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1.
A conventional balance study with 48 male weanling rats was conducted to determine true absorption and endogenous fecal excretion
of manganese (Mn) in relation to dietary Mn supply, following the procedures of a previously adapted isotope dilution technique.
After 10 d on a diet with 1.5 ppm Mn, eight animals each were assigned to diets containing 1.5, 4.5, 11.2, 35, 65, or 100
ppm Mn on a dry-matter basis. Three days later, each rat was given an intramuscular54Mn injection and kept on treatment for a balance period of 16 d.
Apparent Mn absorption assessed for the final 8 d, averaged 8.6 μg/d without significant treatment effects, although Mn intake
ranged from 18.6 to 1200 μg/d, in direct relation to dietary Mn concentrations. Mean fecal excretion of endogenous Mn for
the six treatments was 0.9, 2.7, 7.4, 11.0, 16.3, and 17.7 μg/d, respectively. These values delineate the rates to which true
absorption exceeded apparent rates. True absorption, as percent of Mn intake, averaged 28.7, 15.9, 11.7, 6.1, 3.4, and 2.0,
respectively, as compared with mean values of 23.9, 10.9, 6.2, 3.4, 1.2, and 0.5 for percent apparent absorption. It was concluded
that both true absorption and endogenous fecal excretion markedly responded to Mn nutrition and that the reduction in the
efficiency of true absorption was quantitatively the most significant homeostatic response for maintaining stable Mn concentrations
in body tissues. 相似文献
2.
The ATP-binding-cassette transmembrane transporters (ABC transporters)
known from vertebrates belong to four major subfamilies: (1) the P-
glycoproteins (Pgp); (2) the cystic fibrosis transmembrane conductance
regulators (CFTR); (3) the Tap proteins encoded with the major
histocompatibility complex of mammals; and (4) the peroxisomal membrane
proteins. Both Pgp and CFTR have a structure suggesting a past internal
gene duplication; a phylogenetic analysis indicated that these duplications
occurred independently, while an independent tandem gene duplication
occurred in the case of the Tap family. Both the Pgp and Tap proteins show
evidence of relationship to bacterial ABC transporters lacking internal
duplication, and both are significantly more closely related to the HlyB
and MsbA families of transporters from purple bacteria than they are to ABC
transporters from nonpurple bacteria. The simplest hypothesis to explain
this observation is that eukaryotic Pgp and Tap genes are descended from a
mitochondrial gene or genes that were subsequently translocated to the
nuclear genome. The Pgp genes of eukaryotes are characterized by a
remarkable degree of convergent evolution between the ATP-binding cassettes
of their N- terminal and C-terminal halves, whereas no such convergence is
seen between the two halves of CFTR genes or between the duplicated Tap
genes. Exon 13 of the CFTR gene, which encodes a putative regulatory domain
not found in other ABC transporters apart from CFTR, showed high levels of
both synonymous and nonsynonymous difference in comparisons among different
mammalian species, suggesting that this region is a mutational hot spot.
相似文献
3.
4.
X Xiao G Hintermann AL Demanin J Piret 《Journal of industrial microbiology & biotechnology》1996,16(4):261-262
Streptomyces glaucescens is shown to possess -lactamase activity which is inhibitable by clavulanate. This is important in regard to its use as a cloning host for enzymes of \-lactam biosynthesis. 相似文献
5.
The present study was conducted to investigate the effect of zinc deficiency on fatty acid desaturation in rats fed two different
types of dietary fat, a mixture of coconut oil and safflower oil (7∶1, w/w, “coconut oil diet”) or linseed oil (“linseed oil
diet”). In order to ensure an adequate food intake, all rats were force-fed by gastric tube. Zinc deficiency caused statistical
significant reducion of Δ9-desaturase activity in liver microsomes of rats fed coconut oil diet and tendencial reduction (p<0.15) in rats fed linseed oil diet compared with control rats fed diets with the same type of fat. In agreement with this
effect, zinc deficiency in the rats fed both types of dietary fat increased the ratio between total saturated and total monounsaturated
fatty in liver phospholipids and liver microsomes. Zinc deficient rats on the coconut oil diet had unchanged Δ6-desaturase
activity with linoleic acid as substrate and lowered activity with α-linolenic acid as substrate. In contrast, zinc deficient
rats on the linseed oil diet had increased Δ6-desaturase activity with linoleic acid as substrate and unchanged activity with
α-linolenic acid. Because linoleic acid is the main substrate for Δ6-desaturase in the rats fed coconut oil diet, and α-linolenic
acid is the main substrate in the rats fed linseed oil diet, it is concluded that in vivo Δ6-desaturation was not changed
by zinc deficiency in the rats fed both types of dietary fat. Activity of Δ5-desaturase was also not changed by zinc deficiency
in the rats fed both dietary fats. Levels of fatty acids in liver phospholipids and microsomes derived by Δ4-, Δ5-, and Δ6-desaturation
were not consistently changed by zinc deficiency in the rats fed both types of dietary fat. Thus, the enzyme studies and also
fatty acid composition data of liver phospholipids and microsomes indicate that zinc deficiency does not considerably disturb
desaturation of linoleic and α-linolenic acid. Therefore, it is suggested that similarities between deficiencies of zinc and
essential fatty acids described in literature are not due to disturbed desaturation of linoleic acid in zinc deficiency. The
present study also indicates that zinc deficiency enhances incorporation of eicosapentaenoic acid into phosphatidylcholine
of rats fed diets with large amounts ofn-3 polyunsaturated fatty acids. 相似文献
6.
A review of experimental studies of the effect of zinc nutrition on insulin metabolism is presented. In addition to a short
introduction to the synthesis, secretion, and action of insulin, the effects of zinc deficiency—specifically on glucose tolerance,
insulin secretion, insulin synthesis and storage, and on total insulin-like activity—are dealt with. The concentrations of
zinc and chromium in serum, pancreas, and liver are compared to those of zinc-deficient animals and pair-fed controls.
In contrast to pair-fed controls, zinc-deficient rats had unaltered proinsulin contents after glucose stimulation, but they
showed a diminished glucose tolerance, lowered serum insulin content, and an elevated total insulin-like activity. The serum
zinc concentration of the deficient animals was greatly reduced and did not change during glucose stimulation, whereas it
rose in the case of the pair-fed controls. The serum chromium concentration increased in both groups in response to glucose
stimulation. In the pancreas of the deficient animals, the zinc concentration was reduced 60% and it increased during the
glucose tolerance test. In the liver there were no significant differences. The chromium concentrations were elevated in both
the pancreas and liver of the zinc-deficient rats by 60 and 100%, respectively, and were not influenced by glucose injection.
These studies show clearly that nutritional zinc deficiency influences insulin metabolism and action. 相似文献
7.
A highly polymorphic dinucleotide repeat on the proximal short arm of the human X chromosome: linkage mapping of the synapsin I/A-raf-1 genes. 总被引:4,自引:3,他引:1 下载免费PDF全文
C U Kirchgessner J A Trofatter M M Mahtani H F Willard L J DeGennaro 《American journal of human genetics》1991,49(1):184-191
A compound (AC)n repeat located 1,000 bp downstream from the human synapsin I gene and within the last intron of the A-raf-1 gene has been identified. DNA data-base comparisons of the sequences surrounding the repeat indicate that the synapsin I gene and the A-raf-1 gene lie immediately adjacent to each other, in opposite orientation. PCR amplification of this synapsin I/A-raf-1 associated repeat by using total genomic DNA from members of the 40 reference pedigree families of the Centre d'Etude du Polymorphisme Humaine showed it to be highly polymorphic, with a PIC value of .84 and a minimum of eight alleles. Because the synapsin I gene has been mapped previously to the short arm of the human X chromosome at Xp11.2, linkage analysis was performed with markers on the proximal short arm of the X chromosome. The most likely gene order is DXS7SYN/ARAF1TIMPDXS255DXS146, with a relative probability of 5 x 10(8) as compared with the next most likely order. This highly informative repeat should serve as a valuable marker for disease loci mapped to the Xp11 region. 相似文献
8.
Two groups of 16 rats each were fed the same diet with 12.9 ppm Zn. Nine days after each animal was injected with65Zn for assessing fecal zinc of endogenous origin, zinc intake and excretion were determined for a six-day period at the age
of about five (group I) and nine (II) weeks. At mean growth rates of 5.1 and 5.2 g/day, food consumption per gram of gain
was 2.01 g in group I vs 2.86 g in II. Overall, zinc retention amounted to 21 vs 25 μg Zn/g of gain. Apparent absorption averaged
92 vs 74% of Zn intake (132 vs 189 μg/day), while true absorption averaged 98 vs 92%. It was concluded that endogenous fecal
zinc excretion was limited to the indispensable loss (F
em) in group I (7 μg/day), while it exceeded this minimum loss in group II (33 μg/day). True retention, which reflected total
zinc utilization (true absorption times metabolic efficiency), was derived from apparent absorption plusF
em (11 μg/day for group II according to the greater metabolic body size of the rats). It averaged 98% of Zn intake in group
I vs 80% in group II. The mean metabolic efficiency was 100% vs 87%. The conclusion was that these marked differences between
age groups in utilizing the dietary zinc reflected the efficient homeostatic adjustments in absorption and endogenous excretion
of zinc to the respective zinc supply status. 相似文献
9.
In experiments using rats it was shown that inadequate dietary supply of Ni reduces growth and lowers the erythrocyte count, hematocrit and hemoglobin level in blood, that the Ni supply affects the trace element content of iron, copper and zinc in various body organs, and that the absorption of iron is greatly impaired by Ni deficiency. For further biochemical criteria on the essentiality of nickel, the activities of two dehydrogenases, malate dehydrogenase and glucose-6-phosphate dehydrogenase, were measured in liver homogenates from two generations of rats at 30 and 50 days of age. In the 30-day-old rats of both the F1 and F2 generation, the activity of the malate dehydrogenase fell to about two-thirds the level of control animals. In the liver of the 50-day-old rats the activity of this enzyme was about the same in deficient animals as in the controls. The activity of glucose-6-phosphate dehydrogenase of Ni-deficient rats was reduced by 85% in the F1 generation and by 56% in the F2 generation at 30 days of age as compared with control levels. In 50-day-old rats the activity had fallen to half the level of control animals at 30 days of age. At the age of 50 days, there was no significant difference between the deficient and the control groups of either generation. 相似文献
10.
Luis E. Escobar Sandra Pritzkow Steven N. Winter Daniel A. Grear Megan S. Kirchgessner Ernesto Dominguez‐Villegas Gustavo Machado A. Townsend Peterson Claudio Soto 《Biological reviews of the Cambridge Philosophical Society》2020,95(2):393-408
Prions are misfolded infectious proteins responsible for a group of fatal neurodegenerative diseases termed transmissible spongiform encephalopathy or prion diseases. Chronic Wasting Disease (CWD) is the prion disease with the highest spillover potential, affecting at least seven Cervidae (deer) species. The zoonotic potential of CWD is inconclusive and cannot be ruled out. A risk of infection for other domestic and wildlife species is also plausible. Here, we review the current status of the knowledge with respect to CWD ecology in wildlife. Our current understanding of the geographic distribution of CWD lacks spatial and temporal detail, does not consider the biogeography of infectious diseases, and is largely biased by sampling based on hunters' cooperation and funding available for each region. Limitations of the methods used for data collection suggest that the extent and prevalence of CWD in wildlife is underestimated. If the zoonotic potential of CWD is confirmed in the short term, as suggested by recent results obtained in experimental animal models, there will be limited accurate epidemiological data to inform public health. Research gaps in CWD prion ecology include the need to identify specific biological characteristics of potential CWD reservoir species that better explain susceptibility to spillover, landscape and climate configurations that are suitable for CWD transmission, and the magnitude of sampling bias in our current understanding of CWD distribution and risk. Addressing these research gaps will help anticipate novel areas and species where CWD spillover is expected, which will inform control strategies. From an ecological perspective, control strategies could include assessing restoration of natural predators of CWD reservoirs, ultrasensitive CWD detection in biotic and abiotic reservoirs, and deer density and landscape modification to reduce CWD spread and prevalence. 相似文献