Inhibition of photophosphorylation in spinach chloroplasts by inorganic sulfate.
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Adenine Nucleotides↗
Biomedical subjects
I J Ryrie
Publications and source records attributed to I J Ryrie.
Nicotinate, quinolinate and nicotinamide as precursors in the biosynthesis of nicotinamide-adenine dinucleotide in barley.
1. The relative efficiencies of nicotinate, quinolinate and nicotinamide as precursors of NAD(+) were measured in the first leaf of barley seedlings. 2. In small amounts, both [(14)C]nicotinate and [(14)C]quinolinate were quickly and efficiently incorporated into NAD(+) and some evidence is presented suggesting that NAD(+) is formed from each via nicotinic acid mononucleotide and deamido-NAD. 3. [(14)C]Nicotinamide served equally well as a precursor of NAD(+) and although significant amounts of [(14)C]NMN were detected, most of the [(14)C]NAD(+) was derived from nicotinate intermediates formed by deamination of [(14)C]nicotinamide. 4. Radioactive NMN was also a product of the metabolism of [(14)C]nicotinate and [(14)C]quinolinate but most probably it arose from the breakdown of [(14)C]NAD(+). 5. In barley leaves where the concentration of NAD(+) is markedly increased by infection with Erysiphe graminis, the pathways of NAD(+) biosynthesis did not appear to be altered after infection. A comparison of the rates of [(14)C]NAD(+) formation in infected and non-infected leaves indicated that the increase in NAD(+) content was not due to an increased rate of synthesis.
Ascomycota↗
Metabolic Regulation in Diseased Leaves II. Changes in Nicotinamide Nucleotide Coenzymes in Barley Leaves Infected With Powdery Mildew.
Nicotinamide nucleotide coenzymes were estimated spectrophotometrically in noninfected barley leaves and leaves infected with Erysiphe graminis var hordei (powdery mildew). Amounts of NADH, NADP(+) and NADPH were not altered by infection. In contrast, the NAD(+) content rose sharply and at 144 hours was 100% greater than in noninfected leaves. The respiratory rate was increased in infected leaves and the pattern of this increase was similar to that of NAD(+).The effect of infection on the intracellular distribution of NADP(+) was examined by fractionating lyophilized leaves in a nonaqueous medium. In noninfected leaves almost all of the NADP(+) was localized in the chloroplasts. In infected leaves where some chloroplast breakdown occurs, about 60% of the NADP(+) was detected in the nonchloroplast part of the cell. This intracellular redistribution of NADP(+) is discussed in relation to the increased pentose-P pathway activity occuring after infection.
Journal Article↗