Three experiments were carried out to determine the optimum selenium-vitamin E injection level to maintain acceptable blood selenium (Se) status of does and kids, as well as to determine the relation of that status to mortality rates in kids. In experiment 1, 238 goats were assigned to one of three groups during the mating period: A1-control, A2-0.06mgSe+0.8IU vitE/kgBW and A3-0.125mgSe+1.7IU vitE/kgBW. No differences (P>.05) for fertility and prolificacy were observed among the groups. Blood Se concentration did not differ among Se-vit E groups and control group before injection, and both groups showed Se deficient condition. There was a trend (P<.05, 32%) to increase Se blood level 60 days post-treatment, but difference was not observed between A2 and control groups, while difference (P<.05; 103%) was observed between A1 and A2 groups vs high Se injection (A3 group). In experiment 2, 48 goats were divided into four groups: B1-control, B2-0.125mgSe+1.7IU vitE/kgBW, B3-0.25mgSe+3.4IU vitE/kgBW and B4-0.31mgSe+4.2IU vitE/kgBW. The B4 group reached the highest concentration at the third month after injection (0.11 ppm), then started to decline after 100 days, reaching a value slightly higher than B2 and B3 on the 135 th day of pregnancy. Results of B2 and B3 groups were slightly higher that those of B1 (P<0.05). In experiment 3, 194 kids (3 to 7 days postpartum) born from Se-deficient goats were used to compare the effectiveness of Se injection. They were divided into three groups: C1-control, C2-0.3mgSe+4.2IU vit E/kg BW and C3-0.6mgSe+8.4IU vit E/kg BW. C1 showed the highest percentage of mortality (60%) as compared to treated Se groups, that scored equal percentage of deaths (22% averaged). The concentration of Se in blood, on day 20 th after the onset of the treatment rapidly increased, according with level of Se injection. The 0.3mgSe/kgBW Se injection increased the blood Se concentration in pregnant goats and it was effective to prevent white muscle disease lesions, besides enhancing the survival of kids until weaning. 125mgSe+1,25mgSe+3,31mgSe+4,
SCO2127 and SCO2126 (glkA) are adjacent regions located in Streptomyces coelicolor DNA. glkA encodes glucose kinase (Glk), which has been implicated in carbon catabolite repression (CCR) in the genus Streptomyces. In this work, the glkA and SCO2127 genes from S. coelicolor were used, either individually or together, to transform three mutants of Streptomyces peucetius var. caesius resistant to CCR. These mutants present decreased levels of Glk, and deficiency in glucose transport. When the mutants were transformed with a plasmid containing the SCO2127 sequence, glucose uptake and Glk activity values were increased to levels similar to or higher than those of the original strain, and each strain regained sensitivity to CCR. This result was surprising considering that the putative SCO2127 amino acid sequence does not seem to encode a glucose permease or a Glk. In agreement with these results, an increase in glkA mRNA levels was observed in a CCR-resistant mutant transformed with SCO2127 compared with those of the original strain and the CCR-resistant mutant itself. As expected, recombinants containing the glkA sequence reverted Glk to normal activity values, but glucose uptake remained deficient. The data suggest that the SCO2127 gene product enhances transcription of both genes, and support the first specific role for this region in Streptomyces species. The physiological consequence of this effect is an increase in the glucose catabolites that may be involved in eliciting CCR in this genus.
Potassium efflux in yeast induced by several cationic compounds showed different characteristics. All of the observed efflux required glucose as substrate at the concentrations used. For most of them, the phenomenon required binding of the cationic compound to the cell surface and increased with the negative cell surface charge, and for all the compounds tested, it depended on a metabolizable substrate. Efflux induced with terbium chloride appeared more likely due to the function of a K+/H+ antiporter. With DEAE-dextran and dihydrostreptomycin, potassium efflux was dependent on the cell potassium content and was also sensitive to osmotic changes of the medium. DEAE-dextran-provoked efflux was not due to cell disruption. Dihydrostreptomycin seemed to activate a potassium efflux system which could not be studied in isolation, but its inhibition of potassium uptake may also be involved. Except for cells treated with ethidium bromide, no appreciable cell disruption was observed. The potassium efflux observed appears to be a membrane phenomenon reversible after washing with magnesium chloride.
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