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Title
Conversion of taurine into N-chlorotaurine (taurine chloramine)
and sulphoacetaldehyde in
response to oxidative stress.
Author
Cunningham C; Tipton KF; Dixon HB
Address
Department of Biochemistry, Trinity College, Dublin 2, Ireland.
Source
Biochem J, 1998 Mar, 330 ( Pt 2):, 939-45
Abstract
N-Chlorotaurine (taurine chloramine), formed by treating taurine
with hypochlorous acid,
was shown to decompose to sulphoacetaldehyde with a first-order
rate constant of 9.9+/-0.5
x 10(-4).h-1 at 37 degrees C in 0.1 M phosphate buffer, pH 7.4.
Rat liver homogenates
accelerated this decay in a process that was proportional to
tissue-protein concentration and
saturable, with maximum velocity (Vmax) and Km values of 0.28+/-0.01
nmol/min per mg
of protein and 37+/-9 microM respectively. This activity was
found to be lost on heat
denaturation, but retained after dialysis. There was no detectable
formation of
sulphoacetaldehyde when taurine itself was incubated with the
tissue homogenates under the
same conditions. Activation of human neutrophils (1.67 x 10(6)
cells/ml) with latex beads
resulted in a respiratory burst of oxygen-radical production,
the products of which were
partially sequestered by 12.5 mM taurine. Under these conditions
sulphoacetaldehyde was
generated at a constant rate of 637+/-18 pmol/h per ml for over
7 h. A non-activated
neutrophil suspension contained constant levels of 1.42+/-0.02
nmol/ml
sulphoacetaldehyde, as did activated cells incubated in the absence
of taurine, a basal level
which may indicate a steady turnover of taurine in these cells.
Such formation of
chlorotaurine and its decay to the aldehyde may be the first
steps in the metabolism of
taurine to isethionate (2-hydroxyethanesulphonate) that has been
demonstrated by various
Authors to occur in vivo.
Title
Host defense--a role for the amino acid taurine?
Author
Stapleton PP; OFlaherty L; Redmond HP; Bouchier Hayes DJ
Source
JPEN J Parenter Enteral Nutr, 1998 Jan, 22:1, 42-8
Abstract
Taurine (2-aminoethane sulphonic acid), a ubiquitous beta-amino
acid is conditionally
essential in man. It is not utilized in protein synthesis but
found free or in some simple
peptides. Derived from methionine and cysteine metabolism, taurine
is known to play a
pivotal role in numerous physiological functions. Some of the
roles with which taurine has
been associated include osmoregulation, antioxidation, detoxification
and stimulation of
glycolysis and glycogenesis. Intracellular taurine is maintained
at high concentrations in a
variety of cell types and alteration of cell taurine levels is
difficult. The role of taurine within
the cell appears to be determined by the cell type. Recent research
has determined a
regulatory role for taurinechloramine, the product formed by
the reaction between taurine
and neutrophil derived hypochlorous acid on macrophage function.
Plasma taurine levels are
also high, although decreases are observed in response to surgical
injury and numerous
pathological conditions including cancer and sepsis. Supplementary
taurine replenishes
decreased plasma taurine. Although commonly used as a dietary
supplement in the Far
East, the potential advantages of dietary taurine supplementation
have not as yet been fully
recognized in the Western World; this is an area which could
prove to be beneficial in the
clinical arena.
Title
Intestinal taurine transport: a review.
Author
OFlaherty L; Stapleton PP; Redmond HP; Bouchier Hayes DJ
Source
Eur J Clin Invest, 1997 Nov, 27:11, 873-80
Abstract
Intestinal uptake of dietary taurine is an important contributor
to taurine homeostasis and
may become crucial when taurine metabolism is impaired. This
review aims to assess the
literature documenting taurine transport and review what is currently
known about the
operation of the enterocyte taurine transport protein. Sources
included MedLine searches
from the last 10 years and references from original and review
articles. The aim was to
include human and animal studies directly addressing the subject
of taurine uptake by
enterocytes. Intestinal taurine transport has been well documented
in in vivo studies using
many different animal models. The mechanistic/kinetic aspects
of the transport system have
been extensively documented. However, little is known about what
regulates the system.
The recent development of a cell culture model of intestinal
taurine transport will allow
studies to explore the regulation of gut taurine uptake, which
promises to be a very exciting
area.
Title
Characterization and regulation of taurine transport in Caco-2,
human intestinal cells.
Author
Satsu H; Watanabe H; Arai S; Shimizu M
Source
J Biochem (Tokyo), 1997 Jun, 121:6, 1082-7
Abstract
We characterized the taurine transport system in human intestinal
Caco-2 cells and showed
that it is subject to adaptive regulation. The activity of taurine
transport in Caco-2 cells was
evaluated by means of an Na+- and Cl(-)-dependent high-affinity
transport system, the
characteristics of which were similar to those of the beta-amino
acid-specific taurine
transport system previously described for various tissues. The
activity of taurine transport
was down-regulated on culturing in taurine-containing medium.
This taurine-induced
down-regulation was dependent on both the incubation time with
taurine and the
concentration of taurine. Hypotaurine and beta-alanine were also
capable of inducing this
adaptive regulation, whereas alpha-amino acids and gamma-aminoisobutyric
acid were not.
Kinetic analysis of control and taurine-treated cells suggested
that the down-regulation was
associated with a decrease in the maximal velocity of taurine
transport and also with a
decrease in the affinity of the taurine transporter. Cycloheximide
treatment weakened the
taurine-induced down-regulation. The mRNA level of the taurine
transporter (HTAU type)
in taurine-treated cells was markedly decreased compared with
in control cells. These results
indicate that a complex regulatory mechanism is involved in this
down-regulation.
Title
Renal excretory responses to saline load in the taurine-depleted
and the
taurine-supplemented rat.
Author
Mozaffari MS; Azuma J; Patel C; Schaffer SW
Source
Biochem Pharmacol, 1997 Sep, 54:5, 619-24
Abstract
Taurine is found in high concentrations in mammalian cells. Despite
recognition of its role
as an organic osmolyte in the kidney, information regarding its
effects on renal fluid and
electrolyte excretion is sparse. Therefore, the objective of
the first series of experiments was
to determine the effects of taurine depletion on renal excretory
responses to a saline load. To
induce taurine depletion, male Wistar-Kyoto (WKY) rats were treated
with tap water
containing 3% beta-alanine for 3 weeks. Taurine depletion reduced
the initial rates of fluid
and sodium excretion after an intravenous saline load. This effect
was attributed to taurine
depletion since maintenance of the taurine-depleted rats on tap
water for 2 days to remove
the effects of beta-alanine yielded the same pattern as the taurine-depleted
rats exposed to
beta-alanine at the time of the experiment. Nonetheless, rats
exposed to short-term
beta-alanine treatment, which has no influence on kidney taurine
content, demonstrated a
larger (approximately 25%) natriuretic but not diuretic response
to the isotonic saline load
than either the control or taurine-depleted rats. These data
suggest that beta-alanine-induced
inhibition of tubular reabsorption of taurine may result in subsequent
excretion of taurine
with attendant natriuresis early in the course of beta-alanine
treatment. We also tested the
hypothesis that taurine potentiates the renal excretory responses
to an isotonic saline load in
WKY rats. Inclusion of taurine in the infusate significantly
increased natriuresis and diuresis
after a saline load. This effect was greater in animals fed a
basal than a high NaCl diet. Our
data support a role for taurine as a natriuretic and diuretic
agent.
Title
Glutathione kinetics in normal man and in patients with liver
cirrhosis.
Author
Bianchi G; Bugianesi E; Ronchi M; Fabbri A; Zoli M; Marchesini
G
Source
J Hepatol, 1997 Mar, 26:3, 606-13
Abstract
BACKGROUND/AIMS: The dynamics of glutathione in plasma has always
been studied
by bolus injections. Data are available suggesting that the low
plasma levels of cirrhosis are
due to decreased production in glutathione-producing tissues,
mainly the liver. We aimed to
measure the kinetics of glutathione during controlled steady-state
conditions, and to
determine the reasons for its reduced plasma levels in advanced
cirrhosis. METHODS: The
plasma clearance of glutathione was measured in six control subjects
and in ten patients with
cirrhosis during a 2-step infusion study, producing steady-state
levels approximately 5 and
10 times basal values. The plasma disappearance curve after infusion
stop was used to
determine the apparent volume of distribution and half-life of
glutathione, and the estimated
basal appearance rate. RESULTS: The clearance of glutathione
did not reject 1st-order
kinetics, i.e., it was concentration-independent, and was nearly
doubled in cirrhosis. The
half-life of exogenous glutathione was not different, whereas
the volume of distribution was
larger in cirrhosis, in the same range as extracellular water.
The endogenous basal
appearance rate of glutathione was reduced by 50%, and correlated
with liver function,
measured by routine and dynamic tests. CONCLUSIONS: The data
confirm that the
primary defect responsible for reduced glutathione in liver disease
is a reduced production,
possibly related to hepatocyte dysfunction and a block along
the pathway of methionine
metabolism.
Title
Taurine is an osmolyte in rat liver macrophages (Kupffer cells).
Author
Warskulat U; Zhang F; Häussinger D
Source
J Hepatol, 1997 Jun, 26:6, 1340-7
Abstract
BACKGROUND/AIMS: The availability of betaine as an osmolyte was
recently shown to
interfere strongly with important cell functions of liver macrophages
(Kupffer cells), such as
eicosanoid and tumor necrosis factor-alpha production or phagocytosis.
We therefore
investigated whether taurine is also used as an osmolyte by Kupffer
cells and whether it is
involved in the control of Kupffer cell functions. METHODS/RESULTS:
Hyperosmotic
(hypoosmotic) exposure of cultured rat liver macrophages (Kupffer
cells) for 6-12 h led to
an increase (decrease) in the mRNA levels of the taurine transporter
(TAUT) and an
increase (decrease) in taurine transport into the cells. The
hyperosmolarity-induced increase
in TAUT-mRNA levels was diminished by 37+/-10% upon addition
of taurine, but not
upon addition of betaine. When Kupffer cells were preloaded with
taurine, hypoosmotic
exposure led to a rapid efflux of taurine from the cells, which
was significantly delayed in
the presence of the anion exchanger inhibitor 4,4'-diisothiocyanostilbene-2,2'-disulfonic
acid
(DIDS). Taurine efflux was also stimulated during phagocytosis
of Latex particles;
however, Latex was without effect on the hyperosmolarity-induced
increase of TAUT
mRNA levels. Lipopolysaccharide (LPS) led to an induction of
cyclooxygenase-2, which
was markedly enhanced during hyperosmotic conditions. Taurine
diminished the induction
of cyclooxygenase-2 and inhibited the LPS/hyperosmolarity-induced
stimulation of
prostaglandin E2 formation. CONCLUSIONS: The data suggest that,
in addition to betaine,
taurine also acts as an osmolyte in Kupffer cells, and that taurine
availability may be an
important modulater of Kupffer cell functions such as eicosanoid
synthesis.
Title
Thiosulfate as a metabolic product: the bacterial fermentation
of taurine.
Author
Denger K; Laue H; Cook AM
Source
Arch Microbiol, 1997 Oct, 168:4, 297-301
Abstract
Thiosulfate (S2O32-) is a natural product that is widely utilized
in natural ecosystems as an
electron sink or as an electron donor. However, the major biological
source(s) of this
thiosulfate is unknown. We present the first report that taurine
(2-aminoethanesulfonate), the
major mammalian solute, is subject to fermentation. This bacterial
fermentation was found
to be catalyzed by a new isolate, strain GKNTAU, a strictly anaerobic,
gram-positive, motile
rod that formed subterminal spores. Thiosulfate was a quantitative
fermentation product.
The other fermentation products were ammonia and acetate, and
all could be formed by
cell-free extracts.
Title
An improved synthesis of taurine- and glycine-conjugated bile
acids.
Author
Momose T; Tsubaki T; Iida T; Nambara T
Source
Lipids, 1997 Jul, 32:7, 775-8
Abstract
A simple and efficient method for the synthesis of taurine- and
glycine-conjugated bile acids
is described. The condensation reaction was achieved by the simple
mixing of unconjugated
bile acid (1.0 eq.), taurine (2.0 eq.) (or glycinate ester),
diethyl phosphorocyanidate (1.2 eq.)
in the presence of triethylamine at room temperature for 30-60
min. Sample clean-up was
effected by the use of a prepacked Sep-Pak C18 cartridge for
reversed-phase solid extraction
or by direct recrystallization, yielding the desired taurine
and glycine conjugates in 89-93 and
92-96% isolated yields, respectively.
Title
Biliary bile acids in primary biliary cirrhosis: effect of ursodeoxycholic
acid.
Author
Combes B; Carithers RL Jr; Maddrey WC; Munoz S; Garcia Tsao G;
Bonner GF; Boyer
JL; Luketic VA; Shiffman ML; Peters MG; White H; Zetterman RK;
Risser R; Rossi SS;
Hofmann AF
Source
Hepatology, 1999 Jun, 29:6, 1649-54
Abstract
Bile acid composition in fasting duodenal bile was assessed at
entry and at 2 years in
patients with primary biliary cirrhosis (PBC) enrolled in a randomized,
double-blind,
placebo-controlled trial of ursodeoxycholic acid (UDCA) (10-12
mg/kg/d) taken as a single
bedtime dose. Specimens were analyzed by a high-pressure liquid
chromatography method
that had been validated against gas chromatography. Percent composition
in bile (mean +/-
SD) for 98 patients at entry for cholic (CA), chenodeoxycholic
(CDCA), deoxycholic
(DCA), lithocholic (LCA), and ursodeoxycholic (UDCA) acids, respectively,
were 57.4 +/-
18.6, 31.5 +/- 15.5, 8.0 +/- 9.3, 0.3 +/- 1.0, and 0.6 +/- 0.9.
Values for CA were increased,
whereas those for CDCA, DCA, LCA, and UDCA were decreased when
compared with
values in normal persons. Bile acid composition of the major
bile acids did not change after
2 years on placebo medication. By contrast, in patients receiving
UDCA for 2 years, bile
became enriched with UDCA on average to 40.1%, and significant
decreases were noted for
CA (to 32.2%) and CDCA (to 19.5%). No change in percent composition
was observed for
DCA and LCA. Percent composition at entry and changes in composition
after 2 years on
UDCA were similar in patients with varying severity of PBC. In
patients whose bile was
not enriched in UDCA (entry and placebo-treated specimens), CA,
CDCA, DCA, and the
small amount of UDCA found in some of these specimens were conjugated
to a greater
extent with glycine (52%-64%) than with taurine (36%-48%). Treatment
with UDCA
caused the proportion of all endogenous bile acids conjugated
with glycine to increase to
69% to 78%, while the proportion conjugated with taurine (22%-31%)
fell (P <.05).
Administered UDCA was also conjugated predominantly with glycine
(87%).
Title
Increased fecal bile acid excretion and changes in the circulating
bile acid pool are involved
in the hypocholesterolemic and gallstone-preventive actions of
psyllium in hamsters.
Author
Trautwein EA; Kunath Rau A; Erbersdobler HF
Source
J Nutr, 1999 Apr, 129:4, 896-902
Abstract
The lipid-lowering effect of psyllium (PSY) is well established.
Enhanced fecal bile acid
excretion and a stimulation of hepatic bile acid synthesis are
discussed as primary
mechanisms of this action. To further examine the effect of bile
acid excretion and
specifically of compositional alterations in the bile acid pool
on the cholesterol-lowering and
gallstone-preventing action of PSY, male golden Syrian hamsters
were fed lithogenic diets
containing 5 g/100 g fat, 0.4 g/100 g cholesterol and 0 (control),
4 or 6% PSY or 1%
cholestyramine (CHY). PSY significantly lowered plasma total
cholesterol and
triacylglycerol at a magnitude comparable to that induced by
CHY. Although hepatic
cholesteryl ester accumulation was completely inhibited by CHY,
PSY did not prevent the
hepatic storage of esterified cholesterol. PSY and CHY caused
distinct alterations in the bile
acid profile. PSY caused a selective reduction of taurine-conjugated
bile acids, especially of
taurochenodeoxycholate. As a result, the glycine:taurine conjugation
and the
cholate:chenodeoxycholate ratios were significantly higher in
PSY-fed hamsters. PSY and
CHY normalized the lithogenic index and prevented cholesterol
gallstone formation
compared with controls. Daily fecal bile acid excretion was approximately
400% greater in
hamsters fed 6% PSY, whereas CHY caused an 11-fold increase.
Daily neutral sterol
excretion did not differ in PSY-fed hamsters but was >100%
greater in those fed CHY than
in controls. These data emphasize the potent lipid-lowering effect
of PSY. Increased fecal
bile acid excretion and alterations of the circulating bile acid
pool by removal of dihydroxy
bile acids (e.g., taurochenodeoxycholate) appear to be main modulators
of the
hypocholesterolemic action of PSY by leading to an up-regulation
of hepatic bile acid
synthesis. |
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