Rate Of Oxidative Metabolism Research Articles

Fluorescence mapping of mitochondrial redox changes in heart and brain

Fluorescence techniques may be utilized to map changes in the distribution of mitochondrial redox states in heart and brain during ischemic or hypoxic stress. The basis of these techniques is the intrinsic fluorescence of reduced NADH and oxidized flavoprotein in mitochondria which respond to changes in critical oxygen supply. Ischemic areas in rabbit hearts induced by coronary ligation were detected and mapped based on the increase in NADH fluorescence in the ischemic zone. The width of the jeopardized normoxic tissue surrounding the ischemic area (less than 50--350 mu) was measured by combination of fluorescein angiography and NADH fluorescence. Areas of increased NADH fluorescence in gerbil brains after carotid artery ligation or induction of spreading depression were mapped in a similar manner. Intraoperative monitoring of flavoprotein fluorescence from human cerebral cortex after superficial temporal artery middle cerebral artery (STA-MCA) anastomoses demonstrated increased rates of cortical oxidative metabolism after the surgical procedures.

Use of mass spectrometer to measure CO2 and O2 fluxes in voltage-clamped epithelia

A quadrupole mass spectrometer was coupled to an Ussing chamber in order to evaluate rates of oxidative metabolism in voltage-clamped epithelia. Well-defined mixing characteristics of the continuously perfused chamber allowed CO2 and O2 concentrations to be related to rates of CO2 efflux, JCO2, and oxygen influx, JO2. The use of a model tissue to simulate step changes in JCO2 validated the treatment, with response within a minute. Monitoring of metabolism was facilitated by use of a desk-top computer, which evaluated JCO2 at 6-s intervals. Concurrent measurements of electrical current and JCO2 were made in the toad urinary bladder in order to relate active sodium transport to metabolism; the use of amiloride to eliminate active transport and the associated metabolism then allowed evaluation of the rates of active Na transport (JNa) and suprabasal metabolism (JsbCO2), and their ratio JNa/JsbCO2. We report the ability to resolve a 5 pmol/s change in CO2 efflux or an 11 pmol/s change in O2 influx rates.

The design of cardiac muscle and the mode of metabolism in molluscs

1. 1. The structure of the squid cardiac myofiber differs fundamentally from that of lamellibranchs, most notably in mitochondrial and tubule density. 2. 2. These properties are correlated with a very high rate of oxidative metabolism in the intact animal, little capacity for anaerobiosis and an exceedingly high performance capability of the muscle. 3. 3. It is suggested that the redesign of the cardiac myofiber was a critical step in the transition from a sedentary to a highly pelagic way of life.

Evolution of thinking in fetal respiratory physiology

An outstanding characteristic of intrauterine life is the low oxygen pressure (Po2) of fetal blood. It seemed at one time that in order to tolerate the Po2 of the uterine environment the fetus must have a relatively slow rate of oxidative metabolism or depend upon anaerobic pathways of substrate utilization. Subsequent studies have shown that the fetus has a high rate of oxygen consumption and that lactic acid is a substrate rather than a net product of normal fetal metabolism. The circulatory response of the fetus to acute hypoxia is centered on the requirement of maintaining the arterial oxygen flow to the heart and central nervous system without increasing cardiac output. The arterial oxygen flow concept helps in understanding the physiologic meaning of the high oxygen affinity of fetal blood and the boundary conditions of the fetal defense against hypoxia.

Activation of monooxygenases in human liver by 7,8-benzoflavone.

Addition of 10(-4) M 7,8-benzoflavone to homogenates of human liver samples obtained by autopsy or surgical biopsy increased the rate of benzo[a]pyrene hydroxylation up to 11-fold. 7,8-Benzoflavone also increased the rates of hydroxylation of zoxazolamine and antipyrine at 10(-4) M but inhibited these reactions at 10(-6) M. The effects of 7,8-benzoflavone on the hydroxylation of benzo[a]pyrene and zoxazolamine in microsomes from human liver were similar to those in homogenates. Addition of 7,8-benzoflavone to homogenates of surgical biopsy samples of human liver had little or no effect on the rates of oxidative metabolism of 7-ethoxycoumarin, coumarin, and hexobarbital. Marked individuality for the activating and inhibiting effects of 7,8-benzoflavone was observed in different liver samples. This individuality may result both from the presence of multiple monooxygenases in varying amounts and proportions in the different liver samples and from a selective effect of 7,8-benzoflavone on certain of the monooxygenases.

The effect of dietary lipid peroxides, sterols and oxidised sterols on cytochrome P450 and oxidative demethylation in the endoplasmic reticulum

The effects of dietary linoleate, oxidised linoleate, lipid peroxides, cholesterol, cholesterol hydroperoxides and squalene have been examined on the concentration of cytochrome P450 and rate of oxidative demethylation in the endoplasmic reticulum. Addition of methyl linoleate (5%) to a diet containing 5% lard caused a large increase in the rate of oxidative demethylation, oxidised methyl linoleate (5%) was much less effective and also depressed the rate of oxidation when added to a diet containing corn oil. A supply of dietary linoleic acid or other polyunsaturated fatty acids are essential for maximum rate of oxidative demethylation in the endoplasmic reticulum and for maximum induction by phenobarbitone. Dietary lipid peroxide did not increase the rate of oxidative metabolism in the endoplasmic reticulum or its induction. Feeding a diet which included 10% herring oil, and which contains only 1.7% linoleic acid caused a very rapid rate of oxidative demethylation and a high concentration of cytochrome P450 in the liver endoplasmic reticulum. Induction by phenobarbitone was also very effective after feeding this diet. The unsaponifiable fraction of herring oil, added to the lard diet, very effectively increased the rate of oxidative demethylation to a value similar to that observed after feeding a diet containing 10% herring oil. Addition of cholesterol (2 g/kg diet) or of squalene (1 g/kg diet) to diets containing 10% lard were less effective than the unsaponifiable fraction of herring oil but caused a large increase in the content of cytochrome P450 and rate of oxidative demethylation in the endoplasmic reticulum. Induction of phenobarbitone was also enhanced. Cholesterol hydroperoxide was not more effective than cholesterol. It may be concluded that a supply of dietary sterols is essential for maximum activity of oxidative demethylation in the liver endoplasmic reticulum, especially when linoleic acid is in restricted supply and for maximum induction by phenobarbitone. The non-saponifiable fraction of herring oil cannot be completely replaced in the diet by pure cholesterol, cholesterol hydroperoxide or squalene.

Oxidative metabolism in cerebral ischemia. Part 1. Measurement of oxygen extraction slopes of grey and white matter in vivo.

Regional oxidative metabolism was studied in vivo. Oxygen availability was monitored from polarographic electrodes in frontal cortical and subcortical tissue. The rate of oxygen extraction in these regions was estimated at frequencies of up to 3 measurements per minute. Transient ischemia of the frontal regions was induced and the resultant decay in the oxygen trace was analyzed kinetically. The oxygen extraction slopes (OES) were steeper in grey than in white matter. They were relatively insensitive to alterations of arterial blood gas concentrations within the physiological range. The slopes were predictably influenced by pharmacologic agents known to alter the rate of oxidative metabolism. Artifacts which may interfere with the OES measurments were considered. This method of estimating regional tissue oxygen extraction may be appropriate for studying aspects of focal CI.

Sensitivity of central chemoreceptors controlling blood glucose and body temperature during glucose deprivation.

1. The rise in blood glucose and the fall in body temperature which follows the injection of a glucose analogue, 2-deoxy-D-glucose (2-DG) into the lateral cerebral ventricle (I.C.V) of unanaesthetized rats were studied and found to be dose-dependent. These 2-DG induced responses are elicited by the impairment of glucose metabolism within central "glucoreceptors'. 2. 2DG induced hyperglycaemia and hypothermia were completely prevented and even the converse effects occurred when fivefold equimolar amounts of D-fructose were simultaneously injected I.C.V.; fructose, at equimolar doses, did not modify the effects of 2-DG. 3. D-xylose and D-ribose, even at high doses, did not influence 2-DG hyperglycaemia, but increased slightly the 2-DG induced hypothermia. This suggests that the pentose phosphate pathway is unable to support the metabolism within the glucoreceptors. 4. Pyruvate suppressed the 2-DG induced hyperglycaemia with a marked delay, while acetate (as ethyl ester) and a mixture of malate plus oxaloacetate did not prevent 2-DG induced effects. These results may be accounted for by the low dosage used. 5. Acetoacetate and 3-hydroxybutyrate did not prevent 2-DG hypothermia and hyperglycaemia. 6. An effective prevention of the 2-DG induced hyperglycaemia and hypothermia was achieved with fumarate and glutamate, indicating that the stimulation of the Krebs cycle within "glucoreceptors' removes the glucoprivic effects. 7. The results indicate that prevention of 2-DG induced effects occurred only with alternate source of metabolic fuel which can support high respiratory rates in brain tissue. It is concluded that central chemoreceptors are not specifically responsive to glucose, or hexoses, but to the rate of oxidative metabolism.

Effect of glucagon on phenylalanine metabolism and phenylalanine-degrading enzymes in the rat.

Glucagon administered subcutaneously to rats for 10 days had no significant effect on liver phenylalanine hydroxylase activity, but induced liver dihydropteridine reductase more than twofold. In rats administered a phenylalanine load orally, glucagon treatment stimulated oxidation and depressed urinary phenylalanine excretion. These responses could not be related to an effect of glucagon on hepatic tyrosine-alpha-oxoglutarate aminotransferase activity. Even in rats with phenylalanine hydroxylase activity depressed to 50% of control values by p-chlorophenylalanine administration, glucagon treatment increased the phenylalanine-oxidation rate substantially. Although hepatic phenylalanine-pyruvate aminotransferase was increased tenfold in glucagon-treated rats, glucagon treatment did not increase urinary excretion of phenylalanine transamination products by rats given a phenylalanine load. Glucagon treatment did not affect phenylalanine uptake by the gut or liver, or the liver content of phenylalanine hydroxylase cofactor. It is suggested that dihydropteridine reductase is the rate-limiting enzyme in phenylalanine degradation in the rat, and that glucagon may regulate the rate of oxidative phenylalanine metabolism in vivo by promoting indirectly the maintenance of the phenylalanine hydroxylase cofactor in its active, reduced state.

Oxidative metabolism during recurrent seizures in the penicillin treated hippocampus

Changes in intracellular NADH fluorescence, which directly reflect changes in the rate of oxidative metabolism, were monitored during hippocampal epileptiform activity induced by penicillin. With interictal and ictal activity the oxidation rate would transiently increase and then return to the previous oxidation level after each spike or in the postictal depression period, respectively. Seizures were preceded by increased spike activity with simultaneously increasing oxidation. Maximum oxidation rates were reached at termination of each ictal episode. When the K + concentration of the fluid bathing the hippocampus was increased, repetitive seizures occurred, at first followed by postictal periods, but at higher K + levels ictal activity was more frequent and postictal periods were eliminated. As the K + concentration was increased the interictal or recovery rate of oxidation rose; however, also at the higher K + concentrations oxidation rates during ictal episodes tended not to be as high as at low K +. Thus the overall changes in rate of oxidation observed in the transition from interictal to ictal activity were smaller at high K + than at low K + concentrations. Direct current electrical correlates of epileptiform activity tended to mirror the changes in oxidation with a negative D.C. shift accompanying an increase in oxidation and vice versa. These results indicate a close relationship between extracellular K + concentration, ictal activity and oxidative metabolism which could possibly be explained by the effects of varying K + concentrations on the electrogenic pump (Na-K-ATPase).

The acute action of ammonia on rat brain metabolism in vivo.

1. Acute NH(4) (+) toxicity was studied by using a new apparatus that removes and freezes the brains of conscious rats within 1s. 2. Brains were removed and frozen 5min after intraperitoneal injection of ammonium acetate (2-3min before the onset of convulsions). Arterial [NH(4) (+)] rose from less than 0.01 to 1.74mm at 4-5min. The concentrations of all glycolytic intermediates measured, except glucose 6-phosphate, were increased by the indicated percentage above the control value as follows: glucose (by 41%), fructose 1,6-diphosphate (by 133%), dihydroxyacetone phosphate (by 164%), alpha-glycerophosphate (by 45%), phosphoenolpyruvate (by 67%) and pyruvate (by 26%). 4. Citrate and alpha-oxoglutarate concentrations were unchanged and that of malate was increased (by 17%). 5. Adenine nucleotides and P(i) concentrations were unchanged but the concentration of creatine phosphate decreased slightly (by 6%). 6. Brain [NH(4) (+)] increased from 0.2 to 1.53mm. Net glutamine synthesis occurred at an average rate of 0.33mumol/min per g. 7. The rate of brain glucose utilization was measured in vivo as 0.62mumol/min per g in controls and 0.81mumol/min per g after NH(4) (+) injection. 8. The arteriovenous difference of glucose and O(2) increased by 35%. 9. No significant arteriovenous differences of glutamate or glutamine were detected. Thus, although much NH(4) (+) was incorporated into glutamine the latter was not rapidly released from the brain to the circulation. 10. Plasma [K(+)] increased from 3.3 to 5.4mm. 11. The results indicate that NH(4) (+) stimulates oxidative metabolism but does not interfere with brain energy balance. The increased rate of oxidative metabolism could not be accounted for only on the basis of glutamine synthesis. We suggest that increased extracellular [NH(4) (+)] and [K(+)] decreased the resting transmembrane potential and stimulated Na(+),K(+)-stimulated adenosine triphosphatase activity thus accounting for the increased metabolic rate.

Photosynthetic Production of Hydrogen Peroxide by Anacystis nidulans

A sensitive assay based upon fluorescence of scopoletin allowed continuous recording of H(2)O(2) production in illuminated intact cells of Anacytis nidulans. Onset of illumination was followed by a 5 to 10 second lag, a burst of very rapid production continuing for up to 5 minutes, and finally a slow and continuing steady rate of H(2)O(2) production. Size of the H(2)O(2) burst was decreased by 3-(3,4-dichlorophenyl)-1, 1-dimethylurea, by low O(2), and by certain Calvin cycle intermediates; it was increased by high light intensity, CO(2) depletion, Calvin cycle inhibitors (as iodoacetamide), cold shock, carbonyl cyanide m-chlorophenylhydrazone, and certain organic acids as glycolate). The H(2)O(2) burst was explained by the following hypothesis: a low potential reductant is produced more rapidly than it can be used in the normal pathway to CO(2) reduction and, instead, reacts with oxygen. H(2)O(2) production is regarded as a metabolic defect observable in Anacystis most dramatically during the transition from a very low rate of oxidative dark metabolism to a high rate of photosynthetic metabolism.

Myocardial utilization of carbohydrate and lipids

Myocardial utilization of carbohydrate and lipids

Modification of carbaryl metabolism in rats with monoamine oxidase inhibitors.

The rate of carbaryl metabolism by rats was decreased by simultaneously administering drugs commonly referred to as monoamine oxidase inhibitors and by prolonged exposure of the animals to one of the drugs in the drinking water. Conjugative mechanisms of metabolism were affected most by the drugs although oxidative and hydroxylative metabolism rates were reduced to some degree. Decreasing the rate of metabolism resulted in a slower rate of excretion of the carbamate from rats treated with the drugs. Tranylcypromine at 50 mg/kg, e.g., reduced excretion of carbaryl-14C equivalents from rats by 50% during the 1st 48 hours after treatment. A rat intestine enzyme system, fortified with UDPGA, conjugated 1-naphthol but did not metabolize carbaryl. This in vitro conjugating system was inhibited by the monoamine oxidase inhibitors. The effect of these drugs on conjugation was not sufficient to suggest that they might enhance the action of pesticides under practical conditions. However, the data do demonstrate that conjugation enzyme systems are sensitive to certain foreign chemicals and that more effective inhibitors of conjugation could be important in the safety and efficacy of chemicals used to control insect pests.

The effects of excitatory and inhibitory amino acids on the metabolism of endogenous brain amino acids in the nembutalized mouse

(1) [U- 14C]Glucose was injected intraventricularly into nembutalized mice in the presence and absence of the neuro-excitants N-methyl- d-aspartate (NMDA), l-aspartate and l-glutamate, and the neuro-depressants, 3-aminopropane sulphonic acid (3-APS) and γ-aminobutyric acid (GABA). Incorporation of 14C into amino acids during control and NMDA-affected metabolism in the nembutalized mice was measured at 2.5, 5 and 10 min. All other effects were measured at 5 min only. (2) NMDA caused an increase in the rate of labelling of aspartate, glutamate, glutamine, GABA and alanine. The increased incorporation of 14C into aspartate was greater than that into glutamate, while that into alanine was lower. The increased incorporation into GABA and glutamine were similar to that into glutamate. The effects were considered to be due to increased turnover of glycolytic and Krebs cycle metabolites located within NMDA-activated neurones, with the possible involvement of reciprocally related changes in the amination rates of pyruvate and oxaloacetate. Pools of GABA and glutamine were closely associated with the pool(s) of glutamate involved in the increased metabolism. (3) Both glutamate and aspartate, injected in neuro-excitatory doses equivalent to that of NMDA, similarly increased the incorporation of glucose 14C into endogenous acidic amino acids; however there were differences in the effects on the labelling of other amino acids. Exogenous glutamate depressed the labelling of glutamine, presumably because of uptake into and isotope dilution within one or more endogenous pools of labelled glutamate associated with glutamine-forming systems. Exogenous aspartate (and also glutamate) depressed the labelling of GABA, an effect which does not accord with the known major sites of uptake of extracellular acidic amino acids, and which may have physiological significance. (4) The inhibitory amino acids decreased the incorporation of glucose 14C into acidic amino acids and increased the relative proportion of amino acid radioactivity in alanine. These effects were considered to reflect a decrease in the rate of oxidative metabolism. (5) The metabolic consequence of the pharmacological interaction of the two types of amino acid and Nembutal are discussed. The main effects on amino acid metabolism resulting from neuronal excitation by NMDA are the reverse of those associated with Nembutal anaesthesia. On the other hand, the metabolic effects of depressant amino acid action — though possibly complicated by hypoxia in the present investigation — resemble those of the barbiturate. The results can be explained solely on the basis of the differential energy requirements of active and inactive neurones, but interrelations between the mechanisms of action of Nembutal and those of the amino acids may well be involved.

The mechanism of acquired resistance to Co 2+ and Ni 2+ in gram-positive and gram-negative bacteria

1. 1. Bacteria rendered resistant to the growth-inhibitory action of Co 2+ by serial subculture in the presence of increasing concentrations of the cation, are resistant also to Ni 2+. Resistance is retained on repeated transfer in the absence of Co 2+, provided that the medium contains adequate amounts of Mg 2+. Higher concentrations of Mg 2+ are required for the maintenance of resistance in Co 2+ resistant strains of the Gram-positive organism, Bacillus subtilis, than in those of the Gram-negative bacteria, Aerobacter aerogenes and Escherichia coli. 2. 2. Studies with Aerobacter aerogenes show that resistance to Co 2+ and Ni 2+ is not associated with alterations in the rate of oxidative metabolism of glucose or pyruvate, or in the cellular contents of cation-binding components, but with a reduction in the capacity for the energy-linked uptake of the toxic cations. Since these cations are translocated by the Mg 2+ transport pathway, the resistant bacteria also assimilate Mg 2+ less efficiently than do the parent organisms. Resistant bacteria regain the normal ability to concentrate Mg 2+, but at the same time. lose their resistante to Co 2+ during one subculture in a Mg 2+-limited medium.

Peroneal muscular atrophy. A histochemical study.

Changes in localisation and distribution of enzymes concerned in important metabolic pathways of the spinal cord and muscle in peroneal muscular atrophy are reported. In the spinal cord, particularly at the lumbo-sacral level, nerve cells of the anterior horns exhibited marked losses in activity of two phospholytic and two oxidative enzymes in contrast to increases in these enzymes in glia cells. The same two oxidative enzymes were severely depleted in the nucleus dorsalis suggestive of a lower rate of oxidative metabolism or to greater sensitivity of these enzymes than others to pathological changes. Acetylcholinesterase in this column was also abnormally low. Enzyme changes in muscle fibres which appeared normal were related mainly to phosphate metabolism; oxidative enzymes and phosphorylase appeared unaffected. In atrophic musclfibres enzyme activities varied, Mg2+-ATPase and phosphorylase were relatively absent. Finde ings are compared with other neuropathies.

ATP level and respiration of embryos

ABSTRACT A considerable increase in the rate of oxygen consumption is known to occur during the development of embryos (cf. Needham, 1931; Tuft, 1953; Brachet, 1960; Gustafson, 1965). However, the mechanism of the increase in respiration during embryonic development is still unclear. A certain correlation seems to exist between DNA synthesis and the respiration of embryos (Comita & Whiteleley, 1953; Brachet, 1960). According to Commoner (1964), this correlation is determined by a change in the level of free nucleotides in cells when the rate of DNA synthesis changes. Free nucleotides control cell metabolism, oxidative processes in particular. The ADP+P/ATP ratio is known to control the rate and direction of electron transfer in the respiratory chain (Chance & Hagihara, 1961 ; Klingenberg & Schollmeyer, 1961). The ADP/ATP system is suggested to control the rate of oxidative metabolism in fertilization (Monroy, 1965 a, b;Zotin, Milman & Faustov, 1967).

The effects of stress on the growth rate and food and water intake of rats.

SUMMARY The effects of four types of stress (daily subcutaneous injection of 0·9 % NaCl solution, a forced choice, water gavage, and surgical trauma) on the growth rate, food and water intake, and water excretion of albino rats have been investigated. These stresses caused a slowing of growth which was apparently not associated with decreased food and water intakes. There were, however, some changes in water excretion which varied with the type of stress. Since food consumption was unchanged during stress whereas the rate of growth decreased it is concluded that the rate of oxidative metabolism was increased.

Effect of Puccinia graminis tritici on Organic Acid Content of Wheat Leaves

Although greatly increased rates of oxidative metabolism result from infection of higher plants by rust fungi (1, 6), the significance of the high rates for the development of the rust pathogen is not understood. Previous work has indicated that the increase in respiratory rates may be correlated at least partially with the development of the parasite (5, 6). At the flecking stage, when visible symptoms of infection are first noticed and only vegetative mycelium is present, there is a moderate increase in rates without any detectable change in the nature of the respiratory pathways. The subsequent larger increases in rates associated with the process of sporulation are characterized by a decline in C6/C1 ratios. This latter feature of the metabolic alterations induced by all rust infections studied suggests that an oxidative pentose, or similar, pathway may be of importanice in obligate parasitism. Shu and Ledingham (23) havre shown that the germinating spore of the wheat rust fungus has all the enzymes of the pentose pathway and the respiration is characterized by low C6/C1 ratios. Consequently, if the mycelium of the parasite is largely responsible for the increased rates of respiration via a pathway requiring a C1 decarboxylation (6), major changes should be apparent in the amounts or activity of metabolic components either directly in, or closely related to, the pathways of glucose catabolism. In contrast to other tissues in which low C,/C_ ratios have been induced (2, 17), data to be published on rust-affected plants do show increases in carbohydrate compounds which arise after decarboxylation of the aldehydic group of glucose. The effects of sodium fluoride on the respiration of safflower hypocotyls (8) suggested the cyclic (3) operation of the pentose pathway and suggest also that the tricarboxylic acid cycle (TCA) would not necessarily function at rates appreciably different from those in uninfected tissue. Similar inhibitor experiments with wheat (7, 21) and bean (7) rustaffected plants were not consistent. However, results obtained by Farkas and Kiraly (10) and Bauermeister (4) with malonic and fluoroacetic acids have been interpreted as indicating a change in respiratory pathways, presumably TCA cycle reactions, during disease development. In both instances rust-affected wheat plants were less sensitive to these inhibitors than normal tissue, but the competitive nature of malonate inhibition presents kinetic difficulties (7). A quantitative study of organic acid concentrations in wheat infected with the leaf rust fungus was made by Staples (24) while Bauermeister (4) noted changes in size of spots of organic acids separated by paper chromotography. In each instance moderate increases in malic and citric acids were observed after infections were well established and the major respiratory changes had occurred. The significant unexplained exception noted by both workers was aconitic acid which actually declined 3 to 6 days after infection. The anomalies of the changes among TCA cycle acids and the detection of moderate increases only when infections were well advanced might be explained by a reduction in TCA activity during disease development followed by an active translocation of acids from other leaves as respiration rates increased. Previous work (20) has indicated a capacity of infected tissue to accumulate exogenous metabolites. The data to be presented are part of a comparative study of organic acid changes in wheat and bean tissue infected by rust fungi in which a stage characterized by vegetative growth of the parasites (fleck stage) was compared to the sporulating stage of (levelopment. Particular attention was paid to variables such as infection intensity, ontogenic host drifts in metabolism, diurnal changes in metabolism, and environmental control, aspects which often are not assessed adequately. Since wheat plants under our conditions showed characteristics which normal bean tissue did not possess, more extensive data on bDean rust infections will be discussed elsewhere.