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Route of Metabolization and Detoxication of Paralytic Shellfish

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Route of Metabolization and Detoxication of Paralytic Shellfish Toxicon 55 (2010) 135–144 Contents lists available at ScienceDirect Toxicon journal homepage: www.elsevier.com/locate/toxicon Route of metabolization and detoxication of paralytic shellfish toxins in humans Carlos Garcı´a a,*, Andre´s Barriga b, Juan Carlos Dı´az c, Marcelo Lagos a,Ne´stor Lagos a a Laboratorio Bioquı´mica de Membrana, Programa de Fisiologı´a y Biofı´sica, Facultad de Medicina, Universidad de Chile, Casilla 70005, Correo 7, Santiago, Chile b CEPEDEG, Facultad de Ciencias Quı´micas y Farmace´uticas, Universidad de Chile, Chile c Unidad de Transplante, Departamento de Cirugı´a, Hospital Clı´nico Universidad de Chile, Chile article info abstract Article history: Paralytic shellfish toxins (PST) are a collection of over 26 structurally related imidazoline Received 11 April 2009 guanidinium derivatives produced by marine dinoflagellates and freshwater cyanobacteria. Received in revised form 16 May 2009 Glucuronidation of drugs by UDP-glucuronosyltransferase (UGT) is the major phase II Accepted 14 July 2009 conjugation reaction in mammalian liver. Available online 24 July 2009 In this study, using human liver microsomes, the in vitro paralytic shellfish toxins oxidation and sequential glucuronidation are achieved. Neosaxitoxin (neoSTX), Gonyautoxin 3/2 Keywords: epimers (GTX3/GTX2) and Saxitoxin (STX) are used as starting enzymatic substrates. The Neosaxitoxin Saxitoxin enzymatic reaction final product metabolites are identified by using HPLC-FLD and HPLC/ Gonyautoxins 3/2 epimers ESI-IT/MS. Four metabolites from GTX3/GTX2 epimers precursors, three of neoSTX and two UDP-glucuronic acid of STX are clearly identified after incubating with UDPGA/NADPH and fresh liver micro- Oxidation somes. The glucuronic-Paralytic Shellfish Toxins were completely hydrolysed by treatment Glucuronidation with b-glucuronidase. All toxin analogs were identified comparing their HPLC retention time with those of analytical standard reference samples and further confirmed by HPLC/ ESI-IT/MS. Paralytic Shellfish Toxins (PST) were widely metabolized by human microsomes and less than 15% of the original PST, incubated as substrate, stayed behind at the end of the incubation. The apparent Vmax and Km formation values for the respective glucuronides of neoSTX, GTX3/GTX2 epimers and STX were determined. The Vmax formation values for Glucuronic- GTX3 and Glucuronic-GTX2 were lower than Glucuronic-neoSTX and Glucuronic-STX (6.8 Æ 1.9 Â 10À3; 8.3 Æ 2.8 Â 10À3 and 9.7 Æ 2.8 Â 10À3 pmol/min/mg protein respectively). Km of the glucuronidation reaction for GTX3/GTX2 epimers was less than that of glucur- onidation of neoSTX and STX (20.2 Æ 0.12; 27.06 Æ 0.23 and 32.02 Æ 0.64 mM respectively). In conclusion, these data show for the first time, direct evidence for the sequential oxidation and glucuronidation of PST in vitro, both being the initial detoxication reactions for the excretion of these toxins in humans. The PST oxidation and glucuronidation pathway showed here, is the hepatic conversion of its properly glucuronic-PST synthe- sized, and the sequential route of PST detoxication in human. Ó 2009 Elsevier Ltd. All rights reserved. 1. Introduction produced by some marine dinoflagellates and freshwater cyanobacteria (Sato et al., 2000; Onodera et al., 1997; Lagos, Paralytic Shellfish Toxins (PST) are a collection of over 26 1998, 2003). Eventually, when the PST-contaminated structurally related imidazoline guanidinium derivatives seafood is consumed by humans, the well known paralytic shellfish poison (PSP) syndrome may occur, resulting in * Corresponding author. Tel.: þ56 2 978 6309; fax: þ56 2 777 6916. severe public health problems (Hallegraeff, 1995; Lagos, E-mail address: [email protected] (C. Garcı´a). 1998; Garcı´a et al., 2004). The most characteristic 0041-0101/$ – see front matter Ó 2009 Elsevier Ltd. All rights reserved. doi:10.1016/j.toxicon.2009.07.018 136 C. Garcı´a et al. / Toxicon 55 (2010) 135–144 symptoms of Paralytic Shellfish Poison (PSP) syndrome are: The present study using human liver microsomes, lips paresthesia, astenia, distonia, ataxia, dyspnea, hypo- shows direct evidence of in vitro sequential oxidation and tension, tachycardia, vomiting and muscular weakness. The glucuronidation of neoSTX, GTX3/GTX2 epimers and STX, PSP is the only Harmful Algae Bloom (HAB) poison which is the major toxins of the PSP. For the first time, the mass lethal in South America (Long et al., 1990; Montebruno, spectrum of Glucuronic-neoSTX, Glucuronic-GTX3/GTX2 1993; Lagos and Andrinolo, 2000; Garcı´a et al., 2004). epimers and Glucuronic-STX is shown. Even more, the While being the only lethal HAB poison, still there is not identities of these molecular ion peaks were further direct evidence or clear knowledge about PST detoxication confirmed by the daughter ion spectra, the main decom- in humans. There are two pioneer studies, an in vivo animal position molecular fractions in the mass spectrum are also model (Andrinolo et al., 1999, 2002; Lagos and Andrinolo, identified. The oxidation and the sequential conjugation 2000) and a post-mortem analysis of tissue and body fluid reactions of PST by human liver microsomes are samples obtained from intoxicated and deceased patients demonstrated. (Garcı´a et al., 2004), that showed indirect evidence of PST metabolization in mammalian. 2. Materials and methods The post-mortem analyses of tissue and body fluid samples from people who died poisoned by consumption 2.1. Chemicals of PST-contaminated shellfish in the Patagonia fjords (Southern Chile), have shown biotransformation of some of 1-Heptensulfonic acid sodium salt, periodic acids, these toxins. The detected biotransformation depended on potassium phosphate dibasic, tetrabutylammonium phos- the time that toxins remained in the organism. Detected phate, and HPLC grade solvents were purchased from oxidation of Saxitoxin (STX) into Neosaxitoxin (neoSTX) Fisher Scientific (New Jersey, USA), phosphoric acid, was reported (Garcı´a et al., 2004). ammonium hydroxide were purchased from Merck Recently, in vitro experiment using human liver micro- (MERCK, Darmstadt, Germany). The Sep-PakÒ cartridges for somes, showed N1-oxidation of the GTX3 and GTX2 into the solid phase extraction of silica and C-18 were purchased corresponding hydroxylamine analogs GTX4 and GTX1. from Waters Corporation (Division of MILLIPORE, Milford, This was the first direct evidence of biotransformation of MA, USA). UDP-Glucuronic acid, b-glucuronidase, D-sac- GTX3/GTX2 epimers into GTX4/GTX1 epimers (Garcı´a et al., charic 1,4-lactone monohydrate (saccharolactone) and 2009). They are the most common epimers found in PST alamethicin were purchased from SIGMA (Sigma Chemical shellfish toxin profile worldwide (Shunway, 1995; Lagos, Co., St. Louis, MO, USA). 1998, 2003). There is also indirect evidence of Gonyautoxins (GTXs) 2.2. Microsomes isolation from human liver biotransformation by molluscs. In this case, Gonyautoxins into both Saxitoxin (STX) or Neosaxitoxin (neoSTX) had Human liver samples were obtained from liver donors, been described when GTXs were incubated with homoge- all patients of liver transplant procedures, with the protocol nate of the toxin-accumulating bivalve Placopecten magel- approved by the University of Chile Clinic Hospital Ethics lanicus, suggesting that the conversion detected was Committee. None of the donors were treated or received catalyzed by enzymes within the shellfish homogenate drugs likely to interfere with drug metabolizing enzyme (Shimizu and Yoshioka, 1981; Kotaki et al., 1985). activities. Rifampicin, known to induce P-450 proteins and Liver microsome enzymatic preparation is advanta- UDP-glucuronosyltransferase, was not ingested by any geously used to determine in vitro metabolism of drug patient. The preparation of isolated microsomes was per- candidates, since it is easier than the whole animal assay formed as described by Hiller et al. (1999). Briefly, livers (Wrighton et al., 1995). The in vitro fresh preparation were excised, washed in isotonic saline, and then blotted to should, therefore reflect the in vivo metabolism, detecting dryness. All of the following steps were performed at 4 C. molecular species differences and predicting compound Approximately, 3 g of frozen human liver were thawed and clearance. homogenized in 5 ml of homogenization buffer (154 mM Glucuronidation represents one of the major conjuga- KCl, 1 mM EDTA, 50 mM Tris/HCl pH 7.4) using a mechan- tion reactions involved in the metabolic conversion of ical tissue tearor at 17,000 rpm for 45 s. A post-mitochon- xenobiotics and numerous endogenous compounds, both drial supernatant was prepared by centrifugation of the converted to polar water-soluble metabolites. The resulting homogenate at 10,000g for 20 min. This supernatant was glucuronides, which are frequently the end product of centrifuged at 202,000g for 70 min and microsomes sedi- metabolism, are removed from the body either via urine or ment pellet was washed once in 15 ml of 0.1 M Na2P2O7 (pH via bile. This two-stage process of glucuronidation followed 7.8) using a tissue homogenizer. After centrifugation at by excretion is quantitatively one of the more important 202,000g the pellet was resuspended in approximately pathways of detoxication in man (Burchell et al., 1995). 1 ml of 100 mM KH2PO4/K2HPO4 (pH 7.4), 1 mM EDTA (pH Numerous compounds once within the body are not 8.0), 20% (v/v) glycerol. Aliquots of the microsomal directly glucuronidated, but instead must be first meta- suspension – with a protein concentration of 25 mg/ml – bolically transformed to yield a suitable acceptor for were fast-frozen in liquid nitrogen and stored at À80 C. conjugation. Initial reactions involved in the early meta- Microsomes purity was assessed by a marker-enzyme bolism of xenobiotics have classically been termed phase I analysis (Benedetti et al., 1988). Activities of glucose-6- reactions and encompass oxidative, reductive, and hydro- phosphate, cytochrome c oxidase, and 50-nucleotidase as lytic modifications. markers for endoplasmic reticulum, mitochondria and C. Garcı´a et al. / Toxicon 55 (2010) 135–144 137 plasma membrane, respectively, were determined in total with a stream of nitrogen.
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