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PubMed1986

Methanogenesis and ATP synthesis in a protoplast system of Methanobacterium thermoautotrophicum.

When Methanobacterium thermoautotrophicum cells were incubated in 50 mM potassium phosphate buffer (pH 7.0) containing 1 M sucrose and autolysate from Methanobacterium wolfei, they were transformed into protoplasts. The protoplasts, which possessed no cell wall, lysed in buffer without sucrose. Unlike whole cells, the protoplasts did not show convoluted internal membrane structures. The protoplasts produced methane from H2-CO2 (approximately 1 mumol min-1 mg of protein-1) at about 50% the rate obtained for whole cells, and methanogenesis was coupled with ATP synthesis. Addition of the protonophore 3,5-di-tert-butyl-4-hydroxybenzylidenemalononitrile (SF-6847) to protoplast suspensions resulted in a dissipation of the membrane potential (delta psi), and this was accompanied by a parallel decrease in the rates of ATP synthesis and methanogenesis. In this respect protoplasts differed from whole cells in which ATP synthesis and methanogenesis were virtually unaffected by the addition of the protonophore. It is concluded that the insensitivity of whole cells to protonophores could be due to internal membrane structures. Membrane preparations produced from lysis of protoplasts or by sonication of whole cells gave comparatively low rates of methanogenesis (methylcoenzyme M methylreductase activity, less than or equal to 100 nmol of CH4 min-1 mg of protein-1), and no coupling with ATP synthesis could be demonstrated.

Adenosine Triphosphate↗
PubMed1995

Inhibition of methanogenesis by human bile.

The factors that regulate methanogenesis in humans have not been established. The presence of bile acid, which is lost into the colon from the small intestine, may be an important regulatory factor of methanogenesis. To examine this possibility, the effect of human bile on methane production by faecal cultures, and the in vivo effect of biliary diversion on breath methane excretion in a methanogenic choledochostomy patient, were investigated. Faecal suspensions (0.1%) from five methanogenic humans were incubated anaerobically with bile (0.3-30%) from three choledochostomy patients, and headspace methane measured by gas chromatography. All biles inhibited headspace methane. Inhibition of methanogenesis was dose dependent, plateaued at 10-30% bile concentration, and was abolished by 0.6% cholestyramine. The maximum inhibition by bile, median (range), was 38 (0.9-56)% of control methane values. Reversal of the bile fistula in the fourth choledochostomy patient converted that subject from methanogenic to 'non-methanogenic' status, It is concluded that inhibition of methanogens in the caecum by bile acid could significantly reduce the number of methanogens in the colon. This and the effect of transit time could explain much of the known epidemiology of 'non-methanogenesis', which has been related to obesity, (comparatively) fast colonic transit in healthy persons, and to small intestinal Crohn's disease.

Bile↗
PubMed2003

Attempts to inhibit ruminal methanogenesis by blocking pyruvate oxidative decarboxylation.

The inhibition of pyruvate oxidative decarboxylation as a means of decreasing ruminal methanogenesis in vitro was studied. In the first experiment, the addition of adenosine and adenine (with and without ribose) to ruminal batch cultures did not decrease methanogenesis. In the second experiment, the addition of oxythiamin decreased methanogenesis by 23%. In the third experiment, three pyruvate derivatives did not inhibit methanogenesis, although hydroxypyruvate improved organic matter fermentation from 57.8% to 64.2%. The additives did not seem to inhibit pyruvate oxidative decarboxylation.

Animals↗
PubMed1993

Use of metabolic inhibitors to study H2 consumption by human feces: evidence for a pathway other than methanogenesis and sulfate reduction.

Human fecal bacteria produce and consume hydrogen, and consumption rate is a critical determinant of the volume of H2 liberated into the colonic lumen. Two bacterial reactions that have been reported to be major consumers of H2 are methanogenesis and sulfate reduction. To determine the importance of each of these reactions, we measured the disappearance of exogenous H2 during incubation with human fecal homogenates treated with 20 mmol/L 2-bromoethanesulphonic acid (BES), an inhibitor of methanogenesis, and/or 20 mmol/L sodium molybdate (Mo), an inhibitor of sulfate reduction. Four methanogenic and four nonmethanogenic samples consumed an average of 99% and 85%, respectively, of the initial H2 during 22 hours of incubation. With methanogenic homogenates, 36% of the H2 consumption persisted despite inhibition of methanogenesis. Inhibition of sulfate reduction had no effect on the rate of H2 consumption by these eight fecal specimens. The importance of fecal sulfate availability was determined in fecal samples obtained from an additional 14 randomly selected volunteers. Incubation after supplementation with 20 mmol/L sulfate was associated with an increase in sulfide production in four of the samples, and three of these four samples also demonstrated an increased rate of H2 consumption. No such evidence of sulfate reduction was observed in the other 10 homogenates. We conclude that a bacterial reaction other than methanogenesis and sulfate reduction, perhaps the recently described reduction of CO2 to acetate, represents a major metabolic route of H2 disposal in nonmethanogenic feces and a minor, but appreciable, pathway in methanogenic feces.

Feces↗
PubMed1978

Hydrogen as a substrate for methanogenesis and sulphate reduction in anaerobic saltmarsh sediment.

Hydrogen gas stimulated sulphate reduction in a saltmarsh sediment and the importance of H2 transferred from organotrophic bacteria to the sulphate-reducers is discussed. beta-fluorolactate inhibited sulphate reduction whether lactate, ethanol or hydrogen was being used as growth substrate. When added to sediment beta-fluorolactate inhibited sulphate reduction with a consequent increase in methane production. Addition of H2 stimulated methanogenesis in sediment and this stimulation was greater if CO2 was also present. Hydrogen availability was the primary limitation of methanogenesis but the low concentration of dissolved CO2 in seawater may limit methane production even if H2 is available. The removal of inhibition of methanogenesis by the use of fluorolactate to suppress sulphate reduction or by the provision of hydrogen indicates competitive inhibition of methanogens by sulphate reducers utilizing transferred hydrogen.

Desulfovibrio↗
PubMed2001

Evaluation of kinetic coefficients using integrated monod and haldane models for low-temperature acetoclastic methanogenesis.

The integrated Monod and Haldane models were used to evaluate the kinetic coefficients and their standard deviations using the methane accumulation curves of low-temperature acetoclastic methanogenesis. The linear and exponential approximations and the limitations of their applicability were deduced from the integrated models. The samples of lake sediments and biomass taken from a low-temperature upflow anaerobic sludge blanket (UASB) reactor were used as inoculum in batch assays for acetate methanation. In comparison, the Monod and Haldane models were applied to evaluate the kinetic coefficients for mesophilic acetoclastic methanogenesis accomplished by the pure culture of Methanosarcina barkeri strain MS. The Monod and Haldane models and their approximations were fitted by using non-linear regression. For the wide range of initial acetateconcentrations (4.2-84 mM: 5-100 mM) applied to the UASB biomass at 11 and 22 degrees C and for the lake sediment samples at 6 and 15 degrees C, a better fit was obtained with the Haldane models and their exponential approximations, respectively. For the lake sediments the values of inhibition coefficients decreased at decreasing temperatures. At the highest temperature of 30 degrees C no difference was found between the Haldane and Monod models and the simpler Monod model should be preferred. The values of the maximum growth rate of biomass were highest at 30 degrees C (lake sediment) and 22 degrees C (the UASB biomass) being in a range presented in the literature for mesophilic acetoclastic methanogenesis.

Acetates↗
PubMed1999

Methanogenic archaea and CO2-dependent methanogenesis on washed rice roots.

Washed excised roots of rice (Oryza sativa) immediately started to produce CH4 when they were incubated in phosphate buffer under anoxic conditions (N2 atmosphere), with initial rates varying between 2 and 70nmolh(-1)g(-1) dry weight of root material (mean +/- SE: 20.3 +/- 5.9 nmol h(-1) g(-1) dry weight; n = 18). Production of CH4 continued for at least 500 h, with rates usually decreasing slowly. CH4 production was not significantly affected by methyl fluoride, an inhibitor of acetoclastic methanogenesis. Less than 0.5% of added [2-14C]-acetate was converted to 14CH4, and conversion of 14CO2 to 14CH4 indicated that CH4 was almost exclusively produced from CO2. Occasionally, however, especially when the roots were incubated without additional buffer, CH4 production started to accelerate after about 200h reaching rates of > 100 nmol h(-1) g(-1) dry weight. Methyl fluoride inhibited methanogenesis by more than 20% only in these cases, and the conversion of 14CO2 to 14CH4 decreased. These results indicate that CO2-dependent rather than acetoclastic methanogenesis was primarily responsible for CH4 production in anoxically incubated rice roots. Determination of most probable numbers of methanogens on washed roots showed highest numbers (10(6)g(-1) dry roots) on H2 and ethanol, i.e. substrates that support CH4 production from CO2. Numbers on acetate (10(5) g(-1) dry roots) and methanol (10(4)g(-1) dry roots) were lower. Methanogenic consortia enriched on H2 and ethanol were characterized phylogenetically by comparative sequence analysis of archaeal small-subunit (SSU) ribosomal RNA-encoding genes (rDNA). These sequences showed a high similarity to SSU rDNA clones that had been obtained previously by direct extraction of total DNA from washed rice roots. The SSU rDNA sequences recovered from the H2/CO2-using consortium either belonged to a novel lineage of methanogens that grouped within the phylogenetic radiation of the Methanosarcinales and Methanomicrobiales or were affiliated with Methanobacterium bryantii. SSU rDNA sequences retrieved from the ethanol-using consortium either grouped within the genus Methanosarcina or belonged to another novel lineage within the phylogenetic radiation of the Methanosarcinales and Methanomicrobiales. Cultured organisms belonging to either of the two novel lineages have not been reported yet.

Acetates↗
PubMed2002

Genetic analysis of the archaeon Methanosarcina barkeri Fusaro reveals a central role for Ech hydrogenase and ferredoxin in methanogenesis and carbon fixation.

Ech hydrogenase (Ech) from the methanogenic archaeon Methanosarcina barkeri catalyzes the reversible reduction of ferredoxin by H(2) and is a member of a distinct group of membrane-bound [NiFe] hydrogenases with sequence similarity to energy-conserving NADH:quinone oxidoreductase (complex I). To elucidate the physiological role(s) of Ech a mutant lacking this enzyme was constructed. The mutant was unable to grow on methanol/H(2)/CO(2), H(2)/CO(2), or acetate as carbon and energy sources but showed wild-type growth rates with methanol as sole substrate. Addition of pyruvate to the growth medium restored growth on methanol/H(2)/CO(2) but not on H(2)/CO(2) or acetate. Results obtained from growth experiments, cell suspension experiments, and enzyme activity measurements in cell extracts provide compelling evidence for essential functions of Ech and a 2[4Fe-4S] ferredoxin in the metabolism of M. barkeri. The following conclusions were made. (i) In acetoclastic methanogenesis, Ech catalyzes H(2) formation from reduced ferredoxin, generated by the oxidation of the carbonyl group of acetate to CO(2). (ii) Under autotrophic growth conditions, the enzyme catalyzes the energetically unfavorable reduction of ferredoxin by H(2), most probably driven by reversed electron transport, and the reduced ferredoxin thus generated functions as low potential electron donor for the synthesis of pyruvate in an anabolic pathway. (iii) Reduced ferredoxin in addition provides the reducing equivalents for the first step of methanogenesis from H(2)/CO(2), the reduction of CO(2) to formylmethanofuran. Thus, in vivo genetic analysis has led to the identification of the electron donor of this key initial step of methanogenesis.

Carbon↗
PubMed2004

Rumen simulation technique study on the interactions of dietary lauric and myristic acid supplementation in suppressing ruminal methanogenesis.

The interactions of lauric (C12) and myristic acid (C14) in suppressing ruminal methanogenesis and methanogens were investigated with the rumen simulation technique (Rusitec) using bovine ruminal fluid. The fatty acids were added to basal substrates (grass hay:concentrate, 1:1.5) at a level of 48 g/kg DM, provided in C12:C14 ratios of 5:0, 4:1, 3:2, 2.5:2.5, 2:3, 1:4 and 0:5. Additionally, an unsupplemented control consisting of the basal substrates only was employed. Incubation periods lasted for 15 (n 4) and 25 (n 2) d. CH4 formation was depressed by any fatty acid mixture containing at least 40 % C12, and effects persisted over the complete incubation periods. The greatest depression (70 % relative to control) occurred with a C12:C14 ratio of 4:1, whereas the second most effective treatment in suppressing CH4 production (60 % relative to control) was found with a ratio of 3:2. Total methanogenic counts were decreased by those mixtures of C12 and C14 also successful in suppressing methanogenesis, the 4:1 treatment being most efficient (60 % decline). With this treatment in particular, the composition of the methanogenic population was altered in such a way that the proportion of Methanococcales increased and Methanobacteriales decreased. Initially, CH4 suppression was associated with a decreased fibre degradation, which, however, was reversed after 10 d of incubation. The present study demonstrated a clear synergistic effect of mixtures of C12 and C14 in suppressing methanogenesis, mediated probably by direct inhibitory effects of the fatty acids on the methanogens.

Animal Feed↗
PubMed1988

Electron-transport-driven sodium extrusion during methanogenesis from formaldehyde and molecular hydrogen by Methanosarcina barkeri.

Methanogenesis from formaldehyde or formaldehyde + H2, as carried out by Methanosarcina barkeri, was strictly dependent on sodium ions whereas methane formation from methanol + H2 or methanol + formaldehyde was Na+-independent. This indicates that the reduction of formaldehyde to the formal redox level of methanol exhibits a Na+ requirement. During methanogenesis from formaldehyde, a delta pNa in the range of -62 mV to -80 mV was generated by means of a primary, electron-transport-driven sodium pump. This could be concluded from the following results obtained on cell suspensions of M. barkeri. 1. The addition of proton conductors or inhibitors of the Na+/H+ antiporter had no effect on sodium extrusion. 2. During methanogenesis from formaldehyde + H2 a delta psi of -60 mV to -70 mV was generated even in the presence of proton conductors. 3. ATPase inhibitors, applied in the presence of proton conductors, had no effect on primary sodium extrusion or generation of a delta psi. Evidence for a Na+-translocating ATPase could not be obtained.

Adenosine Triphosphate↗
PubMed2006

Effects of butyrate precursors on electron relocation when methanogenesis is inhibited in ruminal mixed cultures.

AIMS: Inhibition of ruminal methanogenesis often causes accumulation of H(2), formate and ethanol, which are not energy substrates for ruminants. It was hypothesized that the addition of butyrate precursors would avoid the formation of these products and relocate electrons into butyrate. METHODS AND RESULTS: In four ruminal 24-h incubations, two inhibitors of methanogenesis, each at three different initial concentrations (0, 2 or 4 mmol l(-1) for propynoic acid, and 0, 4 or 8 mmol l(-1) for ethyl 2-butynoate), were combined with two butyrate precursors at two different initial concentrations (0 or 4 mmol l(-1) for crotonic acid or 3-butenoic acid). Ground lucerne hay was the substrate. Propynoic acid at 4 mmol l(-1) decreased CH(4) formation by more than two-thirds. Ethyl 2-butynoate at 8 mmol l(-1) suppressed methanogenesis by more than 90%. Butyrate precursors generally did not decrease the accumulation of H(2) and formate or ethanol production. CONCLUSIONS: Butyrate precursors were ineffective as electron acceptors because they were not completely converted to butyrate and were also metabolized through other pathways. SIGNIFICANCE AND IMPACT OF THE STUDY: Effectiveness of butyrate precursors may be improved by adding them to the fermentation continuously or by enhancing the kinetics of their conversion into butyrate.

Alkynes↗
PubMed1977

Association of hydrogen metabolism with methanogenesis in Lake Mendota sediments.

Lake Mendota sediments were studied to determine the role of H2 in sediment methanogenesis. H2 was generally not detectable in sediment. The addition of H2 to sediment significantly increased methanogenensis. The amount of methane produced was proportional to the concentration of hydrogen added. H2 addition stimulated the reduction of CO2 to methane, but did not significantly stimulate the conversion of methanol or the methyl position of acetate to methane. Various organic compounds also stimulated sediment methanogenesis. Formate, ethanol, and glucose were shown to serve as electron donors for CO2 reduction to methane. The addition of formate to sediment resulted in H2 evolution. H2 was not deith the phenomenon of interspecies hydrogen transfer. The results indicate that hydrogen is an important intermediate and a rate-limiting factor in sediment methanogenesis.

Acetates↗
PubMed1982

Sulfate reduction and methanogenesis in the sediment of a saltmarsh on the East coast of the United kingdom.

The rates of sulfate reduction, methanogenesis, and methane loss were measured in saltmarsh sediment at monthly intervals. In addition, dissolved methane and sulfate concentrations together with pS and pH were determined. Methane formation from carbon dioxide, but not from acetate, was detected within the same horizon of sediment where sulfate reduction was most active. Sulfate reduction was about three orders of magnitude greater than annual methanogenesis. The two processes were not separated either spatially or temporally, but occurred within the same layer of sediment at the same time of the year. Their coexistence did not seem to be the result of sulfate-depleted microenvironments within which methanogenesis could occur, but the methanogenic bacteria persisted at very low rates of activity within the same environment as the sulfate reducers.

Journal Article↗
PubMed1982

Methanogenesis and sulfate reduction: competitive and noncompetitive substrates in estuarine sediments.

Sulfate ions did not inhibit methanogenesis in estuarine sediments supplemented with methanol, trimethylamine, or methionine. However, sulfate greatly retarded methanogenesis when hydrogen or acetate was the substrate. Sulfate reduction was stimulated by acetate, hydrogen, and acetate plus hydrogen, but not by methanol or trimethylamine. These results indicate that sulfate-reducing bacteria will outcompete methanogens for hydrogen, acetate, or both, but will not compete with methanogens for compounds like methanol, trimethylamine, or methionine, thereby allowing methanogenesis and sulfate reduction to operate simultaneously within anoxic, sulfate-containing sediments.

Journal Article↗
PubMed1983

Methanogenesis from Choline by a Coculture of Desulfovibrio sp. and Methanosarcina barkeri.

A sulfate-reducing vibrio was isolated from a methanogenic enrichment with choline as the sole added organic substrate. This organism was identified as a member of the genus Desulfovibrio and was designated Desulfovibrio strain G1. In a defined medium devoid of sulfate, a pure culture of Desulfovibrio strain G1 fermented choline to trimethylamine, acetate, and ethanol. In the presence of sulfate, more acetate and less ethanol were formed from choline than in the absence of sulfate. When grown in a medium containing sulfate, a coculture of Desulfovibrio strain G1 and Methanosarcina barkeri strain Fusaro degraded choline almost completely to methane, ammonia, and hydrogen sulfide and presumably to carbon dioxide. Methanogenesis occurred in two distinct phases separated by a lag of about 6 days. During the first phase of methanogenesis choline was completely converted to trimethylamine, acetate, hydrogen sulfide, and traces of ethanol by the desulfovibrio. M. barkeri fermented trimethylamine to methane, ammonia, and presumably carbon dioxide via dimethyl- and methylamine as intermediates. Simultaneously, about 60% of the acetate expected was metabolized. In the second phase of methanogenesis, the residual acetate was almost completely catabolized.

Journal Article↗
PubMed2000

Phosphate inhibits acetotrophic methanogenesis on rice roots.

The contribution of acetate- and H(2)/CO(2)-dependent methanogenesis to total CH(4) production was determined in excised washed rice roots by radiolabeling, methyl fluoride inhibition, and stable carbon isotope fractionation. Addition of > or = 20 mM phosphate inhibited methanogenesis, which then was exclusively from H(2)/CO(2). Otherwise, acetate contributed about 50 to 60% of the total methanogenesis, demonstrating that phosphate specifically inhibited acetotrophic methanogens on rice roots.

Acetates↗
PubMed2002

Differential expression of methanogenesis genes of Methanothermobacter thermoautotrophicus (formerly Methanobacterium thermoautotrophicum) in pure culture and in cocultures with fatty acid-oxidizing syntrophs.

The expression of genes involved in methanogenesis in a thermophilic hydrogen-utilizing methanogen, Methanothermobacter thermoautotrophicus strain TM, was investigated both in a pure culture sufficiently supplied with H(2) plus CO(2) and in a coculture with an acetate-oxidizing hydrogen-producing bacterium, Thermacetogenium phaeum strain PB, in which hydrogen partial pressure was constantly kept very low (20 to 80 Pa). Northern blot analysis indicated that only the mcr gene, which encodes methyl coenzyme M reductase I (MRI), catalyzing the final step of methanogenesis, was expressed in the coculture, whereas mcr and mrt, which encodes methyl coenzyme M reductase II (MRII), the isofunctional enzyme of MRI, were expressed at the early to late stage of growth in the pure culture. In contrast to these two genes, two isofunctional genes (mtd and mth) for N(5),N(10)-methylene-tetrahydromethanopterin dehydrogenase, which catalyzes the fourth step of methanogenesis, and two hydrogenase genes (frh and mvh) were expressed both in a pure culture and in a coculture at the early and late stages of growth. The same expression pattern was observed for Methanothermobacter thermoautotrophicus strain DeltaH cocultured with a thermophilic butyrate-oxidizing syntroph, Syntrophothermus lipocalidus strain TGB-C1. Two-dimensional sodium dodecyl sulfate-polyacrylamide gel electrophoresis of whole proteins of M. thermoautotrophicus strain TM obtained from a pure culture and a coculture with the acetate-oxidizing syntroph and subsequent N-terminal amino acid sequence analysis confirmed that MRI and MRII were produced in the pure culture, while only MRI was produced in the coculture. These results indicate that under syntrophic growth conditions, the methanogen preferentially utilizes MRI but not MRII. Considering that hydrogenotrophic methanogens are strictly dependent for growth on hydrogen-producing fermentative microbes in the natural environment and that the hydrogen supply occurs constantly at very low concentrations compared with the supply in pure cultures in the laboratory, the results suggest that MRI is an enzyme primarily functioning in natural methanogenic ecosystems.

Acetates↗
PubMed2003

Targeting methanopterin biosynthesis to inhibit methanogenesis.

This paper describes the design, synthesis, and successful employment of inhibitors of 4-(beta-D-ribofuranosyl)aminobenzene-5'-phosphate (RFA-P) synthase, which catalyzes the first committed step in the biosynthesis of methanopterin, to specifically halt the growth of methane-producing microbes. RFA-P synthase catalyzes the first step in the synthesis of tetrahydromethanopterin, a key cofactor required for methane formation and for one-carbon transformations in methanogens. A number of inhibitors, which are N-substituted derivatives of p-aminobenzoic acid (pABA), have been synthesized and their inhibition constants with RFA-P synthase have been determined. Based on comparisons of the inhibition constants among various inhibitors, we propose that the pABA binding site in RFA-P synthase has a relatively large hydrophobic pocket near the amino group. These enzyme-targeted inhibitors arrest the methanogenesis and growth of pure cultures of methanogens. Supplying pABA to the culture relieves the inhibition, indicating a competitive interaction between pABA and the inhibitor at the cellular target, which is most likely RFAP synthase. The inhibitors do not adversely affect the growth of pure cultures of the bacteria (acetogens) that play a beneficial role in the rumen. Inhibitors added to dense ruminal fluid cultures (artificial rumena) halt methanogenesis; however, they do not inhibit volatile fatty acid (VFA) production and, in some cases, VFA levels are slightly elevated in the methanogenesis-inhibited cultures. We suggest that inhibiting methanopterin biosynthesis could be considered in strategies to decrease anthropogenic methane emissions, which could have an environmental benefit since methane is a potent greenhouse gas.

4-Aminobenzoic Acid↗