Ethanol inhibition

The absolute pH range for the growth of most yeasts is 2.4-S.6 with the optimum being about 4.5 (Atkinson and Mavituna, 1983). The specific rate of ethanol production is very sensitive to pH values above 5 and at pH 6 it is only 50% of the maximum value (Jones and Greenfield, 1984). With increasing pH there is a reduction in the yield of ethanol from glucose and a rise in the yields of both glycerol and acetic acid. 

Bauer (1986) recommended that the moisture content of pressed baker s yeast pellets should be maintained between 55% and 65% (wwb) for satisfactory fermentation of the feed glucose. The original moisture content of the yeast is about 70% (wwb) and any decline in moisture content in the bed is due to a mismatch between the drying rate in the bed and the rate at which water is added with the feed solufion. Such a mismatch occurred in work reported by Moebus and Teuber (1984) who obtained ethanol yields of 0.36 and 0.21 at final yeasf moisture contents of 55.9% and 32.6% respectively. 

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Strohhacker J, AA de Graaf, SM Schoberth, RM Wittig, H Sahm (1993) P nuclear magnetic resonance studies of ethanol inhibition in Zymomonas mobilis. Arch Microbiol 159 484 90. 

Dorio, RJ. and Forman, H.J., Ethanol inhibition of signal transduction in superoxide production by rat alveolar macrophages. A proposed mechanism for ethanol related pneumonia, Arm. Clin. Lab. Sci. 18, 3, 190, 1988. 

The kinetic parameters for the oxidation of a series of alcohols by ALD are shown in Table 4.1 (74). Methanol and ethylene glycol are toxic because of their oxidation products (formaldehyde and formic acid for methanol and a series of intermediates leading to oxalic acid for ethylene glycol), and the fact that their affinity for ALD is lower than that for ethanol can be used for the treatment of ingestion of these agents. Treatment of such patients with ethanol inhibits the oxidation of methanol and ethylene glycol (competitive inhibition) and shifts more of the clearance to renal clearance thus decreasing toxicity. ALD is also inhibited by 4-methylpyrazole. 

There is an additional factor contributing to the toxicity of cocaine, namely its interaction with ethanol [122] [123], Many cocaine (ab)users simultaneously ingest ethanol, probably to experience potentiation of effects and attenuation of headaches. It is now known that ethanol interferes in two ways with the metabolism of cocaine, first by inhibiting its hydrolysis and second by allowing transesterification to form benzoylecgonine ethyl ester (7.61, Fig. 7.8) commonly known as cocaethylene. These metabolic effects are illustrated by studies in the rat (Table 7.3), with ethanol inhibiting the formation of... 

All novel bioreactors attempt to increase productivity by increasing yeast cell concentration or by reducing ethanol inhibition and much work has been reported on ethanol production in fluidized beds by Bauer, Hayes, Moebus, Rottenbacher, Teuber and their co-workers aqueous glucose solutions can be atomised within a bed of yeast particles with the latent heat for vaporisation of both ethanol and... 

A theoretical model (Beck and Bauer, 1989), based on ethanol inhibition alone as the limiting factor in gas-solid fluidized bed fermenters run with recirculating inert gas, suggested that the potential of this technique has not been fully explored. Hayes (1998) suggested significant improvements to the model and provided experimental confirmation of its validity. 

A summary of the factors which are known to influence ethanol production from glucose in a gas-solid fluidized bed fermenter, or which may have an influence based on observations with submerged fermentations, is shown in Figure 6.1. In anaerobic beds, the key factors are the fermentation temperature and ethanol inhibition, both of which have a dramatic effect on the specific rafe of ethanol production. Bed dehydration and its influence on yeast pellet moisture content is also important, since a failure of fermentation may occur if the pellets become too dry (Bauer, 1986). 

Pamment, N.B., Overall kinetics and mathematical modelling of ethanol inhibition in yeasts, in van Uden, N., (ed.). Alcohol toxicity in yeasts and bacteria, CRC Press, Boca Raton, Florida, 1989,1-75. 

Management of methanol and ethylene glycol poisoning is similar. Symptomatic support of respiration and circulation is augmented by correction of metabolic acidosis with intravenous bicarbonate infusion, and control of seizures with diazepam. Ethanol inhibits the metabolism of methanol and ethylene glycol to the toxic metabolites, and can give time for further treatment. The goal is to maintain blood ethanol concentrations between 100 and 150 mg per decilitre, sufficient to saturate alcohol... 

Abacavir undergoes extensive hepatic metabolism therefore, patients with liver disease should be monitored closely if this drug is given. Ethanol inhibits the metabolism of abacavir because it competes for metab-... 

Intravenous use of ethanol, while once widely employed to inhibit premature labor, is now of historical interest only. Ethanol inhibits oxytocin release from the pituitary and thus indirectly decreases myometrial contractility. Today, pz-adrenomimetics and magnesium sulfate have replaced ethanol for parenteral tocolysis. 

The acute effects of ethanol and other sedative-hypnotics are mediated by actions at a number of receptor systems. For example, ethanol inhibits several excitatory receptor systems, including N-methyl-D-aspartate (NMDA) receptors, kainate receptors, and Ca channels. In addition, ethanol enhances the action of GABA at GABA receptors and appears to modulate serotonergic neurotransmission. Although a component of ethanol reinforcement is mediated by the activation of mesocorticolimbic dopamine neurons, activation of these neurons may not be necessary for ethanol reinforcement, as ethanol remains reinforcing in the absence of these neurons (Samson and Harris, 1992 Koob, 2000b). 

A) Representative experiment showing the effect of ethanol on non-NMDA reseptor-mediated response. (B) Representative experiment showing die influence of crocin on ethanol-induced inhibition of non-NMDA response. Crocin (10 iM) was applied 10 min prior to ethanol (white bar). (C) Concentration-effect curves for ethanol inhibition of non-NMDA response in the absence (O) or presence ( ) of 10 pM crocin. 

In order to confirm the possible interaction of ethanol and crocin on NMDA receptors, we also performed whole-cell patch recording with primary cultured hippocampal neurons and measured membrane currents induced by the application of NMDA in a voltage-clamped condition. Application of 100 pM NMDA induced an inward current of 100.2 9.8 pA (n=10) at a holding potential of -60 mV. The NMDA-induced inward current was not affected by 10 pM CNQX (data not shown), but was completely abolished by 30 pM APV, supporting the fact that the response was mediated by NMDA receptors. Ethanol inhibited NMDA-induced currents in a concentration-dependent manner. Crocin (10 pM) had no effect on NMDA-induced currents by itself (data not shown), but attenuated the inhibitory effect of ethanol on NMDA-induced currents. The concentration-effect curve for ethanol was shifted to the right by the presence of crocin [22]. 

We demonstrated for the first time that crocin selectively antagonizes the inhibitory effect of ethanol on NMDA-receptor-mediated responses in hippocampal neurons. This action of crocin may underlie the antagonism against ethanol-induced memory impairment. Crocin should be useful as a new pharmacological tool for studying the mechanism of ethanol inhibition of NMDA receptor functions. 

The consumption and subsequent metabolism of ethanol inhibits gluconeogenesis, leading to hypoglycemia in individuals with depleted stores of glycogen. Alcohol consumption can also increase the risk for hypoglycemia in patients using insulin. 

Vidal et al. (2001) examined the inhibitory effect of two commonly used pesticides, copper and dichlofluanid, on several strains of O. oeni and on MLF in simulated wine. Sensitivity to these pesticides varied and was enhanced by the presence of ethanol. Inhibition was due to a decrease in cell number and not to a decrease in malolactic activity. Quinoxyfen,... 

Smothers C. T. and Woodward J. J. (2003). Effect of the NR3 subunit on ethanol inhibition of recombinant NMDA receptors. Brain Res. 987 117-121. 

FIGURE 68.4 Ethanol inhibits the secretion of antidiuretic hormone. 

Koyama M, Heerdt PM, Levi R (2003) Increased severity of reperfusion arrhythmias in mouse hearts lacking histamine H3-receptors. Biochem Biophys Res Commun 306 792-6 Koyama S, Brodie MS, Appel SB (2007) Ethanol inhibition of M-current and ethanol-induced direct excitation of ventral tegmental area dopamine neurons. J Neurophysiol 97 1977-85 Kuzhikandathil EV, Yu W, Oxford GS (1998) Human dopamine D3 and D2l receptors couple to inward rectifier potassium channels in mammalian cell lines. Mol Cell Neurosci 12 390 102 Kuzhikandathil EV, Oxford GS (1999) Activation of human D3 dopamine receptor inhibits P/Q-type calcium channels and secretory activity in AtT-20 cells. J Neurosci 19 1698-1707... 

There are numerous reports indicating that many volatile substances such as methanol, ethanol, n-propanol and n-butanol produced by fungi and yeast (4) inhibit the growth of rice and sugar cane at 10 - 10 M. Further, ethanol inhibits the seed... 

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