Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Ethanol utilization”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 829 records · Page 46Linked to original sources

Phospholipid spin probes measure the effects of ethanol on the molecular order of liver microsomes.

Ethanol, in vitro, is known to perturb the molecular order of the phospholipids in biological membranes, while chronic ethanol exposure, in vivo, leads to resistance to disordering. Such changes have usually been measured by electron spin resonance, utilizing fatty acid spin probes. The use of such probes is controversial, since their orientation in the membrane may not accurately represent that of individual phospholipids. We, therefore, compared ethanol-induced structural perturbations in the membranes of rat hepatic microsomes measured with the spin probe 12-doxylstearic acid (SA 12) with those assayed with various phospholipid spin probes. With SA 12, the addition of increasing amounts of ethanol (50-250 mM) in vitro caused a progressive decrease in the membrane molecular order, as measured by electron spin resonance (ESR). By contrast, microsomes obtained from rats chronically fed ethanol were resistant to the disordering effect of ethanol. Microsomes labeled with the phospholipid spin probes 1-palmitoyl-2-(12-doxylstearoyl)phosphatidylcholine, -phosphatidylethanolamine, or -phosphatidic acid also exhibited increased disordering with the addition of increasing amounts of ethanol. However, the effect noted with phospholipid spin probes was less than that observed with the fatty acid probe. Microsomes obtained from the livers of chronically intoxicated animals labeled with the phospholipid probes were also resistant to the disordering effects of ethanol in vitro. These results suggest that fatty acid spin probes are qualitatively valid for measuring membrane perturbations in biological membranes, ethanol affects all microsomal phospholipids, regardless of chemical dissimilarities (e.g., head-group structure), in a qualitatively similar fashion, and the fluidization of fatty acyl chains in microsomal membranes is comparable in different membrane phospholipids.

Animals↗

Characterization of carbon metabolism in a highly adhesive bacterium Acinetobacter sp. Tol 5 capable of assimilating diverse hydrocarbons and aromatic compounds.

Sustainable bioproduction requires developing robust microbial chassis with broad metabolic versatility and suitability for industrial applications. Acinetobacter sp. Tol 5 is a highly adhesive bacterium capable of utilizing various hydrocarbons, making it a promising chassis candidate for immobilized whole-cell catalysis. In this study, we characterized the carbon metabolism of Tol 5 by reconstructing metabolic pathway maps from its genomic data and analyzing the transcriptomes of cells grown on ethanol, hexadecane, toluene, and phenol. Genomic analysis revealed that Tol 5 has limited capacity for sugar utilization but possesses a wide range of metabolic pathways for alkane and aromatic compounds, including five distinct aromatic degradation routes that expand the known metabolic diversity of the genus Acinetobacter. Transcriptome analysis identified the specific pathway genes induced in response to each carbon source. During growth on phenol, alkylbenzene degradation genes were upregulated alongside phenol monooxygenase genes, suggesting possible substrate-dependent cross-regulation between aromatic degradation pathways. Gene disruption experiments indicated that phenol monooxygenase is required for phenol assimilation, whereas toluene dioxygenase may contribute to earlier entry into exponential growth while potentially limiting final biomass accumulation. These findings provide a comprehensive view of the carbon metabolism of Tol 5 and a basis for assessing its potential in bioprocesses using non-sugar carbon sources.

Acinetobacter↗

Energetics of Microbacterium thermosphactum in glucose-limited continuous culture.

Microbacterium thermosphactum was grown at 25 degrees C in glucose-limited continuous culture under aerobic (greater than 120 microM oxygen) and anaerobic (less than 0.2 microM oxygen) conditions. The end products of the anaerobic metabolism of glucose were identified as L-lactate and ethanol. Together these compounds accounted for between 85 and 90% of the glucose utilized over the full range of growth rates studied. In addition, 4% of the glucose utilized was incorporated into cellular material. Under anaerobic conditions the molar growth yield was 40 g (dry weight) of cells per mol of glucose utilized, and the maintenance energy coefficient was 0.4 mmol of glucose utilized per g (dry weight) of cells per h. For cells grown under aerobic conditions in the corresponding values were 73 g/mol and 0.2 mmol/g per h, respectively. The molar growth yield with respect to adenosine 5'-triphosphate varied with the growth rate of the culture, and the true molar growth yield with respect to adenosine 5'-triphosphate was found to be 20 g/mol of adenosine 5'-triphosphate.

Actinomycetales↗

Regulation of sugar and ethanol metabolism in Saccharomyces cerevisiae.

This review briefly surveys the literature on the nature, regulation, genetics, and molecular biology of the major energy-yielding pathways in yeasts, with emphasis on Saccharomyces cerevisiae. While sugar metabolism has received the lion's share of attention from workers in this field because of its bearing on the production of ethanol and other metabolites, more attention is now being paid to ethanol metabolism and the regulation of aerobic metabolism by fermentable and nonfermentable substrates. The utility of yeast as a highly manipulable organism and the discovery that yeast metabolic pathways are subject to the same types of control as those of higher cells open up many opportunities in such diverse areas as molecular evolution and cancer research.

Animals↗

Anxiety-like behaviors following chronic ethanol exposure.

Rodent models of ethanol withdrawal-induced anxiety have been used to explore the neurobiology underlying withdrawal and to evaluate the utility of therapeutic agents aimed at reducing withdrawal severity. Of the many tests of anxiety-like behavior, the elevated plus maze, light/dark box, and open field are the most commonly used. In general, ethanol withdrawal decreases most or all of the individual behaviors recorded in these tasks, indicating the occurrence of an anxiogenic-like effect of withdrawal in rodents, although these effects of withdrawal have not always been found. Potential problems with interpreting the effects of withdrawal as being indicative of an anxiety-like state include the effects of withdrawal on motivation to explore an apparatus, non-specific effects of withdrawal on locomotion, and the use of test parameters that have not been pharmacologically validated. For example, most of the published studies interpreted as having shown increased anxiety-like behavior during ethanol withdrawal have also observed concurrent decreases in locomotion. At a minimum, a given test of anxiety-like behavior during withdrawal should be responsive to the dose and duration of ethanol exposure that was used to produce physical dependence, and should not non-specifically decrease locomotion. In addition, standard anxiolytic drugs should ameliorate the anxiogenic-like effects of withdrawal, preferably in multiple tests of anxiety-like behavior.

Animals↗

Ethanol effects on 2-deoxyglucose uptake into tissues obtained from LS and SS mice.

The uptake of 2-deoxy-D-[14C]glucose (2-DG) has been used with some success to identify neuronal sites of drug action, and has also been useful in identifying brain regions that are differentially sensitive to ethanol in selectively bred rat lines, the alcohol tolerant (AT) and alcohol nontolerant (ANT) lines. The studies reported here utilized the 2-DG method in an attempt to ascertain whether the LS and SS mouse lines, which were selectively bred for differences in sensitivity to high dose, anesthetic effects of ethanol, do so because of disruption of specific neuronal sites. LS and SS mice were injected with saline or a 4.0-g/kg dose of ethanol 15 min before injection with 2-deoxy-D-[14C]glucose, and uptakes into blood, eight brain regions, the liver, and adrenal tissues were measured 2-60 min afterwards. Ethanol produced statistically significant decreases in 2-DG uptake into every region of the LS mouse brain, but only three brain regions showed significant decreases in uptake in the SS brain. Other SS brain regions showed a trend towards decreased uptake, but these trends were not significant. A comparison of percent decrease in 2-DG uptake across all brain regions showed that ethanol decreased 2-DG uptake approximately twice as much in LS brain regions as in SS brain regions. Since 2-DG uptake into adrenal and hepatic tissue was not affected by ethanol injection in either mouse line, it seems likely that the decreased 2-DG uptake, seen more readily in the LS brain, is due to ethanol-induced central nervous system (CNS) depression.(ABSTRACT TRUNCATED AT 250 WORDS)

Adrenal Glands↗

Effects of ethanol drinking on central nervous system functional activity of alcohol-preferring rats.

The [(14)C]-2-deoxyglucose (2-DG) technique was used to assess the rates of local cerebral glucose utilization (LCGU) in key limbic, cerebral cortical, hippocampal, basal ganglionic, and subcortical regions of alcohol-preferring (P) rats following chronic 24-h free-choice ethanol drinking. Adult male P rats were submitted to (1) 8 continuous weeks of two-bottle access to 15% ethanol and water (E-C group); (2) 8 weeks of identical two-bottle access followed by 2 weeks of ethanol deprivation (E-D group); (3) cycles of 2 weeks of two-bottle ethanol access and 2 weeks of deprivation, repeated for four cycles (E-RD group); or (4) water only treatment [ethanol-naive group (E-N group)]. A single pulse of [(14)C]-2-DG (125 microCi/kg) was administered via a venous catheter, and timed arterial blood samples were collected over 45 min and later assayed for plasma glucose and [(14)C]-2-DG concentrations. Quantitative autoradiography was used to determine [(14)C] densities, and LCGU values were calculated. With the exception of a few small differences in the hippocampus, no significant differences were found in any of the central nervous system (CNS) regions examined among the four experimental groups of P rats. Animals in the E-D group had lower LCGU rates in the anterior hippocampal CA1 subregion than animals in the E-N, E-C, and E-RD groups. In the anterior hippocampal CA3 subregion and the anterior hippocampal dentate gyrus, the E-D group had significantly lower LCGU rates than the E-RD group. Overall, the results of this study indicate that 24-h ethanol-drinking experience has little effect on CNS functional neuronal activity in P rats.

Alcohol Drinking↗

Ethanol inhibits muscarinic receptor-stimulated phosphoinositide metabolism and calcium mobilization in rat primary cortical cultures.

In recent years, it has been hypothesized that muscarinic receptor-stimulated phosphoinositide (PI) metabolism may represent a relevant target for the developmental neurotoxicity of ethanol. Age-, brain region-, and receptor-specific inhibitory effects of ethanol on this system have been found, both in vitro and after in vivo administration. As a direct consequence of this action, alterations of calcium homeostasis would be expected, through alterations of inositol trisphosphate formation, which mediates intracellular calcium mobilization. In the present study, the effects of ethanol (50-500 mM) on carbachol-stimulated PI metabolism and free intracellular calcium levels were investigated in rat primary cortical cultures, by measuring release of inositol phosphates and utilizing the two calcium probes fluo-3 and indo-1 on an ACAS (Adherent Cell Analysis and Sorting) Laser Cytometer. Ethanol exerted a concentration-dependent inhibition of carbachol-stimulated PI metabolism. In addition, ethanol's inhibitory effect paralleled the temporal development of the muscarinic receptor signal transduction system, with the strongest inhibition (25-50%) occurring when maximal stimulation by carbachol occurs (days 5-7). Ethanol also exerted a concentration-dependent decrease in free intracellular calcium levels following carbachol stimulation. Both initial calcium spike amplitude, seen in all responsive cells, as well as the total number of cells responding to carbachol, were decreased by ethanol. The inhibitory effects of ethanol seemed dependent upon preincubation time, in that a longer preincubation (30 min) with the lowest dose (50 mM), showed almost the same decrease in responding cell number and reduction in spike amplitude in responding cells, as a shorter incubation (10 min) with the highest ethanol dose (500 mM). The specificity of the response to carbachol was demonstrated by blocking the response with 10 microM atropine. Moreover, experiments with carbachol in calcium-free buffer with 1 mM EGTA indicated that the initial calcium spike was due to intracellular calcium mobilization from intracellular stores. Since calcium is believed to play important roles in cell proliferation and differentiation, these results support the hypothesis that this intracellular signal-transduction pathway may be a target for ethanol, contributing to its developmental neurotoxicity.

Action Potentials↗

Chronic ethanol consumption affects glutathione status in rat liver.

There is no consensus yet on the role of oxidative stress in the nutritional outcome of chronic ethanol feeding and the status of cellular antioxidative defense systems against ethanol toxicity. In this study, chronic alcohol consumption in humans was reproduced in Sprague-Dawley rats to investigate the effect of ethanol ingestion on the regulation of oxidative stress in liver with a special focus on glutathione. Adult male rats were given 36% of total energy as alcohol in the Lieber-DeCarli liquid diet for 6 wk. The control group was pair-fed the diet containing isocaloric dextrin-maltose instead of ethanol. Chronic ethanol ingestion enhanced expression of cytochrome P450 II E1 in the liver, but did not significantly alter either the level of hepatic thiobarbituric acid reactive substances or the carbonyl group content of proteins. The hepatic concentrations of total and reduced glutathione and the activities of catalase, glutathione reductase and glutathione S-transferase were significantly higher in the ethanol group than in the control group. The activities of glutathione peroxidase and glucose-6-phosphate dehydrogenase were significantly lower in the ethanol group than in controls. Chronic ethanol consumption by well-nourished rats for 6 wk increased enzyme activities related to the recycling and utilization of glutathione in the liver. Such an enhancement in the activities of the hepatic antioxidative defense system may be one of the protective mechanisms of the body against oxidative tissue damage caused by ethanol-induced free radicals.

Alcohol Drinking↗

Features of DNA oligonucleosomal fragmentation in human tumor cell lines and its detection by flow cytometry: utility and limitations.

Cultured HL-60, HeLa S3 and WiDr cells were treated with various doses of ethanol, then subjected to flow cytometry and gel electrophoresis of cellular DNA. On electrophoresis of DNA from HL-60 cells treated with 0.5 or 1.0 mM ethanol, a ladder pattern was recognized after 3 h. At higher doses of ethanol (2.0 and 5.0 mM), a smear pattern resulted. On flow cytometry, however, A0 cells (lower fluorescence level than G0+G1 cells) were noted from 0.5 to 5.0 mM ethanol. The observation of A0 cells at higher doses indicated loss of DNA after random DNA degradation. HeLa S3 and WiDr cells were partially detached from flasks after administration of ethanol and separated into adherent and non-adherent categories. In DNA from non-adherent HeLa S3 cells treated with 0.5 mM ethanol, a ladder pattern was observed after 24 h. On flow cytometry, prior to the appearance of A0 cells, an accumulation in the G2 + M-phase became obvious after 3 h. Increased mitotic indices indicated that this phenomenon was due to M-phase arrest. Adherent HeLa S3 cells showed no DNA oligonucleosomal fragmentation or A0 cells. These findings indicate that detection of A0 cells by flow cytometry is not proof of cell death by DNA oligonucleosomal fragmentation.

Apoptosis↗

Detection method for polygalacturonase-producing strains of Saccharomyces cerevisiae.

In the presence of glycerol or ethanol, SCPP (a strain of Saccharomyces cerevisiae that expresses pectinolytic activity) is capable of utilizing galacturonic acid or pectins for growth purposes. We now establish a relationship between the pectinolytic power of various strains of S. cerevisiae and their ability to grow on a pectin/glycerol-based medium. This property is further exploited for the detection of polygalacturonase-producing strains of S. cerevisiae.

Culture Media↗

Role of the brain-gut axis in alcohol-related gastrointestinal diseases--what can we learn from new animal models?

Ethanol exerts multiple actions on nearly all organs of the body, especially on the central nervous system and the gastrointestinal tract. However, little is known about the effects ethanol has on the brain-gut axis, the linkage between the central neural system and the autonomous innervation of the gastrointestinal tract. It is indisputable that ethanol consumption does affect e.g. exocrine pancreatic secretion or intestinal motility, but it is poorly understood, how alcohol consumption may disturb the brain-gut axis and how this may cause damage to gastrointestinal organs. Due to difficulties in directly assessing ethanol effects on the brain-gut axis in humans, animal models represent a versatile tool to study this topic. However, conventional animal models widely utilized in alcohol research, e.g. the Tsukamoto-French model or the Lieber-DeCarli model, do not mimic the human conditions of ethanol consumption and are therefore not suitable for studies of the brain-gut axis. Established models from other alcohol research disciplines, e.g. addiction research, are by far more applicable. Due to this reason, we have established an animal model of alcohol-dependent rats for the use in gastrointestinal alcohol research. In this model, rats are given free access to different of alcohol solutions (5% and 20% v/v) and tap water. Over time, the rats develop signs of alcohol dependence as seen in humans (e.g. deprivation effect). Organs isolated from rats exposed to this model are currently investigated in our laboratory for alcohol-related gene-regulation compared to non-alcoholic littermates. In addition, non-alcoholic components of alcoholic beverages might affect the brain-gut axis or possibly potentiate the toxicity of ethanol. In our model, commonly ingested alcoholic beverages such as beer, wine, cognac, vodka, and whisky and their non-alcoholic constituents will be tested in future animal studies.

Alcohol Drinking↗

Starch fermentation by recombinant saccharomyces cerevisiae strains expressing the alpha-amylase and glucoamylase genes from lipomyces kononenkoae and saccharomycopsis fibuligera.

Lipomyces kononenkoae and Saccharomycopsis fibuligera possess highly efficient alpha-amylase and/or glucoamylase activities that enable both of these yeasts to utilize raw starch as a carbon source. Eight constructs containing the L. kononenkoae alpha-amylase genes (LKA1 and LKA2), and the S. fibuligera alpha-amylase (SFA1) and glucoamylase (SFG1) genes were prepared. The first set of constructs comprised four single gene cassettes each containing one of the individual amylase coding sequences (LKA1, LKA2, SFA1 or SFG1) under the control of the phosphoglycerate kinase gene (PGK1) promoter and terminator, while the second set comprised two single cassettes containing SFA1 and SFG1 linked to their respective native promoters and terminators. The third set of constructs consisted of two double-gene cassettes, one containing LKA1 plus LKA2 under the control of the PGK1 promoter and terminator, and the other SFA1 plus SFG1 controlled by their respective native promoters and terminators. These constructs were transformed into a laboratory strain Saccharomyces cerevisiae (Sigma1278b). Southern-blot analysis confirmed the stable integration of the different gene constructs into the S. cerevisiae genome and plate assays revealed amylolytic activity. The strain expressing LKA1 and LKA2 resulted in the highest levels of alpha-amylase activity in liquid media. This strain was also the most efficient at starch utilization in batch fermentations, utilizing 80% of the available starch and producing 0.61g/100 mL of ethanol after 6 days of fermentation. The strain expressing SFG1 under the control of the PGK1 expression cassette gave the highest levels of glucoamylase activity. It was shown that the co-expression of these heterologous alpha-amylase and glucoamylase genes enhance starch degradation additively in S. cerevisiae. This study has resulted in progress towards laying the foundation for the possible development of efficient starch-degrading S. cerevisiae strains that could eventually be used in consolidated bioprocessing, and in the brewing, whisky, and biofuel industries.

Coenzymes↗

Topical formulation studies with DEET (N,N-diethyl-3-methylbenzamide) and cyclodextrins.

The purpose of this study was to investigate the utility of cyclodextrins as a safer alternative to the commonly used cosolvent ethanol in topical N,N-diethyl-3-methylbenzamide (DEET) formulations. Ethanol is a known penetration enhancer and would ideally not be used in a formulation containing DEET, a compound known for its potential toxicity. DEET formulations were prepared containing up to 20% w/w gamma-cyclodextrin (GCD) or 30% w/w hydroxypropyl-beta-cyclodextrin (HPBCD). These formulations were evaluated by determining the release rate of DEET from its vehicle through a synthetic membrane into a receiver medium with a high affinity for DEET using a fully automated Franz-diffusion cell system. DEET release was measured by ultraviolet spectrophotometry at 260 nm. Both the traditional Higuchi release model and an alternate repeated measures analysis of variance with nested factors were used to analyze the data. The influence of the cyclodextrins on the volatility of DEET was determined by solid-phase microextraction. Morphological characterization of the formulations was performed by light microscopy. Physical stability of the formulations was evaluated by rheology in an accelerated study performed at 50 degrees C for 28 days. The cyclodextrins caused a decrease in the release of DEET from its vehicle compared with an ethanol-containing formulation. This effect became more pronounced as the amount of cyclodextrin in the formulation was increased. The addition of the cyclodextrins resulted in a cream-like product compared with the ethanol formulation, which was a lotion. The DEET formulations had the following rank order of volatility: ethanol < DEET = GCD < HPBCD. Examination of the formulations by light microscopy indicated that the CD-based formulations produced a smaller and more homogeneous droplet size distribution than the ethanol-based formulations. The accelerated physical stability study indicated that cyclodextrin-based formulations are both technically and commercially feasible. Cyclodextrins are a promising alternative to ethanol in DEET-containing formulations. The reduced release rate of DEET from these formulations suggests that the toxic potential of DEET may be decreased in these products, while its repellency and stability are maintained.

Administration, Topical↗

Studies on dissimilatory sulfate-reducing bacteria that decompose fatty acids. I. Isolation of new sulfate-reducing bacteria enriched with acetate from saline environments. Description of Desulfobacter postgatei gen. nov., sp. nov.

Three strains (2ac9, 3ac10 and 4ac11) of oval to rod-shaped, Gram negative, nonsporing sulfate-reducing bacteria were isolated from brackish water and marine mud samples with acetate as sole electron donor. All three strains grew in simple defined media supplemented with biotin and 4-aminobenzoic acid as growth factors. Acetate was the only electron donor utilized by strain 2ac9, while the other two strains used in addition ethanol and/or lactate. Sulfate served as electron acceptor and was reduced to H2S. Complete oxidation of acetate to CO2 was shown by stoichiometric measurements with strain 2ac9 in batch cultures using sulfate, sulfite or thiosulfate as electron acceptors. With sulfate an average growth yield of 4.8 g cell dry weight was obtained per mol of acetate oxidized; with sulfite or thiosulfate the growth yield on acetate was about twice as high. None of the strains contained desulfoviridin. In strain 2ac9 cytochromes of the b- and c-type were detected. Strain 2ac9 is described as type strain of the new species and genus, Desulfobacter postgatei.

Acetates↗

Computer programming for nucleic acid studies. III. Calculated ultraviolet absorption spectra of protected oligodeoxyribonucleotides.

A computer program called UV. FOR was written in FORTRAN. This program primarily utilizes the digitized UV absorption spectra of 8 protected deoxyribonucleosides in 95% ethanol solution to compose the UV spectrum of a oligodeoxynucleotide of any sequence. Both calculated and observed UV spectra of 2 protected oligodeoxynucleotides are carefully compared. The results show that the calculated UV spectrum is virtually identical to the observed spectrum. Thus, the calculated spectra provide rapid confirmation of oligonucleotide compositions during the course of oligonucleotide synthesis by the phosphotriester method.

Computers↗

Central and peripheral components of the inhibitory actions of 5-HTP on ethanol consumption in the rat.

When administered under a backward conditioning paradigm, 5-HTP administration resulted in a decrease in ethanol intake followed by a persistently decreased ethanol consumption. A central component to this inhibitory effect was suggested by the inability of xylamidine to significantly reduce the initial inhibitory effect of 5-HTP. The persistent rejection was prevented by xylamidine. Methysergide reduced the initial as well as the persistent effects of 5-HTP. In studies utilizing a forward conditioning paradigm, 5-HTP and lithium were each effective in developing CTAs to ethanol and saccharin. Only the ethanol-5-HTP pairing showed a persistent aversion. A peripheral component to the actions of 5-HTP was suggested by xylamidine blocking the CTAs induced by 5-HTP. Xylamidine also prevented the persistent ethanol avoidance induced by 5-HTP, but was ineffective in antagonizing lithium-induced CTAs. These results suggest central as well as peripheral components associated with the inhibitory effects of 5-HTP on ethanol consumption. Central actions appear to mediate the initial inhibitory effects while peripheral actions appear to be associated with persistent avoidance of ethanol following 5-HTP treatment.

5-Hydroxytryptophan↗

Increased microsomal interaction with iron and oxygen radical generation after chronic acetone treatment.

In vivo administration of acetone influences a variety of reactions catalyzed by rat liver microsomes. The effect of chronic treatment with acetone (1% acetone in the water for 10-12 days) on interaction with iron and subsequent oxygen radical generation by liver microsomes was evaluated. Microsomes from the acetone-treated rats displayed elevated rates of H2O2 generation, an increase in iron-dependent lipid peroxidation, and enhanced chemiluminescence upon the addition of t-butylhydroperoxide. The ferric EDTA-catalyzed production of formaldehyde from DMSO or of ethylene from 2-keto-4-thiomethylbutyrate was increased 2-fold after acetone treatment. This increase in hydroxyl radical generation was accompanied by a corresponding increase in NADPH utilization and was sensitive to inhibition by catalase and a competitive scavenger, ethanol, but not to superoxide dismutase. In vitro addition of acetone to microsomes had no effect on oxygen radical generation. Associated with the chronic acetone treatment was a 2-fold increase in the microsomal content of cytochrome P-450 and in the activity of NADPH-cytochrome-P-450 reductase. It appears that increased oxygen radical generation by microsomes after chronic acetone treatment reflects the increase in the major enzyme components which comprise the mixed-function oxidase system.

Acetone↗