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PubMed1976

Transport of 5-hydroxy-3-indoleacetic acid by spinal cord during subarachnoid perfusion.

The transport of [14C]5-hydroxy-3-indoleacetic acid (5-HIAA) by the spinal cord was investigated with spinal subarachnoid perfusions of 20 rhesus monkeys. For spinal white matter, [14C]5-HIAA was found to distribute in a tissue space of 50-55% and to exchange readily between tissue and blood across parenchymal capillaries. The data were analyzed with a model of the spinal cord as a cylinder and a mean capillary transfer half-time of 20 min determined. The spinal cord cleared [14C]5-HIAA from 19 mul/min of CSF. Administration of probenecid yielded a somewhat lower mean tracer clearance rate (14 mul/min) but did not alter the capillary exchange half-time or the distribution volume of [14C]5-HIAA in the spinal cord. The data suggest that capillaries within spinal white matter transport 5-HIAA by a mechanism which is insensitive to inhibition by probenecid and that lumbar CSF concentrations reflect only a small portion of total 5-HIAA production by the central nervous system.

Animals↗
PubMed1982

Does in vivo voltammetry in the hippocampus measure 5-HT release?

In vivo voltammetry enables catecholamine and 5-hydroxytryptamine (5-HT) release to be directly determined in the brains of conscious unrestrained animals. This study concerned the validation of the measurement of 5-HT release using scanning voltammetry at chronically implanted carbon paste/epoxy resin glass microelectrodes in the rat hippocampus. Automated recordings of the current produced by applying a ramp (100 mV/s) potential (0-1 V) to the electrode at 5 min intervals were made over a period of several hours. A current peak at 0.35-0.4 V corresponded to that produced by solutions of 5-HT in vitro. The effect of a number of drug known to affect 5-HT synthesis and release was then studied in vivo. p-Chloroamphetamine (PCA) caused an increase in the peak which correlated with a '5-HT behavioural syndrome'. p-Chlorophenylalanine caused a reduction in the peak and prevented both the increase seen with PCA and the PCA induced behavior. Fluoxetine and L-tryptophan also led to increases in signal; all these results were consistent with the signal reflecting extraneuronal 5-HT. However 5-hydroxyindoleacetic acid (5HIAA) also oxidizes at 0.35-0.4 V in vitro. Probenecid, which blocks 5HIAA egress from the brain caused a large increase in the hippocampal signal. The monoamine oxidase inhibitors pargyline and nialamide, which increases 5-HT and reduce 5HIAA levels, had no significant effect on the signal. These results, together with the greater increase in signal following probenecid than tryptophan and the delayed increase after tryptophan, and interpreted as implying that extraneuronal 5HIAA and 5-HT contribute approximately equally to the hippocampal signal. We conclude that this method gives information distinct from and complementary to biochemical estimations, and offers great scope for the investigation of the role of 5-hydroxyindole release in drug and environmental effects on behaviour.

Animals↗
PubMed1977

Changes in striatal dopamine metabolism during precipitated morphine withdrawal.

Precipitation of withdrawal in morphine tolerant/dependent rats by either naloxone or the partial agonist ZK 48491 caused a significant increase in the contration of striatal DA, which persisted for at least 1 h. During the same time the probenecid-induced accumulation of HVA and DOPAC was reduced in the striatum in relation to probenecid-treated tolerant/dependent controls. 20 min after precipitation of withdrawal by naloxone, the striatal concentration of 3-methoxytyramine was decreased by about 40%, while the activity of the DA metabolizing enzymes, MAO and COMT, remained unchanged. Naloxone-precipitated withdrawal was, further, found to delay the depletion of striatal DA caused by inhibition of synthesis 90 min after alpha-methyl-p-tyrosine treatment. All these results provide evidence for a decreased release of DA from the striatum during precipitated morphine withdrawal.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1983

Drug-induced alterations in the efflux of 5-hydroxytryptamine and of 5-hydroxyindoleacetic acid into superfusates of the rat spinal cord.

The effect of dl-p-chloroamphetamine, fluoxetine and probenecid on the efflux of endogenous 5-hydroxytryptamine (5HT) and 5-hydroxyindoleacetic acid (5HIAA) into superfusates of the spinal cord of anesthetized rats was examined. Mean basal efflux of 5HT and 5HIAA was 0.27 and 15.56 ng/ml superfusate, respectively. The addition of dl-p-chloroamphetamine to the superfusate produced a dose-dependent increase in the efflux of 5HT into the superfusate, but did not increase the efflux of 5HIAA. Probenecid (200 mg/kg i.p.) increased the basal efflux of both 5HT and 5HIAA as compared to control values. When administered systemically, fluoxetine (10 mg/kg i.p. or s.c.) decreased the basal efflux of 5HIAA, but did not alter the basal efflux of 5HT as compared to control values. In contrast, when administered in the superfusate, fluoxetine produced a dose-dependent increase in the basal efflux of 5HT, but did not alter the basal efflux of 5HIAA. The release of 5HT produced by the addition of 2.5 X 10(-4) M dl-p-chloroamphetamine to the superfusate was not prevented in rats pretreated systemically with fluoxetine, although when administered in the superfusate fluoxetine inhibited the dl-p-chloroamphetamine-induced release of 5HT.

Animals↗
PubMed1993

The AMPA receptor antagonist NBQX exerts antidystonic effects in an animal model of idiopathic dystonia.

The effects of the AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate) antagonist NBQX (2,3-dihydroxy-6-nitro-7-sulfamoyl-benzo(F)quinoxaline) were studied in an inbred line of Syrian golden hamsters with paroxysmal dystonia. The severity of dystonia in these mutant hamsters was significantly reduced by NBQX at doses of 10-20 mg/kg i.p. Coadministration of the transport inhibitor probenecid prolonged the antidystonic action of NBQX, indicating that NBQX may be rapidly eliminated by a process sensitive to probenecid. A similar potent and long-lasting antidystonic effect was obtained when NBQX was administered as an aqueous suspension rather than an aqueous solution, which may be explained by retarded absorption of NBQX after its injection as a suspension. The antidystonic activity of the AMPA antagonist NBQX may indicate that an overactivity of excitatory acidergic neurotransmission is involved in the pathophysiology of dystonia in genetically dystonic hamsters.

Animals↗
PubMed1996

Capillary electrophoresis of diuretics.

The review surveys the application of capillary electrophoresis to the screening, identification and determination of diuretics and probenecid. The number of publications is still limited, but the studies already published clearly show that capillary zone electrophoresis (CZE) and micellar electrokinetic chromatography are excellent alternatives for the investigation of diuretics. High accuracy identifications of diuretics and probenecid, even in urine samples, can be obtained when CZE is used with the marker techniques. This review paper has been written from the viewpoint of practical use and some hints are given for future CE studies on diuretics.

Diuretics↗
PubMed1993

Conjugation of phenylacetic acid and m- and p-hydroxyphenylacetic acids in the rat striatum.

Two factors that might regulate the levels of the trace acids, phenylacetic acid (PAA), m-hydroxyphenylacetic acid (mHPAA) and p-hydroxyphenylacetic acid (pHPAA) in the rat striatum were investigated: first, formation of conjugates of these acids and second, transport out of the brain by a probenecid-sensitive system. The presence of conjugates of these acids was investigated by subjecting homogenates of rat striatum to hydrolysis. The concentrations of PAA were increased ten-fold by hydrolysis, pHPAA increased two-fold, and mHPAA was unaffected. These findings coupled with the failure of parglyline to decrease free or total PAA levels suggest that conjugation of PAA is an important factor regulating free PAA levels. The transport inhibitor, probenecid, increased the concentrations of free mHPAA, free pHPAA and the total concentrations of all three acids indicating that all three trace acids can be removed from the rat brain by a transport system.

Animals↗
PubMed1989

N-acetyl S-(1,2-dichlorovinyl)-L-cysteine produces a similar toxicity to S-(1,2-dichlorovinyl)-L-cysteine in rabbit renal slices: differential transport and metabolism.

Renal cortical slices were used to determine the toxicity of N-acetyl-S-(1,2-dichlorovinyl)-L-cysteine (N-acetyl-DCVC) as well as to investigate the transport and metabolism of S-(1,2-dichlorovinyl)-L-cysteine (DCVC) and the N-acetyl derivative. N-Acetyl-DCVC produced dose- and time-dependent decreases in intracellular K+ content and lactate dehydrogenase activity. Histopathology demonstrated an initial S3 lesion followed by a lesion inclusive of all proximal tubules. N-Acetyl-DCVC was shown to be transported via the organic anion system by its ability to inhibit PAH transport by the cells and the ability of probenecid to decrease uptake (80%) and toxicity of N-acetyl-DCVC. DCVC, in contrast, was not transported by the organic anion system, but may be transported by one or more amino acid systems. N-Acetyl-DCVC must be deacetylated before undergoing metabolism by beta-lyase. This process must occur since covalent binding of a 35S-labeled reactive product from N-acetyl [35S]DCVC is observed within 1 hr. Both the uptake inhibitor, probenecid, and aminooxyacetic acid (AOAA), a beta-lyase inhibitor, decreased the covalent binding from N-acetyl [35S]DCVC (80 and 50%, respectively), but only AOAA inhibited the covalent binding of DCVC. AOAA also partially inhibited the toxicity of DCVC and N-acetyl-DCVC as determined by intracellular K+ content, lactate dehydrogenase activity, and histopathology. Despite the fact that a separate transport system and an additional enzymatic step (deacetylation) are required, N-acetyl-DCVC produces a lesion with similar intratubular specificity to that seen with DCVC. Therefore, the S3 specificity seen in vivo could be produced by either compound.

Acetylation↗
PubMed1991

Cadmium inhibition of basolateral solute fluxes in rabbit renal tubules and the nature of cycloleucine uptake.

The objective of this investigation was to determine whether Cd inhibition of amino acid transport across basolateral (BL) cell membranes in renal tubules results from a direct toxic action at that site. The concentration ratio (R) of cycloleucine in cell water/arterial plasma at steady state in nonfiltering rabbit kidneys consistently exceeded 1.0, thus confirming the active nature of BL amino acid uptake. BL cycloleucine extrusion, though down the concentration gradient, has previously been shown to be greatly slowed in Cd-poisoned animals; nevertheless, R remained unchanged. Active uptake and passive extrusion of cycloleucine must therefore be equally sensitive to Cd, a fact strongly suggesting an indirect action of the metal on BL solute transfer. This hypothesis is strengthened by the observation that R for paraaminohippurate (PAH), another solute actively accumulated across BL membranes, also remained unaffected by Cd poisoning. The reduction in R(PAH) by the direct transport inhibitor probenecid served as positive control. The additional finding that R(cycloleucine) is also depressed by probenecid, as well as by excess PAH, indicates some overlap in substrate specificities of the two carrier systems. The systems are not identical, however, as can be deduced from the observation that L-leucine affected only transport of cycloleucine, not that of PAH.

Animals↗
PubMed1982

Value of monoamine metabolite determinations in CSF as an index of their concentrations in rat brain following various pharmacological manipulations.

Using reversed-phase high performance liquid chromatography with electrochemical detection it is possible to measure concomitantly the concentration of several monoamines, their metabolites and aminoacid precursors in 100 microliters of rat cerebrospinal fluid. To study the quantitative relationship between CSF and brain, alterations in brain monoamines and monoamine metabolites were effected by treatment with L-DOPA or L-5HTP administered with or without concomitant inhibition of extracerebral aromatic amino acid decarboxylase and by treatment with alpha-monofluoromethyldopa, probenecid, haloperidol, or probenecid plus haloperidol. The concentrations of the monoamine metabolites, 5-hydroxyindoleacetic acid, 3,4-dihydroxyphenylacetic acid, and homovanillic acid as well as of the L-DOPA metabolite, 3-methoxy-4-hydroxyphenylalanine in the cerebrospinal fluid were linearly correlated with the concentrations of these metabolites in the brain. However, these correlations need to be interpreted cautiously, since the slopes of the individual regression lines obtained after different pharmacological treatments differed significantly.

5-Hydroxytryptophan↗
PubMed1990

Identification of cholate as a shared substrate for the unidirectional efflux systems for methotrexate in L1210 mouse cells.

The bidirectional transport properties of cholate have been examined in leukemic L1210 mouse cells and compared with the transport of methotrexate. The cell entry of [3H]cholate was Na(+)-independent, linear with increasing concentrations of substrate, enhanced by decreasing pH, and uneffected by excess unlabeled cholate or by various anion-transport inhibitors and hence had the characteristics of passive diffusion or a pH-dependent mediated process with a high Kt for cholate. The efflux of [3H]cholate, however, could be attributed to carrier-mediated and energy-dependent transport. Efflux was rapid (t1/2 = 1.5 min) and could be increased with glucose and decreased with metabolic inhibitors, and it was inhibited by various compounds including bromosulfophthalein, probenecid, prostaglandin A1, reserpine, verapamil, quinidine, diamide, 1-methyl-3-isobutylxanthine and vincristine. The most potent inhibitor was prostaglandin A1, which reduced efflux by 50% at a concentration of 0.10 microM. Half-maximal inhibition by vincristine occurred at 4.8 microM. The maximum extent of inhibition with most of the inhibitors was 95%, although a lower value was observed with bromosulfophthalein (85%). When cholate efflux was compared with the efflux of methotrexate, both processes responded similarly to changes in the metabolic state of the cell. Moreover, the various inhibitors of cholate efflux also inhibited the efflux of methotrexate and the same concentration of each inhibitor was required for half-maximal inhibition of both processes. The efflux of folate and urate also proceeded via outwardly directed, unidirectional processes which were sensitive to bromosulfophthalein and probenecid. The results suggest that L1210 cells have the capacity for the unidirectional extrusion of cholate, methotrexate and probably other large, structurally dissimilar organic anions and that this efflux occurs via two or more very similar transport systems with a broad anion specificity. The function of an organic anion efflux system in vivo may be to facilitate the extrusion of cytotoxic metabolic anions which are too large to exit via the general anion-exchange carrier of these cells. Similarities in inhibitor specificity were also apparent between unidirectional anion efflux in L1210 cells and the drug efflux pump which is over-produced in cells with multidrug resistance.

Animals↗
PubMed1992

Failure of Borrelia burgdorferi to survive in the skin of patients with antibiotic-treated Lyme disease.

BACKGROUND: Borrelia burgdorferi has been cultivated from clinically normal skin (previous erythema migrans sites) after antibiotic therapy for Lyme disease. OBJECTIVE: We investigated the possibility of similar findings in 13 of our patients with antibiotic-treated Lyme disease from whom B. burgdorferi was cultivated from their erythema migrans lesions before antibiotic therapy. METHODS: After treatment with doxycycline or a combination of amoxicillin and probenecid, skin biopsy specimens were obtained from clinically normal skin adjacent to the previous biopsy sites and cultured. RESULTS: B. burgdorferi was not cultivated from these posttreatment biopsy sites. CONCLUSION: The failure of B. burgdorferi to survive in the former erythema migrans sites of our antibiotic-treated patients, as well as their favorable clinical response, supports the use of doxycycline or combined amoxicillin and probenecid in the treatment of early Lyme disease but does not preclude the survival of the organism in other tissues.

Adult↗
PubMed1993

Renal clearance of domoic acid in the rat.

The renal clearance (Clr) of the seafood toxin domoic acid (DA) was investigated in the rat. Following cannulation of the right femoral artery, the left femoral vein and the bladder of anaesthetized rats, a single bolus injection of either [3H]DA, [14C]p-aminohippuric acid (PAH) or [3H]inulin was administered through the venous cannula. Blood samples were taken from the arterial cannula at 1, 2, 10, 30, 50, 70, 90, 110 and 130 min following injection, and urine samples were collected at 20-min intervals starting from the time of bolus injection. Based on plasma concentration-time profiles, the total clearances (Clt) for DA, PAH and inulin were 9.12, 33.17 and 7.50 ml/min/kg body weight, respectively. The Clr calculated from urinary excretion rates were not significantly different from the Clt. Probenecid significantly reduced the Clr of PAH but did not affect that of DA. When DA was given at doses of 0.5 ng, 0.5 mg and 2.0 mg/kg body weight, the pharmacokinetic parameters Clt, Clr, elimination-rate constant and apparent volume of distribution at steady state were not statistically different between doses. The entire dose of 3H was recovered in the urine by 160 min after dosing, and analysis of urine samples by HPLC confirmed that the radiolabel (3H) was associated predominantly with the parent form of DA. The results of the present study demonstrate that DA is cleared from plasma primarily through the kidneys. DA clearance occurs primarily by renal glomerular filtration since its Clt is comparable with that of inulin, is less than that of PAH and is not affected by probenecid.

Animals↗
PubMed1985

Inhibition of cephaloridine-induced lipid peroxidation.

The present study was designed to elucidate whether cephaloridine-induced lipid peroxidation is inhibited by probenecid, cobalt chloride and antioxidants such as alpha-tocopherol and N,N'-diphenyl-p-phenylenediamine (DPPD). Kidney slices obtained from the renal cortex of male Wistar rats were incubated for 1 h in a cephaloridine or cefotaxime (1.25-10 mg/ml) containing medium. In another series of experiments, kidney slices were incubated with cephaloridine or cefotaxime (5 mg/ml) for different periods of time (30-120 min). Lipid peroxidation was monitored by measuring the production of malondialdehyde (MDA). Subsequently, kidney slices were incubated in both series of experiments, in a cephalosporin free medium containing tetraethylammonium (TEA). Accumulation of TEA in renal cortical slices, expressed as slice to medium ratio (S/M), was used to measure changes in the transport capacity of the kidney cells. While cefotaxime had only a slight effect, cephaloridine induced a significant time- and concentration-dependent increase of MDA production and a significant time- and concentration-dependent decrease of TEA accumulation. Inhibition of the renal uptake of cephaloridine by probenecid induced a decrease in MDA production and complete recovery of TEA accumulation. The antioxidants DPPD and alpha-tocopherol inhibited cephaloridine-induced lipid peroxidation in a concentration-dependent manner. Recovery of TEA accumulation accompanied the decrease in lipid peroxidation. DPPD was a more potent inhibitor of lipid peroxidation than alpha-tocopherol. Cobalt chloride, known for its ability to decrease cellular concentration of cytochrome P-450, effectively decreased cephaloridine-induced lipid peroxidation. Thus, these findings support the concept that lipid peroxidation has an important role in the development of cephaloridine-induced nephrotoxicity.

Animals↗
PubMed1986

The toxicity of tetrahydrobiopterin: acute and subchronic studies in mice.

Tetrahydrobiopterin (BH4) is presently being employed in clinical trials for the therapy of various neurological disorders. The toxicity of BH4 in mice was analyzed by acute and subchronic intraperitoneal and acute oral survival studies. Organ weight analysis and histopathology were performed after acute and subchronic i.p. administration. The effect of probenecid on BH4 toxicity was also tested. An LD50 of approximately 260 mg/kg was obtained from acute (14-day) intraperitoneal survival studies. A dose-dependent increase in kidney weights and histopathologic evidence of acute toxic tubular necrosis were noted in acute i.p. studies. Acute oral administration of up to 1318 mg/kg BH4 did not cause any significant morbidity or mortality, nor did subchronic (92-day) i.p. administration of 10 or 50 mg/kg BH4. Probenecid pretreatment did not decrease the toxicity of BH4. The importance of further evaluation of the potential toxicity of tetrahydrobiopterin in clinical utilization is emphasized.

Administration, Oral↗
PubMed1991

In vivo nephrotoxic action of an isomeric mixture of S-(1-phenyl-2-hydroxyethyl)glutathione and S-(2-phenyl-2-hydroxyethyl)glutathione in Fischer-344 rats.

An isomeric mixture of S-[(1 and 2)-phenyl-2-hydroxyethyl]glutathione (PHEG), a glutathione conjugate of styrene, is moderately nephrotoxic. Its in vivo nephrotoxicity was characterized by significant elevations in the urinary excretion of glucose, gamma-glutamyl transpeptidase, glutamate dehydrogenase, N-acetyl-beta-D-glucosaminidase and lactic dehydrogenase 24 h after an i.v. administration of PHEG (0.5 mmol/kg) in male Fischer-344 rats. The histologic alterations consisted of moderate tubular damage with proximal tubule vacuolization and accumulation of tubular cast material, indicating an early sign of tubular necrosis. The data suggest that nephrotoxic injury induced by PHEG lies preferentially at the tubular region of the rat kidney involving several subcellular targets. The nephrotoxicity of PHEG was blocked by acivicin, a specific inhibitor of gamma-glutamyl transpeptidase, by phenylalanylglycine, an inhibitor of cysteinylglycine dipeptidase, as well as by probenecid, a competitive inhibitor of renal organic anion transport system. On the other hand, pretreatment with aminooxyacetic acid, a specific inhibitor of renal cysteine conjugate beta-lyase, failed to inhibit the nephrotoxicity of this glutathione conjugate. Similarly, prior administration of alpha-ketobutyrate, an inducer of renal cysteine conjugate beta-lyase, failed to potentiate its nephrotoxicity, suggesting an insignificant role of beta-lyase in such toxicity. A modest decline in renal cellular GSH due to PHEG but without any concomitant oxidation of GSH to GSSG and without any increase in lipid peroxidation indicates that oxidative stress may not be an important mechanism of its nephrotoxicity. Therefore, the following steps at least, are involved in the development of its nephrotoxicity: (1) renal tubular accumulation of PHEG via a probenecid-sensitive transport process; and (2) its renal metabolism via gamma-glutamyl transpeptidase and cysteinylglycine dipeptidase to the corresponding cysteine-S-conjugate.

Acetylglucosaminidase↗
PubMed1992

Urate excretion by the cat kidney.

1. The renal handling of urate by the cat kidney was investigated during continuous infusion of urate. 2. Fractional urate excretion (FE(UA)) in cats was 0.57 +/- 0.04, indicating net reabsorption of urate. In contrast, FE(UA) in rabbits was 1.76 +/- 0.08, reflecting net secretion of urate. 3. Fractional PAH excretion (FE(PAH)) was 3.94 +/- 0.26 in cats and 4.12 +/- 0.76 in rabbits, showing net secretion in both species. 4. FE(UA) in cats was dependent on urine flow, but was independent of plasma urate concentration. 5. The urate excretion in cats was enhanced by probenecid, but was insensitive to PAH and PZA. 6. The PAH excretion in cats was reduced by probenecid, but was unaltered by urate and PZA. 7. These results indicate that urate is handled in the cat kidney by a unique transport system which is distinct from that for organic anions.

Animals↗
PubMed1994

Thyrotropin regulation of basolateral Cl- and I- effluxes in thyroid follicles in culture.

This report describes chloride and iodide effluxes across the basolateral membrane of porcine thyroid follicles reconstituted in culture. Basolateral chloride efflux is activated by thyrotropin (TSH). TSH (10 mU/ml) induces a twofold increase in the initial rate of chloride efflux. Forskolin (FSK, 5 microM) which increases intracellular cAMP also stimulates the initial rate of chloride efflux 3.5-fold, whereas an increase in the free cytosolic Ca2+ with the ionophore A23187 or thapsigargin, fails to mimic the TSH effect. The chloride channel blocker 5-nitro-2(3-phenylpropylamino)benzoic acid (NPPB) dose dependently inhibits chloride efflux rates with the maximal and half maximal effects observed for 100 microM and 30 microM, respectively. Basolateral chloride efflux rates are also inhibited in the presence of the organic anion transporter blocker probenecid (5 mM) or the Cl-/HCO3- exchanger blocker 4-acetamido-4'-isothiocyanostilbene-2,2'-disulfonic acid (SITS, 250 microM), respectively, by 60% and 40%, whereas it is not affected by ClO4 (100 microM). The initial rate of iodide efflux is weakly activated (1.4-fold) by TSH (10 mU/ml). TSH effect could be reproduced by agents known to activate Ca(2+)-dependent processes as A23187, ionomycin (1 microM), phorbol 12-myristate 13-acetate (TPA, 0.1 microM) and epidermal growth factor (EGF, 0.1 microM) which increase the initial rate of iodide efflux from 1.2- to 1.8-fold, whereas FSK is without effect. The chloride channel blocker NPPB (500 microM) is required to significantly inhibit the initial rate of iodide efflux by 30%. The initial rate of iodide efflux is also reduced by 30% in the presence of SITS (250 microM) or probenecid (5 mM) whereas it is activated by ClO4 (100 microM). We conclude that basolateral chloride and iodide effluxes are both regulated by TSH, using two different transduction pathways. Chloride efflux regulation may involve a cAMP transduction signal, whereas the regulation of iodide efflux may involve a Ca2+ signal. Furthermore, as the sensitivities of chloride and iodide effluxes for the anion transporter blockers (especially NPPB) are different, it seems likely that chloride and iodide use two different transport pathways.

4-Acetamido-4'-isothiocyanatostilbene-2,2'-disulfo↗