Do puroindolines affect the impact of enzymatic lipid hydrolysis on loaf volume in bread making?

This paper is the first to study whether and how interactions between puroindolines (PINs) and lipids affect bread loaf volume (LV). Flour from near-isogenic wheat lines differing in PIN haplotype and lipases were used in bread making. That lipase impact on LV strongly depended on the flour used supported the hypothesis that PINs modify the impact of enzymatic lipid hydrolysis on LV. In dough prepared from gluten-starch blends (GSB) differing in PIN levels, PINs did not affect enzymatic lipid hydrolysis itself. Gas cells in these GSB doughs were apparently not surrounded by surface-active compounds so that the impact of PIN-lipid interactions on LV could not be evaluated. This allowed concluding that lipase impact on LV is exclusively related to stabilization of gas cell interfaces in dough since lipase application did not change GSB LVs. Our results advance knowledge on PIN-lipid interactions and the impact of lipases in bread making.

Improvement of the energy status of hypoxic hepatocytes by calcium channel blockers.

Isolated hepatocytes from rat liver in primary culture rapidly lost viability under hypoxic conditions. Hypoxic injury was significantly decreased by the calcium channel blockers nifedipine (5 microM) and diltiazem (10 microM). The concentrations of the inhibitors which afforded maximum protection also produced the maximum increase in the energy level of the hypoxic hepatocytes, as evidenced by their ATP, ADP, AMP, and total adenine nucleotide content and by their energy charge. The increased hypoxic energy level caused by these calcium channel blocking agents was not due to an increased rate of anaerobic glycolysis; nifedipine did not have any effect on lactate production while diltiazem slightly decreased its rate. During the first 2 h under hypoxic conditions the cytosolic Ca2+ concentration remained constant around 100 nM, subsequently increasing to 400 nM first slowly and later more rapidly. The calcium channel blockers delayed the Ca2+ increase by about 1 h but were without any effect on the rate of this increase. The results suggest that the well-known beneficial effects of calcium channel blockers on hypoxic liver injury are due in large measure to an improved energetic situation of the hepatocytes rather than to the increase in the cytosolic Ca2+ concentration being blocked.

Late steady increase in cytosolic Ca2+ preceding hypoxic injury in hepatocytes.

Upon initiation of hypoxia, the ATP content of hepatocytes in monolayer cultures fell within 5 min from 22 to 12 nmol of ATP/10(6) cells. This decrease in ATP was not followed by early alterations in the cytosolic Ca2+ concentration; for up to 60 min it remained around 100 nM. However, after the period cytosolic free Ca2+ steadily increased, up to 400 nM. This increase began around 60 min before the cells lost their viability, and primarily resulted from an influx of extracellular Ca2+. Likewise, in experiments where the mitochondrial respiratory chain was blocked by KCN and glycolysis was blocked by iodoacetate, the ATP content fell within minutes to 10 nmol/10(6) cells, whereas the cytosolic Ca2+ concentration only began to increase 30 min later (up to 600 nM). However, also under these conditions of 'chemical hypoxia' this increase was clearly (about 10 min) earlier than the loss of viability.

Comparative surfact structure of 16S ribosomal ribonucleic acid of 30S ribosomes of procaryotic cells.

Ribonuclease T(1) treatment of 30S ribosomes of Escherichia coli converts a large region at the 3' OH end of 16S ribosomal ribonucleic acid (rRNA) to low-molecular-weight RNA. The final 25 nucleotides at the 3' terminus of the molecule emerge relatively intact, whereas most of the region "upstream," for about 150 nucleotides, is converted to oligonucleotides. Identical enzyme treatment generates a fragment of about 60 nucleotides from the middle of 16S rRNA (section D'). To determine whether there are similar sequences in other bacteria, which occupy similar accessible surface locations, we treated 30S ribosomes from Azotobacter vinelandii and Bacillus stearothermophilus with RNase T(1). In each case, a fragment of RNA about 25 nucleotides in length containing the 3' OH end of 16S rRNA and a fragment of about 60 nucleotides in length similar, but not identical, in oligonucleotide composition to section D' of E. coli 16S rRNA were obtained from nuclease-treated 30S ribosomes. These data indicate that, although the primary structure at the 3' end and the middle (section D') of the various 16S rRNA's is not completely conserved, their respective conformations are conserved. A number of identical oligonucleotides were found in the low-molecular-weight fraction obtained from RNase T(1)-treated E. coli, A. vinelandii, and B. stearothermophilus 30S ribosomes. These results show that identical RNase T(1)-sensitive sequences are present in all three bacteria. Hydrolysis of these regions leads to the production of the fragments 25 and 60 nucleotides in length.