Degradation Of Taurine Research Articles

Diet and the gut microbiome in patients with Parkinson’s disease

It has been suggested that gut microbiota influence Parkinson’s disease (PD) via the gut–brain axis. Here, we examine associations between diet and gut microbiome composition and its predicted functional pathways in patients with PD. We assessed gut microbiota in fecal samples from 85 PD patients in central California using 16S rRNA gene sequencing. Diet quality was assessed by calculating the Healthy Eating Index 2015 (HEI-2015) based on the Diet History Questionnaire II. We examined associations of diet quality, fiber, and added sugar intake with microbial diversity, composition, taxon abundance, and predicted metagenomic profiles, adjusting for age, sex, race/ethnicity, and sequencing platform. Higher HEI scores and fiber intake were associated with an increase in putative anti-inflammatory butyrate-producing bacteria, such as the genera Butyricicoccus and Coprococcus 1. Conversely, higher added sugar intake was associated with an increase in putative pro-inflammatory bacteria, such as the genera Klebsiella. Predictive metagenomics suggested that bacterial genes involved in the biosynthesis of lipopolysaccharide decreased with higher HEI scores, whereas a simultaneous decrease in genes involved in taurine degradation indicates less neuroinflammation. We found that a healthy diet, fiber, and added sugar intake affect the gut microbiome composition and its predicted metagenomic function in PD patients. This suggests that a healthy diet may support gut microbiome that has a positive influence on PD risk and progression.

Characterization of the gut microbiota and fecal and blood metabolomes under various factors in urban children from Northwest China.

Children have regional dynamics in the gut microbiota development trajectory. Hitherto, the features and influencing factors of the gut microbiota and fecal and plasma metabolites in children from Northwest China remain unclear. Shotgun metagenomic sequencing and untargeted metabolomics were performed on 100 healthy volunteers aged 2-12 years. Age, body mass index (BMI), regular physical exercise (RPE), and delivery mode (DM) significantly affect gut microbiota and metabolites. Lactobacillus, Butyricimonas, Prevotella, Alistipes, and predicted pathway propanoate production were significantly increased with age while Bifidobacterium breve, B. animalis, B. pseudocatenulatum, Streptococcus infantis, and carbohydrate degradation were decreased. Fecal metabolome revealed that the metabolism of caffeine, amino acids, and lipid significantly increased with age while galactose metabolism decreased. Noticeably, BMI was positively associated with pathogens including Erysipelatoclostridium ramosum, Parabacteroides distasonis, Ruminococcus gnavus, and amino acid metabolism but negatively associated with beneficial Akkermansia muciniphila, Alistipes finegoldii, Eubacterium ramulus, and caffeine metabolism. RPE has increased probiotic Faecalibacterium prausnitzii and Anaerostipes hadrus, acetate and lactate production, and major nutrient metabolism in gut and plasma, but decreased pathobiont Bilophila wadsworthia, taurine degradation, and pentose phosphate pathway. Interestingly, DM affects the gut microbiota and metabolites throughout the whole childhood. Bifidobacterium animalis, Lactobacillus mucosae, L. ruminis, primary bile acid, and neomycin biosynthesis were enriched in eutocia, while anti-inflammatory Anaerofustis stercorihominis, Agathobaculum butyriciproducens, Collinsella intestinalis, and pathogenic Streptococcus salivarius, Catabacter hongkongensis, and amino acid metabolism were enriched in Cesarean section children. Our results provided theoretical and data foundation for the gut microbiota and metabolites in preadolescent children's growth and development in Northwest China.

Ruminal Degradation of Taurine and Its Effects on Rumen Fermentation In Vitro

Taurine accounts for approximately 0.1% of an animal’s body. It cannot be used for protein synthesis but plays a wide range of important roles in the animal body. Taurine does not exist in plants, while mammals can only synthesize 30–40% of the taurine they need. Supplementing taurine to beef cattle may be necessary to improve their nutrient utilization and health status. However, no data are available regarding the metabolism of taurine in the rumen. Two in vitro trials were conducted to investigate the ruminal degradability of taurine and its effects on rumen fermentation. In Trial 1, Tilley and Terry’s in vitro rumen fermentation technique was used for incubation. As treatments, two levels of taurine, i.e., 0 and 10 mg, were added into plastic tubes containing 0.4000 g of feed mixture with a calibrated volume of 50 mL. Three adult cattle fitted with rumen cannulas were used as the donors for rumen fluid. The incubation was carried out at 39 °C for 48 h. The results showed that the taurine degradability increased with incubation time (p < 0.001) while its 2 h-degradability reached 99%. Taurine decreased the 48 h-dry matter degradability (DMD) (p = 0.008) and increased the 24 h- and 48 h-pH (p = 0.005; p = 0.018), respectively. In Trial 2, the Hohenheim gas test was used for incubation. Four levels of taurine, i.e., 0, 5, 10 and 20 mg, were added into glass syringes containing 0.2000 g feed mixture with a calibrated volume of 100 mL as treatments. The rumen fluid donors were the same as in Trial 1. The incubation was carried out at 39 °C for 48 h. The results showed that taurine increased the 48 h-pH (p < 0.001) linearly, decreased the cumulative gas production (p < 0.001) and the total volatile fatty acids (VFA) concentration (p = 0.014), and quadratically affected the ammonia–nitrogen (p < 0.001) and microbial crude protein (MCP) concentrations (p < 0.001). It was concluded that taurine was highly degradable in rumen fermentation. Taurine inhibits ruminal fermentation by decreasing DMD, VFA and gas production while improving MCP synthesis on a dose-dependent basis.

Osmotic Gradient Is a Factor That Influences the Gill Microbiota Communities in Oryzias melastigma.

Simple SummaryThis study was applied to the laboratory medaka to understand how the osmotic gradient could influence the composition of the gill microbiota communities. The data suggested that the shift of the gill microbiota community has relied on the first sense of osmolality differences, and such changes were accomplished by the enriched osmosensing and metabolic pathways.The fish gill is the first tissue that is exposed to the external media and undergoes continuous osmotic challenges. Recently, our group published an article entitled “Integrated Omics Approaches Revealed the Osmotic Stress-Responsive Genes and Microbiota in Gill of Marine Medaka” in the journal mSystems (e0004722, 2022), and suggested the possible host-bacterium interaction in the fish gill during osmotic stress. The previous study was performed by the progressive fresh water transfer (i.e., seawater to fresh water transfer via 50% seawater (FW)). Our group hypothesized that osmotic gradient could be a factor that determines the microbiota communities in the gill. The current 16S rRNA metagenomic sequencing study found that the direct transfer (i.e., seawater to fresh water (FWd)) could result in different gill microbiota communities in the same fresh water endpoints. Pseduomonas was the dominant bacteria (more than 55%) in the FWd gill. The Kyoto Encyclopedia of Genes and Genomes and MetaCyc analysis further suggested that the FWd group had enhanced osmosensing pathways, such as the ATP-binding cassette transporters, taurine degradation, and energy-related tricarboxylic acid metabolism compared to the FW group.

The role and molecular mechanism of gut microbiota in Graves' orbitopathy.

Graves' orbitopathy (GO) is an autoimmune orbital disorder. Gut microbiota dysfunction plays a vital role in autoimmune diseases, including Graves' disease (GD) and GO. In the present study, we aimed to investigate the change of gut microbiota in GD/GO using mouse model. The murine model of GD/GO was established by the challenge of adenovirus expressing thyroid-stimulating hormone (TSH) receptor (TSHR) (Ad-TSHR). The histological changes of orbital and thyroid tissues were analyzed by hematoxylin and eosin (H&E), Masson staining, and immunohistochemistry (IHC) staining. The fecal samples were collected for 16SrRNA gene sequencing and bioinformatics analysis. The GD/GO model was established successfully, as manifested as the broadened eyelid, exophthalmia and conjunctive redness, severe inflammatory infiltration among thyroid glands and between extraocular muscle space, hypertrophic extraocular muscles, elevated thyroxine (T4) and decreased TSH, and positive CD34, CD40, collagen I, and α-SMA staining. A total of 222 operational taxonomic units (OUTs) were overlapped between mice in the Ad-NC and Ad-TSHR groups. The microbial composition of the samples in the two groups was mainly Bacteroidia and Clostridia, and the Ad-NC group had a significantly lower content of Bacteroidia and higher content of Clostridia. KEGG orthology analysis results revealed differences in dehydrogenase, aspartic acid, bile acid, chalcone synthase, acetyltransferase, glutamylcyclotransferase, glycogenin, and 1-phosphatidylinositol-4-phosphate 5-kinase between two groups; enzyme commission (EC) analysis results revealed differences in several dehydrogenase, oxidase, thioxy/reductase between two groups; MetaCyc pathways analysis results revealed differences in isoleucine degradation, oxidation of C1 compounds, tricarboxylic acid (TCA) cycle IV, taurine degradation, and biosynthesis of paromamine, heme, colonic acid building blocks, butanediol, lysine/threonine/methionine, and histidine/purine/pyrimidine between two groups. This study induced a mouse model of GD/GO by Ad-TSHR challenge, and gut microbiota characteristics were identified in the GD/GO mice. The Bacteroidia and Clostridia abundance was changed in the GD/GO mice. These findings may lay a solid experimental foundation for developing personalized treatment regimens for GD patients according to the individual gut microbiota. Given the potential impact of regional differences on intestinal microbiota, this study in China may provide a reference for the global overview of the gut-thyroid axis hypothesis.

The role of fecal sulfur metabolome in inflammatory bowel diseases

Sulfur metabolism and sulfur-containing metabolites play an important role in the human digestive system, and sulfur compounds and pathways are associated with inflammatory bowel diseases (IBD). In fact, cysteine metabolism results in the production of taurine and sulfate, and gut microbes catabolize them into hydrogen sulfide, a signaling molecule with various biological functions. Besides metabolites originating from sulfur metabolism, several other sulfur-containing metabolites of different classes were detected in human feces, consisting of non-volatile and volatile compounds. Sulfated steroids and bile acids such as taurine-conjugated bile acids are the major classes along with sulfur amino acids and sulfur-containing peptides. Indeed, sulfur-containing metabolites were described in stool samples from healthy subjects, patients suffering from colorectal cancer or IBD. In metabolomics-driven studies, around 50 known sulfur-containing metabolites were linked to IBD. Taurine, taurocholic acid, taurochenodeoxycholic acid, methionine, methanethiol and hydrogen sulfide were regularly reported in IBD studies, and most of them were elevated in stool samples from IBD patients. We summarized from this review that there is strong interplay between perturbed gut microbiota in IBD, and the consistently higher abundance of sulfur-containing metabolites, which potentially represent substrates for sulfidogenic bacteria such as Bilophila or Escherichia and promote their growth. These bacteria might shift their metabolism towards the degradation of taurine and cysteine and therefore to a higher hydrogen sulfide production.

Comparative characterization of bacterial communities in digestive glands of Crassostrea gigas fed with different microalgal diets

The digestive glands of marine molluscs are colonized by a large number of microorganisms, and the structure and function of bacterial community could be severely affected by diets. Microalgae is the main food and energy sources for bivalves, while the impact of phytoplankton composition on the bacterial community as well as the health of bivalves are still not well understood. In the present study, the bacterial communities in digestive glands of oyster Crassostrea gigas fed with different diets were compared based on the high-throughput sequencing of partial 16S rRNA gene. There were significant differences of bacterial composition rather than diversity in digestive glands between the oysters fed with diatom dominant diet (Group N, mainly made up of Nitzschia closterium f.minutissima) and dinoflagellate dominant diet (Group P, mainly made up of Prorocentrum micans). The abundances of Prevotella, Vibronaceae, Ruminococcaceae, and Polaribacter were significantly higher in Group N (p < 0.05), and the abundances of Streptophyta and Acidimicrobiales were significantly higher in Group P (p < 0.05). According to the functional prediction results, the bacterial community in Group P displayed weaker capacities of Kdo2-lipid A biosynthesis as well as taurine degradation, and a stronger capacity of glycolysis compared with the bacterial community in Group N. The higher phylogenetic clustering degree of the bacterial community in Group P (p < 0.05) indicated the higher host selectivity on bacteria. These results suggested that the change of phytoplankton composition of diet would have large effects on bacterial communities in oyster digestive glands. The bacterial community in digestive glands of oysters living in dinoflagellate dominant waters would produce harmful impact to hosts. The present study provided a new perspective to explore the potential mechanism for the massive mortalities of oysters.

Sulfite oxidation in Sinorhizobium meliloti

Sulfite-oxidizing enzymes (SOEs) are crucial for the metabolism of many cells and are particularly important in bacteria oxidizing inorganic or organic sulfur compounds. However, little is known about SOE diversity and metabolic roles. Sinorhizobium meliloti contains four candidate genes encoding SOEs of three different types, and in this work we have investigated the role of SOEs in S. meliloti and their possible link to the metabolism of the organosulfonate taurine. Low level SOE activity (∼1.4 U/mg) was present under all conditions tested while growth on taurine and thiosulfate induced high activities (5.5–8.8 U/mg) although S. meliloti cannot metabolize thiosulfate. Protein purification showed that although expression of two candidate genes matched SOE activity patterns, only a single group 2 SOE, SorT (SMc04049), is responsible for this activity. SorT is a heme-free, periplasmic homodimer (78 kDa) that has low homology to other bacterial SOEs. SorT has an apparent kcat of 343 s−1 and high affinities for both sulfite (KMapp_pH8 15.5 μM) and ferricyanide (KMapp_pH8 3.44 μM), but not cytochrome c, suggesting a need for a high redox potential natural electron acceptor. KMapp_sulfite was nearly invariant with pH which is in contrast to all other well characterized SOEs. SorT is part of an operon (SMc04049-04047) also containing a gene for a cytochrome c and an azurin, and these might be the natural electron acceptors for the enzyme. Phylogenetic analysis of SorT-related SOEs and enzymes of taurine degradation indicate that there is no link between the two processes.

The DUF81 protein TauE in Cupriavidus necator H16, a sulfite exporter in the metabolism of C2 sulfonates

The degradation of taurine, isethionate and sulfoacetate in Cupriavidus necator (Ralstonia eutropha) H16 was shown by enzyme assays to be inducible, and each pathway involved sulfoacetaldehyde, which was subject to phosphatolysis by a common sulfoacetaldehyde acetyltransferase (Xsc, H16_B1870) to yield acetyl phosphate and sulfite. The neighbouring genes encoded phosphate acetyltransferase (Pta, H16_B1871) and a hypothetical protein [domain of unknown function (DUF)81, H16_B1872], with eight derived transmembrane helices. RT-PCR showed inducible transcription of these three genes, and led to the hypothesis that H16_B1872 and orthologous proteins represent a sulfite exporter, which was named TauE.

Roseovariussp. strain 217: aerobic taurine dissimilation via acetate kinase and acetate-CoA ligase

The genome sequence of Roseovarius sp. strain 217 indicated that many pathway enzymes found in other organisms for the degradation of taurine are represented, but that a novel, apparently energy-dependent pathway is involved in the conversion of acetyl phosphate to acetyl CoA. Thus, an ABC transporter for taurine could be postulated, while inducible taurine: pyruvate aminotransferase, alanine dehydrogenase, sulfoacetaldehyde acetyltransferase and sulfite dehydrogenase could be assayed. Whereas phosphate acetyltransferase has been found in other organisms, none was indicated in the genome sequence and no activity was found in cell-free extracts. Instead, acetate kinase was active as was acetate-CoA ligase.

Sulphoacetaldehyde acetyltransferase yields acetyl phosphate: purification from Alcaligenes defragrans and gene clusters in taurine degradation.

The facultatively anaerobic bacterium Alcaligenes defragrans NKNTAU was found to oxidize taurine (2-aminoethanesulphonate) with nitrate as the terminal electron acceptor. Taurine was transaminated to 2-sulphoacetaldehyde. This was not converted into sulphite and acetate by a "sulphoacetaldehyde sulpho-lyase" (EC 4.4.1.12), but into sulphite and acetyl phosphate, which was identified by three methods. The enzyme, which required the addition of phosphate, thiamin diphosphate and Mg(2+) ions for activity, was renamed sulphoacetaldehyde acetyltransferase (Xsc; EC 2.3.1.-). Inducible Xsc was expressed at high levels, and a three-step 11-fold purification yielded an essentially homogeneous soluble protein, which was a homotetramer in its native form; the molecular mass of the subunit was found to be between about 63 kDa (SDS/PAGE) and 65.3 kDa (matrix-assisted laser-desorption ionization-time-of-flight MS). The N-terminal and two internal amino acid sequences were determined, and PCR primers were generated. The xsc gene was amplified and sequenced; the derived molecular mass of the processed protein was 65.0 kDa. The downstream gene presumably encoded the inducible phosphate acetyltransferase (Pta) found in crude extracts. The desulphonative enzymes ("EC 4.4.1.12") from Achromobacter xylosoxidans NCIMB 10751 and Desulfonispora thiosulfatigenes GKNTAU were shown to be Xscs. We detected at least three subclasses of xsc in Proteobacteria and in Gram-positive bacteria, and they comprised a distinct group within the acetohydroxyacid synthase supergene family. Genome sequencing data revealed xsc genes in Burkholderia fungorum (80% sequence identity) and Sinorhizobium meliloti (61%) with closely linked pta genes. Different patterns of regulation for the transport and dissimilation of taurine were hypothesized for S. meliloti and B. fungorum.

Genetic analysis of a Rhodobacter capsulatus gene region involved in utilization of taurine as a sulfur source

Rhodobacter capsulatus was shown to grow efficiently with taurine as sole source of sulfur. We identified a gene region exhibiting similarity to the Escherichia coli tauABC genes coding for a taurine-specific ABC transporter. The R. capsulatus tauABC genes were flanked by two putative operons ( orf459- 484- 590 and cysE- srpI- nifS2) both reading in opposite direction relative to tauABC. Orf459 shows strong similarity to taurine:pyruvate aminotransferase (Tpa) from Bilophila wadsworthia catalyzing the initial transamination during anaerobic taurine degradation, and Orf590 exhibits clear similarity to sulfoacetaldehyde sulfo-lyase from Desulfonispora thiosulfatigenes probably catalyzing the step following the taurine:pyruvate aminotransferase (Tpa) reaction, whereas nifS2 might code for a putative cysteine desulfurase. Expression of R. capsulatus tauABC and nifS2 was inhibited by sulfate, suggesting that tauABC and nifS2 might belong to the same regulon. In contrast, transcription of orf459 was not inhibited by sulfate but was induced by taurine. A tauAB deletion mutant showed significantly reduced growth compared to the wild-type with taurine as sole sulfur source in the presence of serine as a nitrogen source, whereas normal growth was observed in the presence of taurine and ammonium. Deletion of orf459- 484- 590 completely abolished growth with taurine/serine. Single mutations in any of the three genes resulted in the same phenotype, indicating that all three genes of this putative operon are essential for taurine sulfur utilization in the presence of serine. A model for anaerobic taurine sulfur assimilation in R. capsulatus is discussed.

Genetic analysis of aRhodobacter capsulatusgene region involved in utilization of taurine as a sulfur source

Rhodobacter capsulatus was shown to grow efficiently with taurine as sole source of sulfur. We identified a gene region exhibiting similarity to the Escherichia coli tauABC genes coding for a taurine-specific ABC transporter. The R. capsulatus tauABC genes were flanked by two putative operons (orf459-484-590 and cysE-srpI-nifS2) both reading in opposite direction relative to tauABC. Orf459 shows strong similarity to taurine:pyruvate aminotransferase (Tpa) from Bilophila wadsworthia catalyzing the initial transamination during anaerobic taurine degradation, and Orf590 exhibits clear similarity to sulfoacetaldehyde sulfo-lyase from Desulfonispora thiosulfatigenes probably catalyzing the step following the taurine:pyruvate aminotransferase (Tpa) reaction, whereas nifS2 might code for a putative cysteine desulfurase. Expression of R. capsulatus tauABC and nifS2 was inhibited by sulfate, suggesting that tauABC and nifS2 might belong to the same regulon. In contrast, transcription of orf459 was not inhibited by sulfate but was induced by taurine. A tauAB deletion mutant showed significantly reduced growth compared to the wild-type with taurine as sole sulfur source in the presence of serine as a nitrogen source, whereas normal growth was observed in the presence of taurine and ammonium. Deletion of orf459-484-590 completely abolished growth with taurine/serine. Single mutations in any of the three genes resulted in the same phenotype, indicating that all three genes of this putative operon are essential for taurine sulfur utilization in the presence of serine. A model for anaerobic taurine sulfur assimilation in R. capsulatus is discussed.

Ethanedisulfonate is degraded via sulfoacetaldehyde in Ralstonia sp. strain EDS1.

Aerobic enrichment cultures (11) yielded three cultures able to utilise ethane-1,2-disulfonate as sole source of carbon and energy in salts medium. Two pure cultures were obtained and we worked with strain EDS1, which was assigned to the genus Ralstonia on the basis of its 16S rDNA sequence and simple taxonomic tests. Strain EDS1 utilised at least seven alkane(di)sulfonates, ethane-1,2-disulfonate, taurine, isethionate, sulfoacetate, sulfoacetaldehyde and propane-1,3-disulfonate, as well as methanesulfonate and formate. Growth with ethanedisulfonate was concomitant with substrate disappearance and the formation of 2 mol sulfate per mol substrate. The growth yield, 7 g protein (mol C)(-1), indicated quantitative utilisation of the substrate. Ethanedisulfonate-dependent oxygen uptake of whole cells during growth rose to a maximum before the end of growth and then sank rapidly; this was interpreted as evidence for an inducible desulfonative oxygenase that was not active in cell extracts. Inducible sulfoacetaldehyde sulfo-lyase was detected at high activity. Inducible degradation of taurine or isethionate or sulfoacetate via sulfoacetaldehyde sulfo-lyase is interpreted from the data.

Dissimilatory sulfite reductase (desulfoviridin) of the taurine-degrading, non-sulfate-reducing bacterium Bilophila wadsworthia RZATAU contains a fused DsrB-DsrD subunit.

A dissimilatory sulfite reductase (DSR) was purified from the anaerobic, taurine-degrading bacterium Bilophila wadsworthia RZATAU to apparent homogeneity. The enzyme is involved in energy conservation by reducing sulfite, which is formed during the degradation of taurine as an electron acceptor, to sulfide. According to its UV-visible absorption spectrum with maxima at 392, 410, 583, and 630 nm, the enzyme belongs to the desulfoviridin type of DSRs. The sulfite reductase was isolated as an alpha2beta)gamma(n) (n > or = 2) multimer with a native size of 285 kDa as determined by gel filtration. We have sequenced the genes encoding the alpha and beta subunits (dsrA and dsrB, respectively), which probably constitute one operon. dsrA and dsrB encode polypeptides of 49 (alpha) and 54 kDa (beta) which show significant similarities to the homologous subunits of other DSRs. The dsrB gene product of B. wadsworthia is apparently a fusion protein of dsrB and dsrD. This indicates a possible functional role of DsrD in DSR function because of its presence as a fusion protein as an integral part of the DSR holoenzyme in B. wadsworthia. A phylogenetic analysis using the available Dsr sequences revealed that B. wadsworthia grouped with its closest 16S rDNA relative Desulfovibrio desulfuricans Essex 6.

Purification, properties and primary structure of alanine dehydrogenase involved in taurine metabolism in the anaerobe Bilophila wadsworthia.

Alanine dehydrogenase [L-alanine:NAD+ oxidoreductase (deaminating), EC 1.4.1.4.] catalyses the reversible oxidative deamination of L-alanine to pyruvate and, in the anaerobic bacterium Bilophila wadsworthia RZATAU, it is involved in the degradation of taurine (2-aminoethanesulfonate). The enzyme regenerates the amino-group acceptor pyruvate, which is consumed during the transamination of taurine and liberates ammonia, which is one of the degradation end products. Alanine dehydrogenase seems to be induced during growth with taurine. The enzyme was purified about 24-fold to apparent homogeneity in a three-step purification. SDS-PAGE revealed a single protein band with a molecular mass of 42 kDa. The apparent molecular mass of the native enzyme was 273 kDa, as determined by gel filtration chromatography, suggesting a homo-hexameric structure. The N-terminal amino acid sequence was determined. The pH optimum was pH 9.0 for reductive amination of pyruvate and pH 9.0-11.5 for oxidative deamination of alanine. The apparent Km values for alanine, NAD+, pyruvate, ammonia and NADH were 1.6, 0.15, 1.1, 31 and 0.04 mM, respectively. The alanine dehydrogenase gene was sequenced. The deduced amino acid sequence corresponded to a size of 39.9 kDa and was very similar to that of the alanine dehydrogenase from Bacillus subtilis.

Microbial desulfonation.

Organosulfonates are widespread compounds, be they natural products of low or high molecular weight, or xenobiotics. Many commonly found compounds are subject to desulfonation, even if it is not certain whether all the corresponding enzymes are widely expressed in nature. Sulfonates require transport systems to cross the cell membrane, but few physiological data and no biochemical data on this topic are available, though the sequences of some of the appropriate genes are known. Desulfonative enzymes in aerobic bacteria are generally regulated by induction, if the sulfonate is serving as a carbon and energy source, or by a global network for sulfur scavenging (sulfate-starvation-induced (SSI) stimulon) if the sulfonate is serving as a source of sulfur. It is unclear whether an SSI regulation is found in anaerobes. The anaerobic bacteria examined can express the degradative enzymes constitutively, if the sulfonate is being utilized as a carbon source, but enzyme induction has also been observed. At least three general mechanisms of desulfonation are recognisable or postulated in the aerobic catabolism of sulfonates: (1) activate the carbon neighboring the C-SO3- bond and release of sulfite assisted by a thiamine pyrophosphate cofactor; (2) destabilize the C-SO3- bond by addition of an oxygen atom to the same carbon, usually directly by oxygenation, and loss of the good leaving group, sulfite; (3) an unidentified, formally reductive reaction. Under SSIS control, different variants of mechanism (2) can be seen. Catabolism of sulfonates by anaerobes was discovered recently, and the degradation of taurine involves mechanism (1). When anaerobes assimilate sulfonate sulfur, there is one common, unknown mechanism to desulfonate the inert aromatic compounds and another to desulfonate inert aliphatic compounds; taurine seems to be desulfonated by mechanism (1).

Taurine synthesis and cysteine metabolism in cultured rat astrocytes: effects of hyperosmotic exposure.

We investigated mechanisms controlling taurine synthesis in cultured rat cerebral astrocytes. The mean +/- SE rate of taurine synthesis from extracellular cysteine was 21.2 +/- 2.0 pmol.mg protein-1.min-1, whereas taurine degradation was < 1.3% of this rate. Eliminating cellular glutathione and inhibiting glutathione biosynthesis increased taurine synthesis from extracellular cysteine by 39%. In cell homogenates, cysteine dioxygenase (CDO) and cysteine-sulfinate decarboxylase activities were 2.4 +/- 0.2 and 8.3 +/- 2.8 nmol.mg protein-1.min-1, respectively. CDO activity was strongly dependent on cysteine concentration over physiological and pathophysiological ranges of intracellular cysteine concentration. Growth in hyperosmotic medium caused a greater increase in culture medium taurine content than that measured from cells in isosmotic growth medium. Hyperosmotic treatment transiently increased the rate of cysteine accumulation and cellular cysteine and glutathione contents but had no effect on the synthesis rate of taurine from extracellular cysteine. Thus cysteine is accumulated and then metabolized to taurine through CDO, whose activity depends on the intracellular cysteine concentration and appears to be rate limiting for taurine synthesis. Hyperosmotic exposure increases net taurine production yet has no effect on taurine synthesis from exogenously applied cysteine. Availability of substrate from intracellular pools must contribute to maintenance of high intracellular taurine during hyperosmotic exposure.

Dietary Antibiotics Decrease Taurine Loss in Cats Fed a Canned Heat-Processed Diet

In a crossover design, cats were fed a canned heat-processed diet (18 g dry matter/kg initial body wt) either with (+) or without (-) antibiotics [a mixture of penicillin G, procaine (25 mg/18 g diet) and tetracycline (50 mg/18 g diet)]. The (-/+) group received no antibiotics during the first 5-wk period and received antibiotics during the second 5-wk period; the (+/-) group received the reverse. Plasma, whole blood, urinary and fecal concentrations of taurine, fecal bile acid excretion and cholyltaurine hydrolase activities were measured. Consumption of antibiotics for 5 wk resulted in a lower rate of depletion of plasma taurine. Taurine concentrations decreased more over the first 5 wk in cats in the (-/+) group than in cats in the (+/-) group [from 116 ± 26 to 26 ± 6 µmol/L (-/+) and from 109 ± 6 to 77 ± 7 µmol/L (+/-) for plasma, and from 546 ± 8 to 292 ± 29 µmol/L (-/+) and from 560 ± 11 to 431 ± 20 µmol/L (+/-) for whole blood]. Urinary total taurine excretions during the 5th week were 54 µmol/d for the (-/+) group and 135 µmol/d for the (+/-) group (pooled SEM, ±13). Fecal total taurine excretions during the 5th week were 184 and 53 µmol/d for the (-/+) and (+/-) groups, respectively, (pooled SEM ± 9). Most of the fecal taurine was unconjugated (free). Fecal bile acid excretions during the 5th week were 235 ± 18 and 106 ± 11 µmol/d for the (-/+) and (+/-) groups, respectively. Dietary antibiotics suppressed fecal cholyltaurine hydrolase activity of cats. Fecal cholyltaurine hydrolase activities during the 5th week were 279 ± 54 and 42 ± 10 nmol cholic acid released · min-1 · g dry feces-1 in the (-/+) and (+/-) groups, respectively. After the crossover, mean values for the groups were reversed, showing that the observed changes were due to the antibiotic treatment. These results support the hypothesis that the dietary taurine requirement of cats is largely determined by the extent of microbial degradation of taurine in the gastrointestinal tract.

Maillard reaction products in purified diets induce taurine depletion in cats which is reversed by antibiotics.

The effects of heat processing (Maillard reaction) and addition of antibiotics to diets on the metabolism of taurine in adult cats were studied. Groups of four cats were given daily 22 g/kg body weight one of four purified diets based on casein and starch. All diets contained the same major ingredients as the control (diet 1), except for starch substitutions. Diet 2 was autoclaved; in diet 3, 50 g glucose replaced 50 g starch before autoclaving; in diet 4, only the casein component was autoclaved with 50 g glucose before addition to the diet. Diets were fed for 5 wk, then a mixture of antibiotics was added to all diets and they were fed for a further 5 wk. In the first (no antibiotics) period, cats given the Maillard reaction products (diets 3 and 4) had a significant depletion of plasma and whole blood taurine and had twice the fecal, but less than half the urinary total taurine excretion of control cats. The addition of antibiotics to the diets restored plasma and whole blood concentration in cats given diets 3 and 4, reduced fecal and increased urinary taurine excretion, and decreased fecal cholyltaurine hydrolase activity. These results suggest that Maillard reaction products promote an enteric flora that favors degradation of taurine and decreases recycling of taurine by the enterohepatic route.