The expulsion of a primary infection of Trichinella spiralis was studied in rats fed diets containing (per kg diet) either 3 mg Zn [zinc deficient (Zn-)] or 40 mg Zn [zinc adequate (Zn+)]. A dose of 2000 muscle larvae (ML) impaired weight gain (mg/g body wt) in all groups compared with uninfected controls [eg, 0-7 d postinfection (dpi): infected Zn-, -105 +/- 10 (means +/- SEM); uninfected Zn-, 54 +/- 19 (p less than 0.001)]. In a study with 20.5 ML/g body wt, some Zn- rats were transferred at the time of infection to the zinc-adequate diet. [This was the zinc-repleted group (ZnR).] Both groups retained a group of pair-fed controls (Zn-PF and ZnRPF). The percentage dose established at 7 dpi was similar in all groups (32.5-39.3%) but at 13 dpi recoveries were 19.4 +/- 2.2% for Zn-, 0.1 +/- 0.1% for Zn-PF, 1.6 +/- 0.9% for ZnR, 0.6 +/- 0.2% for ZnRPF, and 4.1 +/- 2.2% for Zn+ (p less than 0.001). Up to 13 dpi, all groups except ZnR lost weight. These results show that zinc deficiency impairs the expulsion of T spiralis in rats.

The effect of picolinic acid (pyridine-2-carboxylic acid) on the efflux of divalent metal ions from multilamellar liposomes was examined to determine the possible specificity and mechanism for its reported beneficial effects on the intestinal absorption and systemic metabolism of zinc. Extraliposomal picolinic acid increased the efflux of Zn, Cu, Co, Mn, Ni, Cd, Pb, Fe(II) and Ca from the vesicles. However, when picolinic acid was trapped with Co, Cu and Zn within the liposomes, the loss of metals was reduced. In a partition study, picolinic acid increased the aqueous solubility of Zn, Cu, Co and Cd at alkaline pH, but did not transfer the metal to an organic bulk phase of chloroform. It is proposed that picolinic acid does not act as an ionophore and that any effect it may have on zinc metabolism is dependent upon its unselective chelating properties, which may also lead to altered dietary and systemic compartmentation of other divalent cations.

The course of a subcutaneous weight-related infection with Strongyloides ratti was followed in rats fed diets containing either 3 mg Zn/kg diet [zinc deficient (Zn-)] or 40 mg Zn/kg diet [zinc adequate (Zn+)]. At 19 d postinfection (dpi) the proportions of larvae persisting in the intestines as adult worms were 52 +/- 2% (means +/- SEM) for Zn-, 39.5 +/- 2.5% for pair-fed Zn- (Zn-PF), and 31.6 +/- 3.2% for Zn+ (p less than 0.001, analysis of variance); some Zn- rats were then transferred to the zinc-adequate diet [This was the zinc-repleted group (ZnR).] Both groups retained a group of pair-fed controls (Zn-PF and ZnRPF). Between 19 and 28 dpi ZnR animals gained weight faster than did Zn- animals and had heavier thymuses relative to body weight. Zinc deficiency enhances the establishment of S ratti larvae in the intestine of rats and alters the characteristics of intestinal expulsion of the nematodes; however, spontaneous cure was achieved by 38 dpi in both Zn- and control groups.

No abstract

The role of zinc (Zn) in the immunological expulsion of the nematode Nippostrongylus brasiliensis (Nb) from the small intestine of the rat was investigated. Three groups of 28 rats each were fed a basal diet providing either 3 mg Zn/kg for the zinc-deficient group (-Zn) or 40 mg Zn/kg for ad libitum-fed and pair-fed controls. After 6 wk each group was divided into two equal subgroups and infected with either 1000 or 4000 infective Nb larvae/rat. The -Zn rats showed significant reductions (P less than 0.001) in food intake, weight gain and food conversion efficiency when compared to the rats fed ad libitum but not when compared to the pair-fed controls. Plasma zinc concentration in the -Zn rats (0.50 microgram/ml) was significantly lower than in both ad libitum-fed (1.33 micrograms/ml) and pair-fed (1.45 micrograms/ml) controls (P less than 0.001). The recovery of worms from the rats 3, 7 and 12 d postinfection was similar for the corresponding day and dose of infection in all groups. Expulsion was almost complete in all groups by 12 d post-infection. There were no significant differences in size and fecundity of worms recovered from the different groups of rats on 7 d postinfection. However, over the whole period of infection, the -Zn rats excreted significantly more parasite eggs than did controls (P less than 0.001). These results indicate that although zinc deficiency affected growth performance of the rats, it did not affect the establishment or expulsion of Nb. Impairment of the immune response of the zinc-deficient rat was manifested only by a significant increase in the number of parasite eggs excreted in feces.