We have investigated the thiamine metabolism in Schizosaccharomyces pombe and shown that: (1) Thiamine-repressible acid phosphate, coded for by the gene pho4, dephosphorylates thiamine phosphates indicating that the enzyme acts as a thiamine phosphate phosphatase. (2) In vivo synthesized thiamine is present intracellularly mainly as thiamine diphosphate. Starving cells for glucose decreases the intracellular thiamine pool. (3) The genes thi2, thi3 and thi4 control thiamine biosynthesis and probably code for thiamine biosynthetic enzymes. Thi3, which is involved in the synthesis of the pyrimidine moiety of the thiamine molecule, is allelic to the thiamine repressible gene nmt1. (4) Thiamine uptake is a thiamine regulated process, probably occurs by active transport and is controlled by the gene ptr1.
The influence of 50 and 100 μm Ni on membrane integrity, hydrogen peroxide content, lipid peroxidation as well as total fatty acid composition was studied in shoots and roots of wheat seedlings. In both organs, treatment with Ni led to significant increase in electrolyte leakage reflecting the metal‐induced enhancement of membrane permeability. In the shoots, it was accompanied by significant increase in lipid peroxidation. Accumulation of hydrogen peroxide, more pronounced in the shoots, was also found in Ni‐treated wheat. Exposure of wheat seedlings to Ni altered the total fatty acid composition, leading to decrease in their unsaturation, which was indicated by reduction in double bond index. In both organs, a significant decrease in linolenic acid (C18 : 3) content was observed. It was accompanied by increased linoleic (C18 : 2) and oleic (C18 : 1) acid contents in shoots and roots, respectively. In the shoots, parallel increase in palmitic acid (C16 : 0) and decrease in palmitoleic acid (C16 : 1) were found at the end of the experiment. Our results suggest that modification of fatty acid profile in Ni‐treated wheat seedlings is partly related to lipid peroxidation and increased electrolyte leakage and may reflect damage of cells caused by the metal.
To investigate the response of the tributyltin-degrading fungal strain Cunninghamella elegans to the organotin, a comparative lipidomics strategy was employed using an LC/MS-MS technique. A total of 49 lipid species were identified. Individual phospholipids were then quantified using a multiple reaction monitoring method. Tributyltin (TBT) caused a decline in the amounts of many molecular species of phosphatidylethanolamine or phosphatidylserine and an increase in the levels of phosphatidic acid, phosphatidylinositol and phosphatidylcholine. In the presence of TBT, it was observed that overall unsaturation was lower than in the control. Lipidome data were analyzed using principal component analysis, which confirmed the compositional changes in membrane lipids in response to TBT. Additionally, treatment of fungal biomass with butyltin led to a significant increase in lipid peroxidation. It is suggested that modification of the phospholipids profile and lipids peroxidation may reflect damage to mycelium caused by TBT.
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