Iodothyronine deiodinase activity in methionine-deficient rats fed selenium-deficient or selenium-sufficient diets

We examined the effect of methionine deficiency on iodothyronine 5’-deiodinase activity in selenium-deficient rats or selenium-sufficient rats fed sodium selenate or selenomethionine. Forty-two weanling male Wistar rats were divided into six groups and pair fed the respective purifiedl-amino acid-based diets for 4 wk.l-methionine concentrations in the diet were 8.0 g/kg for sufficient rats, and 2.0 g/kg for deficient rats. Selenium concentrations in the diet were 0.5 mg/kg (as sodium selenate or selenomethionine) for selenium-sufficient rats and less than 0.005 mg/kg for selenium-deficient rats. Type I 5’-deiodinase activities were significantly lower in liver and higher in kidney of methionine-deficient rats than in those of methionine-sufficient rats fed either the selenium-sufficient or the selenium-deficient diets. The type I 5’-deiodinase activity in brain was significantly lower in the methionine-deficient rats than in the methionine-sufficient rats fed the selenium-deficient diet. Type II 5’-deiodinase activity in brain was significantly higher in the methionine-deficient rats than in the methionine-sufficient rats fed selenium-sufficient diet as sodium selenate. Both thyroxine and 3,3’,5-triiodothyronine concentrations in plasma were significantly higher in the methionine-deficient rats than in the methionine-sufficient rats. It is suggested that the methionine deficiency affects the 5’-deiodinase activity and thyroid hormones level in the rats.     

Activities of liver microsomal fatty acid desaturases in zinc-deficient rats force-fed diets with a coconut oil/safflower oil mixture of linseed oil

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.     

Effects of Mg(OH)2-fertilization on nutrient cycling in a heavily damaged Norway spruce ecosystem (NE Bavaria/FRG)

Main objective of this study was to test the effects of Mg(OH)₂-fertilization in a Norway spruce ecosystem showing severe symptoms of Mg-deficiency.The site is characterized by high atmospheric inputs with deposition rates of 1.25 kg H, 42 kg S, and 32 kg N per ha and year. The typic Dystrochrept derived from granite is acidified down to greater depths. The pH-values in soil solution of the organic surface layer and the upper mineral soil are around 3.5. Concentrations of Al, SO₄ ^2-, and especially NO₃ ^- and DOC are very high. The element balance indicates a significant influence of N-inputs and processes of N-turnover on the chemical status of the soil and probably on tree nutrition. Nitrification in the upper mineral soil leads to a transformation of a major part of NH₄ ⁺ into NO₃ ^-, which is quantitatively leached, resulting in an ecosystem-internal H⁺-production of 1.8 keq ha^-1yr^-1. NO₃ ^- and SO₄ ^2- govern the seepage output from the ecosystem.Mg(OH)₂ fertilization resulted in manifold increased Mg²⁺ concentrations in soil solution down to 70 cm soil depth and to a significant increase of pH down to 25 cm mineral soil depth. Nitrate concentrations were elevated after fertilization, but decreased within 15 months below the level of the control plot. As a mean over the whole experimental period, N-output was not increased by fertilization. Despite an elevated internal proton production due to nitrification, acid buffering in the soil was clearly increased, but enhanced Al-mobilization was not observed. Mg/Al- and Ca/H-ratios in soil solution indicate much more favourable conditions for fine root growth. Fertilization also increased the amount of exchangeable Mg down to 40cm mineral soil depth. Mg contents in current-year needles increased after three vegetation periods. Thirty months after application, only 10% and 4% of the fertilized Mg had left the organic surface layer and the mineral soil with seepage water output, respectively.     

Immunological characterization of a 36 kDa Fe deficiency specific peptide in barley roots

In a previous paper we reported that an acidic 36 kDa peptide is the most strongly induced peptide among several peptides induced by Fe deficiency in barley roots. In this paper, polyclonal antibodies were raised against the 36 kDa peptide. This peptide appeared in the roots of all the graminaceous species tested (barley, rye, wheat, oat, maize, sorghum and rice) in response to Fe deficiency. More of the peptide was found in the roots of graminaceous species which secrete higher amounts of mugineic acids (MAs) under Fe deficient nutrition status. Induction of the 36 kDa peptide was first observed on the third day of Fe deficiency, rising to a maximum value on the seventh day. The trend has a positive correlation with secretion of MAs during Fe deficiency. Further, resupply of Fe resulted in a decrease in peptide production on the second day, reaching a control level on the seventh day. The rate of decrease in peptide production was observed to be slower than that of MA secretion. Other nutrient stresses such as B excess, B deficiency, Cu excess, Cu deficiency, Mn excess, Mn deficiency, Zn excess and Zn deficiency induced far less of the peptide. The specific expression of the 36 kDa peptide in roots of graminaceous species under Fe deficiency suggested the positive association of the peptide with a specific Fe deficiency tolerance mechanism in graminaceous plants.     

Regional alterations of thiamine phosphate esters and of thiamine diphosphate-dependent enzymes in relation to function in experimental Wernicke's encephalopathy

Thiamine phosphate esters (thiamine monophosphate-TMP; thiamine diphosphate-TDP and thiamine triphosphate-TTP) were measured as their thiochrome derivatives by High Performance Liquid Chromatography in the brains of pyrithiamine-treated rats at various stages during the development of thiamine deficiency encephalopathy. Severe encephalopathy was accompanied by significant reductions of all three thiamine phosphate esters in brain. Neurological symptoms of thiamine deficiency appeared when brain levels of TMP and TDP fell below 15% of normal values. Activities of the TDP-dependent enzyme -ketoglutarate dehydrogenase were more severely reduced in thalamus compared to cerebral cortex, a less vulnerable brain structure. On the other hand, reductions of TTP, the non-cofactor form of thiamine, occurred to a greater extent in cerebral cortex than thalamus. Early reductions of TDP-dependent enzymes and the ensuing metabolic pertubations such as lactic acidosis impaired brain energy metabolism, and NMDA-receptor mediated excitotoxicity offer rational explanations for the selective vulnerability of brain structures such as thalamus to the deleterious effects of thiamine deficiency.     

Guanosine triphosphate catabolism in purine nucleoside phosphorylase deficient human B lymphoblastoid cells

GTP catabolism induced by sodium azide or deoxyglucose was studied in purine nucleoside phosphorylase (PNP) deficient human B lymphoblastoid cells. In PNP deficient cells, as in control cells, guanylate was both dephosphorylated and deaminated but dephosphorylation was the major pathway. Only nucleosides were excreted during GTP catabolism by PNP deficient cells and the main product was guanosine. The level of nucleoside excretion was largely affected by intracellular orthophosphate (P_i) level. In contrast, normal cells excreted nucleosides only at low P_i level while at high P_i levels, purine bases (guanine and hypoxanthine) were exclusively excreted. PNP deficiency had no effect on the extent of GMP deamination.     

Development and characterisation of a line of bread wheat,Triticum aestivum,which lacks the short-arm satellite of chromosome 1B and the Gli-B1 locus

Summary About 360 offspring of a tri-parental cross were screened by gel electrophoresis and unexpectedly one of them did not contain chromosome 1B -gliadins derived from either of the primary parents. A line disomic for the -gliadin null was developed from the surviving embryo half of the unique grain. Two dimensional electrophoresis revealed that all the storage protein genes at Gli-B1, coding for -gliadins, -gliadins and low-molecular-weight subunits of glutenin as well as the -gliadin, were not expressed. The nuclei of dividing root-tip cells were shown by light microscopy to lack the normal short-arm satellites of chromosome 1B, indicating that the genes for the missing storage proteins had been lost through a terminal deletion. Using a radioactive ribosomal RNA probe, the deficient 1B chromosomes were shown to contain ribosomal RNA genes demonstrating that at least two-thirds of the short arm was still present. Examination of serial sections of chromosome 1B at metaphase by low-power electron microscopy showed that the point of scission of this chromosome was within the secondary constriction where the ribosomal RNA genes are located. The Gli-B1 locus must therefore be carried on the short-arm satellite. Transmission of the deficient chromosome from female gametes to progeny was normal (i.e., about 50%) but from pollen it was poor (8.8%). Recombination mapping indicated that the distance from the ribosomal RNA genes (Nor1) to Glu-B1 was 22 cM, equivalent to 13 cM from Nor1 to the centromere.     

Nickel requirement in Chlorella emersonii

The dependence of growth on nickel supply was studied in Chlorella emersonii 211-8b. After transfer to Ni²⁺ deficient medium containing only 0.5±0.2 g/l of Ni²⁺, production of biomass or daughter cells dropped to 55±5% of the controls, and the cells became chlorotic. These symptoms of deficiency disappeared completely by supplying adequate amounts of nickel. They were, however, only partially reversible by cobalt. It is concluded that nickel is an essential micronutrient for C. emersonii, although this organism lacks the nickel enzyme, urease.Gratefully dedicated to Prof. Hans Adolf von Stosch on the occasion of his 70th birthday     

EFFECTS OF IRON DEFICIENCY ON ISOCHRYSIS GALBANA (CHRYSOPHYCEAE) AND PHAEODACTYLUM TRICORNUTUM (BACILLARIOPHYCEAE)1

Cultures of Isochrysis galbana Parks and Phaeodactylum tricornutum Bohlin were grown in iron-limited chemostats. With increasing iron deficiency, photosynthetic rate per cell and assimilation number decreased. The pattern of photosynthesis was also altered; in Fe deficient cells the proportion of ¹⁴C fixed in glycine and serine decreased with an accompanying increase into alanine after 3 min assimilation. Although there was no significant effect of Fe deficiency on the proportion of ¹⁴C incorporated into total amino acids and amides, the percentage of total ¹⁴C fixed in protein increased with increasing Fe deficiency. Cellular levels of chlorophyll a, carotenoids, cytochromes and protein also decreased with increasing Fe deficiency. However, the reduction in chlorophyll a/cell was not as great as that of cytochrorne f₁ and Fe deficient cells therefore showed a marked increase in chlorophyll a:cytochrorne f₁ ratio.     

Platte Valley Yellows,a chlorotic condition of soybeans: Symptoms and preliminary chemical analyses

Summary A chlorotic condition of soybeans in the river valleys of eastern Nebraska was studied. The pattern of chlorosis, presence of petiolar necrosis, reductions in rhizobial and mycorrhizal infection, and plant and soil chemical analyses suggest that the condition is more complex than normal iron deficiency chlorosis or other mineral deficiencies or toxicities. Nodulation is almost totally inhibited in affected plants. Mycorrhizal fungi, while able to infect early in the season, do not persist on affected plants. Breakdown of endodermis was observed in the roots of affected plants. The factors contributing to this condition have not yet been determined. Published with the approval of the director as Paper No. 5672, Journal Series, Nebraska Agricultural Experiment Station.