Alcohol dehydrogenase and ethanol in the stems of trees : evidence for anaerobic metabolism in the vascular cambium

Anaerobic fermentation in plants is usually thought to be a transient phenomenon, brought about by environmental limitations to oxygen availability, or by structural constraints to oxygen transport. The vascular cambium of trees is separated from the air by the outer bark and secondary phloem, and we hypothesized that the cambium may experience sufficient hypoxia to induce anaerobic fermentation. We found high alcohol dehydrogenase activity in the cambium of several tree species. Mean activity of alcohol dehydrogenase in Populus deltoides was 165 micromoles NADH oxidized per minute per gram fresh weight in May. Pyruvate decarboxylase activity was also present in the cambium of P. deltoides, with mean activity of 26 micromoles NADH oxidized per minute per gram fresh weight in May. Lactate dehydrogenase activity was not present in any tree species we examined. Contrary to our expectation, alcohol dehydrogenase activity was inversely related to bark thickness in Acer saccharum and unrelated to bark thickness in two Populus species. Bark thickness may be less important in limiting oxygen availability to the cambium than is oxygen consumption by rapidly respiring phloem and cambium in actively growing trees. Ethanol was present in the vascular cambium of all species examined, with mean concentrations of 35 to 143 nanomoles per gram fresh weight, depending on species. Ethanol was also present in xylem sap and may have been released from the cambium into the transpiration stream. The presence in the cambium of the enzymes necessary for fermentation as well as the products of fermentation is evidence that respiration in the vascular cambium of trees may be oxygen-limited, but other biosynthetic origins of ethanol have not been ruled out.     

Metabolism of Transpired Ethanol by Eastern Cottonwood (Populus deltoides Bartr.)

Ethanol has previously been shown to be present in the xylem sap of flooded and nonflooded trees. Because of the constitutive presence of alcohol dehydrogenase in the mature leaves of woody plants, we hypothesized that the leaves and shoots of trees had the ability to metabolize ethanol supplied by the transpiration stream. 1-[14C]Ethanol was supplied to excised leaves and shoots of eastern cottonwood (Populus deltoides Bartr.) in short- and long-term experiments. More than 99% of the radiolabel was incorporated into plant tissue in short-term experiments, with more than 95% of the label remaining in plant tissue after 24 h. In all experiments, less than 5% of the label was transpired as ethanol and less than 1% was emitted as CO2. In excised leaf experiments, less than 0.5% of the radiolabel escaped from the leaf. Fifty percent of the label was incorporated into the petioles of excised leaves; 56% was incorporated into the stems of excised shoots. Very little label reached the leaf mesophyll cells of excised shoots, as revealed by autoradiography. Radiolabel appeared primarily in the water- and chloroform-soluble fractions in short-term experiments, whereas in long-term experiments, label was also incorporated into protein. These results demonstrate that the leaves and stems of trees appear to have substantial ability to scavenge ethanol from the transpiration stream, allowing efficient recovery of ethanol produced elsewhere by hypoxic tissues. When labeled ethanol was supplied to excised petioles in a 5-min pulse, 41% of the label was incorporated into organic acids. Some label was also incorporated into amino acids, protein, and the chloroform-soluble fraction, with very little appearing in neutral sugars, starch, or the insoluble pellet. Labeled organic acids were separated by high performance liquid chromatography and were composed of acetate, isocitrate, [alpha]-ketoglutarate, and succinate. There was no apparent incorporation of label into phosphorylated compounds. We conclude that, in higher plants, ethanol is metabolized to acetaldehyde and then to acetate by alcohol and aldehyde dehydrogenases, and then into general metabolism.     

Diurnal pattern of acetaldehyde emission by flooded poplar trees

The emission of the tropospheric trace gas acetaldehyde was determined in leaves of 4-month-old poplar trees ( Populus tremula × P. alba ) grown under controlled environmental conditions in a greenhouse. Using a dynamic cuvette system together with a high sensitivity laser-based photoacoustic detection unit, rates of acetaldehyde emission were measured with the high time resolution of about 15 min. Submergence of the roots resulted in the emission of acetaldehyde by the leaves. The emission increased linearly before reaching more or less steady-state values (ca 350 nmol m⁻² min⁻¹; ca 470 ng g⁻¹ dry weight min⁻¹) after approximately 6 h. Prolonged flooding of poplar trees resulted in a clear diurnal rhythm of acetaldehyde emission. The emission rates decreased when the light was switched off in the evening and peaked in the morning after the light was turned on again. This pattern significantly correlated with diurnal rhythms of stomatal conductance, photosynthesis, transpiration and with the concentrations of ethanol, the assumed precursor of acetaldehyde, in the xylem sap of flooded poplar trees. It may be concluded that under conditions of diminished stomatal conductance, acetaldehyde emission declines because its diffusive flux is reduced. Alternatively, reduced transpiration may decrease ethanol transport from the roots to the shoots and appreciable amounts of the acetaldehyde precursor ethanol are lacking in the leaves. The present results support the view that acetaldehyde emitted by the leaves of plants is derived from ethanol produced by alcoholic fermentation in submerged roots and transported to the leaves with the transpiration stream.     

Acetaldehyde emission by the leaves of trees – correlation with physiological and environmental parameters

The leaves of trees emit significant amounts of acetaldehyde which is synthesized there by the oxidation of ethanol. In the present study, we examined plant internal and environmental factors controlling the emission of acetaldehyde by the leaves of young poplar ( Populus tremula × P. alba ) trees. The enzymes possibly involved in the oxidation of ethanol in the leaves of trees are catalase (CAT; EC 1.11.1.6) and alcohol dehydrogenase (ADH; EC 1.1.1.1), both expressed constitutively in the leaves of poplars. Inhibition of ADH in excised leaves caused a significant decrease of acetaldehyde emission accompanied by an increased ethanol emission. Since inhibition of CAT by aminotriazole did not affect acetaldehyde and ethanol emission, it is concluded that the oxidation of ethanol in the leaves is mediated by ADH rather than by CAT. Further studies indicated that aldehyde dehydrogenase (ALDH; EC 1.2.1.5) seems to be responsible for the oxidation of acetaldehyde. The present results demonstrate that acetaldehyde emission is clearly dependent on its production in the leaves as controlled by the delivery of ethanol to the leaves via the transpiration stream. Environmental factors that control stomatal conductance seem to be of less importance for acetaldehyde emission by the leaves.     

Metabolic origin of acetaldehyde emitted by poplar (Populus tremula x (P. alba) trees

The metabolic origin and emission by the leaves of the tropospheric trace gas acetaldehyde were examined in 4-month-old poplar trees (Populus tremula x P. alba) cultivated under controlled environmental conditions in a greenhouse. Treatments which resulted in increased ethanol concentration of the xylem sap caused significantly enhanced rates of acetaldehyde and ethanol emission by the leaves. Leaves fed [¹⁴C]-ethanol via the transpiration stream emitted [^<14C]-acetaldehyde. These findings suggest that acetaldehyde in the leaves is synthesized by a metabolic pathway that operates in the opposite direction of alcoholic fermentation and results in oxidation of ethanol. Enzymatic studies showed that this pathway is mediated either by alcohol dehydrogenase (ADH; EC 1.1.1.1) or catalase (CAT; EC 1.11.1.6), both constitutively present in the leaves of poplar trees. Labelling experiments with [¹⁴C]-glucose indicated that the ethanol delivered to the leaves by the transpiration stream is produced in anaerobic zones of submersed roots by alcoholic fermentation. Anoxic conditions in the rhizosphere caused by flooding of the root system resulted in an activation of alcoholic fermentation and led to significantly increased ethanol concentrations in the xylem sap. These results support the hypothesis that acetaldehyde emitted by the leaves of trees is derived from xylem transported ethanol which is synthesized during alcoholic fermentation in the roots.Keywords: Acetaldehyde, emission, ethanol, anaerobiosis, Populus tremula x P. alba      

Influence of flood‐stress on ambrosia beetle host‐selection and implications for their management in a changing climate

• 1 Xylosandrus germanus (Blandford) is a key pest of ornamental nursery trees. Ethanol is the most attractive semiochemical known for X. germanus, and its emission from trees represents a primary host‐selection cue. Ethanol production is induced by a variety of abiotic and biotic stressors, which could thereby predispose trees to attack by ethanol‐responsive ambrosia beetles.
• 2 To better understand X. germanus host‐selection behaviour within ornamental nurseries, a series of experiments examined the influence of flood‐stress on the attractiveness and susceptibility of flowering dogwood Cornus florida L. Under field conditions, more X. germanus were attracted to experimentally flood‐stressed dogwoods than neighbouring nonflooded controls in 2009, 2010 and 2011. Flood‐stressed dogwoods were also preferentially attacked in 2009–2011, although no attacks occurred on any of the neighbouring nonflooded trees.
• 3 Solid‐phase microextraction‐gas chromatography‐mass spectrometry detected ethanol in stem tissue from flooded dogwoods but not nonflooded trees. Acetaldehyde, acetic acid and ethanol were also emitted from the outer bark of flooded dogwoods but not nonflooded trees.
• 4 These results demonstrate that X. germanus preferentially lands on and attacks physiologically‐stressed hosts, and further support the role of ethanol in mediating this interaction.
• 5 Attacks by X. germanus have previously been suspected to occur on trees viewed as ‘apparently‐healthy’, although the possibility of such trees being in apparently‐stressed at the time of attack cannot be ruled out given the results obtained in the present study. Minimizing the impact of stressors known to induce the production of ethanol should be the primary foundation of a management plan for X. germanus and other ethanol‐responsive ambrosia beetles.

     

Interaction of flooding with carbon metabolism of forest trees

Waterlogging and flooding cause oxygen deprivation in the root system of trees. Since oxygen is essentially for mitochondrial respiration, this process cannot be maintained under anoxic conditions and must be replaced by other pathways. For the roots it is therefore a matter of survival to switch from respiration to alcoholic fermentation. Due to the low efficiency of this process to yield energy equivalents (ATP), energy and carbon metabolism of trees are usually strongly affected by oxygen deprivation, even if a rapid switch from respiration to fermentation is achieved. The roots can compensate for the low energy yield of fermentation either (1) by decreasing the demand for energy by a reduction of energy-dependent processes such as root growth and/or nutrient uptake, or (2) by consuming more carbohydrates per unit time in order to generate sufficient energy equivalents. In the leaves of trees, flooding and waterlogging cause a decline in the rates of photosynthesis and transpiration, as well as in stomatal conductance. It is assumed that, due to reduced phloem transport, soluble sugars and starch accumulate in the leaves of flooded trees, thereby negatively affecting the sugar supply of the roots. Thus, root growth and survival is negatively affected by both changes in root internal carbon metabolism and impaired carbon allocation to the roots by phloem transport. In addition, accumulation of toxic products of fermentation in the roots, such as acetaldehyde, can further impair root metabolism. A main feature of tolerance against flooding and waterlogging of trees seems to be the steady supply of carbohydrates to the roots in order to maintain alcoholic fermentation; in addition, roots of tolerant trees seem to avoid accumulation of fermentation-derived ethanol and acetaldehyde. From studies with flooding tolerant and non-tolerant tree species, it is hypothesized that (1) the transport of ethanol produced in the roots under hypoxic conditions into the leaves via the transpiration stream, (2) its conversion into acetyl-CoA in the leaves, and (3) its use in the plant's general metabolism, are mechanisms of flooding tolerance of trees.     

乙醇与乙醛对心脏的影响及其可能机制的探讨

通过研究乙醇、乙醛对离体心脏和神经干的影响,探讨乙醇、乙醛对心脏作用的可能机制.用不同浓度的乙醇和乙醛处理牛蛙蛙心灌流标本和坐骨神经标本,用BL-420 系统对给药前后心脏的心率和振幅以及神经干最小刺激强度作记录.乙醇和乙醛可以引起神经兴奋性的改变从而影响神经冲动的传导,而且其影响具有明显的量效依赖关系,低浓度的乙醇和乙醛能使神经的兴奋性增加,高浓度则降低;乙醇对心脏的心率和振幅均有抑制作用,低浓度的乙醛对心脏心率和振幅有促进作用,高浓度的乙醛对心脏造成不可恢复的损伤.乙醇、乙醛对心脏的影响效果不同,但两者均可直接影响及通过神经而间接影响心脏的活动.     

The phytotoxic effect of exogenous ethanol on Euphorbia heterophylla L.

This study investigated the effects of exogenously applied ethanol on Euphorbia heterophylla L., a troublesome weed in field and plantation crops. Ethanol at concentrations ranging from 0.25 to 1.5% caused a dose-dependent inhibition of germination and growth of E. heterophylla. Measurements of respiratory activity and alcohol dehydrogenase (E.C. 1.1.1.1) activity during seed imbibition and initial seedling growth revealed that ethanol induces a prolongation of hypoxic conditions in the growing tissues. In isolated mitochondria, ethanol inhibited the respiration coupled to ADP phosphorylation, an action that probably contributed to modifications observed in the respiratory activity of embryos. A comparison of the effects of methanol, ethanol, propanol and acetaldehyde on germination and growth of E. heterophylla indicates that alcohol dehydrogenase activity is required for the observed effects, with the conversion of ethanol to acetaldehyde playing a role in the ethanol-induced injuries.     

Effect of chronic ethanol or acetaldehyde on hepatic alcohol and aldehyde dehydrogenases, aminotransferases and glutamate dehydrogenase

Ethanol or acetaldehyde orally administered (15% and 2% respectively in drinking water) to male Wistar rats for three months induced alterations in the main liver enzymes responsible for ethanol metabolism, aspartate and alanine aminotransferases and NAD glutamate dehydrogenase. Ethanol produced a significant decrease in the activity of soluble alcohol dehydrogenase, while acetaldehyde induced alterations both in soluble and mitochondrial aldehyde dehydrogenases: soluble activity was significantly higher than in the control and ethanol-treated groups, and mitochondrial activity was significantly diminished. Both soluble aspartate and alanine aminotransferases showed pronounced increases by the chronic effect of acetaldehyde, while mitochondrial activities were practically unchanged by the effect of ethanol or acetaldehyde. Mitochondrial NAD glutamate dehydrogenase showed a rise in its activity both by the effect of chronic ethanol and acetaldehyde consumption. The level of metabolites assayed in liver extracts showed marked differences between ethanol and acetaldehyde treatment which indicates that ethanol produced a remarkable increase in glutamate, aspartate and free ammonia together with marked decrease in pyruvate and 2-oxoglutarate concentrations. Acetaldehyde consumption induced a significant decrease in 2-oxoglutarate and pyruvate concentrations. These observations suggest that ethanol has an important effect on the urea cycle enzymes, while the effect of acetaldehyde contributes to the impairment of the citric acid cycle.     

Whole plant aspects of heavy metal induced changes in CO2, uptake and water relations of spruce (Picea abies) seedlings

Spruce seedlings [ Picea abies (L.) Karst.] were exposed to a range of concentrations of Zn, Cd, Hg and methyl-Hg for 5 weeks. The chlorophyll and water content of the needles were then estimated. The rates of photosynthesis, transpiration and dark respiration of the intact plant were determined using a Li-cor portable photosynthesis measuring system. Chlorophyll and water contents of needles decreased in response to all metal treatments, as did CO₂ uptake. At 1 μ M Cd, 0.1 μ M Hg and 30 and 60 μ M Zn, the decrease in CO₂ uptake could be accounted for by decreased chlorophyll concentrations. Decreased transpiration was only found at 5 μ M Cd and 0.01 μ M methyl-Hg. At 5 μ M Cd most of the decrease in CO₂ uptake could be explained by decreased chlorophyll levels and stomatal closure induced by water stress. At 0.01 μ M methyl-Hg, besides a decrease in chlorophyll concentration and partial stomatal closure, photosynthetic reactions may have been directly affected. Respiration rates were not influenced by exposure to heavy metals.     

The role of ethanol and acetaldehyde in flower senescence and fruit ripening – A review

Ethanol and acetaldehyde are present in carnation flowers during the senescence process. If applied to cut carnations, flower longevity is increased. These same compounds are found in increasing concentrations during fruit ripening, and the application of acetaldehyde can promote the ripening process. If the natural concentrations are increased by means of external application of either acetaldehyde or ethanol, ripening of some fruits may be inhibited. Acetaldehyde apparently inhibits the formation of ethylene, by preventing the action of ACC synthase and ACC oxidase. Low concentrations of ethanol may prevent normal climacteric respiration from occurring. If ethanol is present in high concentrations, it leads to increased membrane permeability and damages the lipid bilayers, where the site of ethylene action is suspected to be. The effect of both acetaldehyde and ethanol on binding sites, respiration and ethylene production are reviewed. An attempt is also made to provide some understanding of the interrelationship between ethanol and acetaldehyde. The role played by alcohol dehydrogenase in this relationship remains largely unexplored.     

Novel mitochondrial alcohol metabolizing enzymes of <Emphasis Type="Italic">Euglena gracilis</Emphasis>

Ethanol is one of the most efficient carbon sources for Euglena gracilis. Thus, an in-depth investigation of the distribution of ethanol metabolizing enzymes in this organism was conducted. Cellular fractionation indicated localization of the ethanol metabolizing enzymes in both cytosol and mitochondria. Isolated mitochondria were able to generate a transmembrane electrical gradient (Δψ) after the addition of ethanol. However, upon the addition of acetaldehyde no Δψ was formed. Furthermore, acetaldehyde collapsed Δψ generated by ethanol or malate but not by D-lactate. Pyrazole, a specific inhibitor of alcohol dehydrogenase (ADH), abolished the effect of acetaldehyde on Δψ, suggesting that the mitochondrial ADH, by actively consuming NADH to reduce acetaldehyde to ethanol, was able to collapse Δψ. When mitochondria were fractionated, 27% and 60% of ADH and aldehyde dehydrogenase (ALDH) activities were found in the inner membrane fraction. ADH activity showed two kinetic components, suggesting the presence of two isozymes in the membrane fraction, while ALDH kinetics was monotonic. The ADH Km values were 0.64–6.5 mM for ethanol, and 0.16–0.88 mM for NAD⁺, while the ALDH Km values were 1.7–5.3 μM for acetaldehyde and 33–47 μM for NAD⁺. These novel enzymes were also able to use aliphatic substrates of different chain length and could be involved in the metabolism of fatty alcohol and aldehydes released from wax esters stored by this microorganism.     

Inhibition of acetaminophen activation by ethanol and acetaldehyde in liver microsomes

Mechanisms of the inhibitory effect of ethanol on acetaminophen hepatotoxicity are controversial. We studied the effects of ethanol and acetaldehyde, an oxidative metabolite of ethanol, on NADPH-dependent acetaminophen-glutathione conjugate production in liver microsomes. Ethanol at concentrations as low as 2mM prevented the conjugate production noncompetitively. Acetaldehyde also inhibited acetaminophen-glutathione conjugate production at concentrations as low as 0.1mM that is comparable with those observed in vivo after social drinking. Acetaldehyde may be involved in ethanol-induced inhibition of acetaminophen hepatotoxicity.     

The effect of ethanol and acetaldehyde on [14C]pantothenate incorporation into CoA in cultured rat liver parenchymal cells

The effect of ethanol on [¹⁴C]pantothenate incorporation into CoA and on total CoA levels was measured in 3-day-old primary cultures of adult rat liver parenchymal cells. Ethanol decreased the incorporation of radioactivity into CoA a maximum of 67%, 5 mm ethanol was saturating for the inhibitory effect and 0.2 mm ethanol was sufficient for half-saturation. This inhibitory effect did not result from a loss of CoA precursors or from cell death. Ethanol concentrations up to 10 mm did not decrease the ATP content of cells or the total protein content of cells which adhered to the incubation flask. Ethanol (5 mm) had no effect on the cyteine + cystine content of the cells. Intracellular pantothenate concentrations were not affected by 5 mm ethanol, and increasing the pantothenate concentration did not affect ethanol inhibition. Ethanol inhibition of [¹⁴C]pantothenate conversion to CoA could be fully reversed by rinsing the cells free of ethanol. The ethanol inhibition could also be fully reversed by addition of 4-methylpyrazole, indicating that ethanol must be oxidized via alcohol dehydrogenase to exert its inhibitory effect. Acetaldehyde, the immediate product of alcohol dehydrogenase, was also an inhibitor of the incorporation of [¹⁴C]pantothenate into CoA; the maximum inhibition was 63%. Acetaldehyde concentrations maintained between 18 and 103 μm inhibited incorporation by 57%. The inhibition by acetaldehyde did not correlate well with changes in the NADH and NAD⁺ ratio of the cells (as determined by measuring changes in the lactate-to-pyruvate ratio). The ability of glucagon, dibutyryl cAMP + theophylline, or dexamethasone to stimulate [¹⁴C]pantothenate conversion to CoA was not decreased by the addition of ethanol or acetaldehyde, indicating that ethanol inhibition does not occur by reversal of the cAMP-mediated regulatory mechanism for CoA biosynthesis.     

Effect of ethanol on the hemolytic stability of erythrocytes

The stability of rabbit erythrocytes to hemolysis induced by different compounds in the presence or absence of ethanol or acetaldehyde has been analyzed. Ethanol slightly reduced erythrocyte stability against acidic hemolysis only after long-term preincubation, but the effect of ethanol on stability to oxidative hemolysis manifested itself immediately after its addition to the cells. Ethanol decreased both stability of cells to oxidative damage and dispersion of the hemolytic curve. Comparison of the effects of ethanol and acetaldehyde showed that the destabilizing effect of ethanol might be caused by either its direct action or the effect of its metabolites formed during preincubation of ethanol with erythrocytes. Possible mechanisms of ethanol and acetaldehyde effects on erythrocyte stability are discussed.     

Destruction of highly purified cytochromes P-450 associated with metabolism of fluorinated ether anesthetics

The effects of ethanol and acetaldehyde on rat intestinal microvillus membrane integrity and glucose transport function were examined in vitro with purified membrane vesicles. Ethanol could influence glucose transport function by alterations in the conformation of the carrier, the lipid environment surrounding the carrier, or in the transport driving force (Na⁺ electrochemical gradient). Due to the rapid nature of glucose uptake, transport was assayed with the use of an apparatus that permitted uptake measurements as early as 1 s. Ethanol (340 mm) partially and acetaldehyde (44 mm) completely inhibited concentrative glucose uptake throughout the 1-min time course. Their inhibitory effects were reversible and irreversible, respectively. Kinetic measurements made during the initial rate of uptake (at 2 s) with various concentrations of glucose (0.05–8 mm) showed that ethanol and acetaldehyde both caused a decrease in V. Although ethanol did not substantially alter the transport K_m, acetaldehyde increased the K_m almost 50%. To determine whether ethanol or acetaldehyde directly interfered with glucose carrier function, uptake was measured in the presence of equilibrated Na⁺. Only acetaldehyde had a significant inhibitory effect under these conditions. Membrane permeability, as determined by efflux of preloaded 6-carboxyfluorescein dye, increased upon exposure of the vesicles to ethanol or acetaldehyde. Membrane fluidity measurements by fluorescence polarization showed that only acetaldehyde had a significant fluidizing effect. These results indicate that ethanol and acetaldehyde acted to perturb membrane integrity and inhibited glucose uptake indirectly by allowing the Na⁺ gradient to dissipate. Acetaldehyde, which had a stronger inhibitory effect than ethanol, appeared also to directly inhibit carrier function.     

Assimilate Transport in the Xylem Sap of Pedunculate Oak (Quercus robur) Saplings

Abstract: The rates of photosynthesis and transpiration, as well as the concentrations of organic compounds (total soluble non-protein N compounds [TSNN], soluble carbohydrates), in the xylem sap were determined during two growth seasons in one-year-old Quercus robur saplings. From the data, the total C gain of the leaves, by both photosynthesis and the transpiration stream, was calculated. Large amounts of C were allocated to the leaves by the transpiration stream; depending on the time of day and the environmental conditions the portion of C originating from xylem transport amounted to 8 to 91% of total C delivery to the leaves. Particularly under conditions of reduced photosynthesis, e.g., during midday depression of photosynthesis, a high percentage of the total C delivery was provided to the leaves by the transpiration stream (83 to 91 %). Apparently, attack by phloem-feeding aphids lowered the assimilate transport from roots to shoots; as a consequence the portion of C available to the leaves from xylem transport amounted to only 12 to 16 %. The most abundant organic compounds transported in the xylem sap were sugars (sucrose, glucose, fructose) with concentrations of ca. 50 to 500 μmol C ml^-1, whereas C from N compounds was of minor significance (3 to 20 μmol ml^-1 C). The results indicate a significant cycling of C in the plants because the daily transport of C with the transpiration stream exceeded the daily photosynthetic CO₂ fixation in several cases. This cycling pool of C may sustain delivery of photosynthate to heterotrophic tissues, independent of short time fluctuations in photosynthetic CO₂ fixation.     

Acetaldehyde induces histamine release from purified rat peritoneal mast cells

Acetaldehyde is a widely distributed compound in the human environment and it is also formed in the human body from various endogenous and exogenous sources, exogenous ethanol being the most important one. Many alcohol-associated hypersensitivity reactions, e.g. Oriental flushing reaction, appear to be attributable to acetaldehyde rather than to ethanol itself. The pathogenetic mechanism behind such hypersensitivity reactions has been suggested to be histamine release from mast cells or blood basophils. However, the direct effects of acetaldehyde on mast cells, the main source of histamine in a mammalian body, have not been studied. The aim of the present study was, thus, to evaluate whether physiological concentrations of acetaldehyde could release histamine from purified rat peritoneal mast cells. The effects of ethanol were studied similarly. The results show that acetaldehyde, already at a concentration of 50 microM, significantly increases the release of histamine from mast cells. Ethanol has a similar effect but only at molar concentrations. These results indicate that acetaldehyde may contribute to the development of various hypersensitivity reactions by directly increasing histamine release from mast cells.     

The inhibition of human leukocyte elastase by basic pancreatic trypsin inhibitor

The effects of 30-min intravenous infusions of ethanol (about 50 mm blood concentration), acetaldehyde (about 100 μm blood concentration), and acetate (equimolar dose to acetaldehyde) were studied in normal and adrenalectomized rats. Blood glucose, plasma free fatty acids (FFA), plasma immunoreactive insulin, and glucagon and hepatic glycogen concentrations were measured. Ethanol itself in the presence of 4-methylpyrazole (4-MP) produced no marked changes in the parameters measured. Its infusion without 4-MP reduced plasma insulin by 35% in the normal rats, but not in the adrenalectomized rats, with no simultaneous changes in blood glucose. Acetaldehyde infusion produced hyperglycemia and relatively slight hyperinsulinemia in the normal rats, but not in the adrenalectomized rats. Equimolar acetate was not as potent a stimulator of glycogenolysis as acetaldehyde. Plasma FFA concentrations were markedly reduced by ethanol (without 4-MP), acetaldehyde and acetate both in the normal and adrenalectomized rats, but in the presence of 4-MP ethanol was without effect. The results indicate that metabolites of ethanol (mostly acetaldehyde) produced during ethanol oxidation in vivo are responsible for the stimulation of glycogenolysis through the release of catecholamines from the adrenal glands. The ethanol-induced decrease in plasma FFA is also attributable to the metabolites of ethanol, acetaldehyde having a more potent depressing action than acetate. The mode of inhibition of lipolysis is not related to hormonal factors.