the effect of oral zinc supplementation during pregnancy on pregnancy outcome.

Women in different trimesters of pregnancy (Group B; n = 106) were administered 200 mg zinc sulphate (elemental Zn 45 mg) orally/day from the day of reporting till delivery. Untreated group of 62 served as control. Levels of zinc in maternal serum, umbilical cord blood serum, and urine were estimated. Pregnancy outcome was assessed in terms of incidence of prematurity, IUGR, birth weight; apgar score and gestational age. Serum zinc levels in Gp. A declined significantly from 113.00 +/- 2.80 ug/dl in I trimester to 83.78 +/- 2.20 ug/dl in III (P < 0.001). Following zinc supplementation (Gp. B) serum zinc levels increased significantly from 109.70 + 3.23 micrograms/dl to 205.40 +/- 4.47 micrograms/dl (P < 0.001). Urinary excretion of zinc in Gp. A declined significantly with increase in the period of gestation. However in Gp. B, elimination of Zn increased significantly in proportion with the serum levels (P < 0.001) cord blood serum zinc level was normal irrespective of maternal serum Zn levels. Following oral Zn supplementation, levels increased significantly from below 127.0 micrograms/dl to above 158.0 micrograms/dl in Gp. B (P < 0.001). Maternal serum and cord blood serum zinc ratios were fairly constant in Gp. A as well as in Gp. B. Birth weight of babies born with Zn supplementation was significantly higher than control and was related to duration of oral zinc supplementation (P < 0.001). Gestational age of babies in Gp. B was significantly higher than respective controls when Zn supplementation was given for more than 3 months (P < 0.01), and was related to duration of zinc therapy (P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)