Background: Ciguatera fish poisoning (CFP) is a disease caused by the ingestion of poisonous coral reef fish. To the best of the author’s knowledge, no attempt has so far been made to consolidate available reports of outbreaks in order to characterize the toxidrome of CFP in the Philippines. Objective: To review and consolidate data from epidemiologically-documented CFP outbreaks in order to characterize the toxidrome of CFP in the Philippines and identify the areas of high risk for outbreaks. Methods: Epidemiologic reports of CFP outbreaks in the Philippines were reviewed. A compilation of symptoms of CFP patients was done to describe the toxidrome. High risk areas in the Philippines were identified. Results: Ten reports were retrieved related to 17 CFP outbreaks from 1988 to 2010. No epidemiologic reports were found after 2010. Consolidation of reported symptoms showed a CFP toxidrome with prominent paresthesia, muscle weakness, and myalgia with some gastrointestinal symptoms. Based on the reports, the high risk islands identified were Palawan, Panay, Romblon, the islands in the Cuyo Pass, and Basilan. Cases of CFP continue to be encountered but are not reported to public health epidemiologists. Conclusion When put together, the reports describe a CFP toxidrome where the neurologic symptoms predominate over the gastrointestinal symptoms. Most of the cases occurred in the west central and southern portion of the archipelago suggesting a higher risk for CFP in that area. Cases of what appear to be CFP continue to be diagnosed although they are not reported to government epidemiology units. More systematic surveillance of CFP by government agencies is needed.
Ciguatera Poisoning ; Philippines

Animals ; Breath Tests ; methods ; Carbon Isotopes ; Carbon Tetrachloride ; Carbon Tetrachloride Poisoning ; Chemical and Drug Induced Liver Injury ; etiology ; physiopathology ; Liver Function Tests ; methods ; Male ; Phenylalanine ; Rats ; Rats, Sprague-Dawley

Adjuvants, Immunologic ; therapeutic use ; Animals ; Carbon Tetrachloride ; Carbon Tetrachloride Poisoning ; Cell Wall Skeleton ; Chemical and Drug Induced Liver Injury ; therapy ; Male ; Mice

OBJECTIVETo find out the reason of three ciguatera fish poisoning cases in Xiamen in 2005 and identify the fish species.

METHODSThe grouper implicated in food poisoning and seven other coral reef fishes collected from market were tested by mice bioassay and ciguatoxin-test kit. The mtDNA was extracted from toxic grouper meat, and Cty b gene segment was amplified and the PCR products were sequenced. The sequences were compared with those in the GenBank.

RESULTSThe result turned out to be positive by the ciguatoxin-test kit, while the toxicity of the toxic grouper implicated in food poisoning was 0.11 mouse unit (MU)/g by mice bioassay. A 475 bp segments of Cty b gene was amplified by PCR and the sequence was 99% homologous with Epinephelus fuscoguttatus (GenBank: AY950695).No ciguatoxin in six grouper species collected from market was detected.

CONCLUSIONAll three food poisoning cases were caused by consumption of ciguatoxin-carrying groupers.

Animals ; China ; Ciguatera Poisoning ; epidemiology ; Ciguatoxins ; toxicity ; Foodborne Diseases ; epidemiology ; Humans ; Male ; Mice ; Mice, Inbred Strains ; Perciformes ; Toxicity Tests

No abstract available.
Cadmium Poisoning* ; Cadmium* ; Zinc*

Animals ; Antioxidants ; pharmacology ; Carbon Tetrachloride Poisoning ; drug therapy ; Chemical and Drug Induced Liver Injury ; drug therapy ; etiology ; Enzyme Inhibitors ; pharmacology ; Male ; Mice ; Protective Agents ; pharmacology ; Ribonucleases ; antagonists & inhibitors

Bicyclol is a new generation of anti-hepatitis drug with China's own intellectual property rights. The chemical structure of bicyclol is new and original. Pharmacological research showed that it has high clinical efficacy in treating chronic hepatitis (HBV) patients and lower side effects. Two metabolites of bicyclol have been isolated: M2 (4-hydroxy-4'-methoxy-5, 6, 5', 6'-bis (methylenedioxy)-2-hydroxylmethyl-2'-methoxycarbonyl biphenyl) and M3 (4'-hydroxy-4-methoxy-5, 6, 5', 6'-bis (methyl enedioxy)-2-hydroxylmethyl-2'-methoxycarbonyl biphenyl). To further study the mechanism, safety, and effectiveness of bicyclol, the M2 and M3 have been total synthesized. The synthesis route is as following: the carboxyl and phenolic hydroxyl group of the aromatic bromide had been separately protected by bromobenzyl, coupling through the intermolecular asymmetric Ullmann reaction and then catalyst hydrogenated, borane reducted, two metabolites of bicyclol M2 and M3 were obtained. The structures were determined by IR, 1H NMR, HRMS. Comparison of hepatoprotective activity of bicyclol and the two metabolites on experimental liver injury, the potency of the metabolites were lower than that of bicyclol.
Alanine Transaminase ; blood ; Animals ; Benzodioxoles ; chemical synthesis ; chemistry ; pharmacology ; Biphenyl Compounds ; metabolism ; Carbon Tetrachloride Poisoning ; Chemical and Drug Induced Liver Injury ; blood ; etiology ; Mice

Two rat hepatic intoxication models by high doses CCl4 and PAR were used. The experimental results showed that the oral administration of Panax Notoginseng (aqueous extract) with the dose of 5g/kg body weight has significantly reduced the serum concentrations of SGOT and SGPT with 29.1% and 43.1% respectively in comparison with that of CCl4 - treated control . In PAR - intoxicated group, Panax Notoginseng with the dose of 5g/kg body weight resulted in a marked decrease of SGOT and SGPT serum concentration 97.0% and 75.5%, respectively, which were significantly different from that of group without Panax Notoginseng. The hepatoprotective effect of Panax Notoginseng with the dose of 5g/kg and Silymarin with the dose of 25mg/kg on both CCl4 and PAR hepatic-intoxication models is the same. In histopathological examinations, Panax Notoginseng has improved CCl4 and PAR induced hepatic injuries
Panax notoginseng ; Carbon Tetrachloride ; poisoning ; liver ; rats ; Animal Experimentation

OBJECTIVETo study the active ingredients in liver protection from Erzhi Wan (AIEP) on acute hepatic injury induced by carbon tetrachloride (CCl4) in mice.

METHODSixty Kunming mice were randomly divided into six groups: the normal group, the model group, bifendate group (150 mg x kg(-1)), high AIEP group (19.8 g x kg(-1)), middle AIEP group (13.2 g x kg(-1)) and low AIEP group (6.6 g x kg(-1)). The treatment groups were orally administered once per day for 7 d separately, whereas the normal and model groups were orally administered with saline. Except normal rats, all the other rats were injected intraperitoneally CCl4 20 mL x kg(-1) once. The rats were sacrificed 16 h after CCl4 administration. Serum and liver samples were collected for analysis. The acute hepatic injury model was prepared by CCl4 injected intraperitoneally. Then, the therapeutic effects of AIEP on the model were evaluated by the activity determination of serum alanine aminotransferase and aspirate aminotransferase (ALT and AST), superoxide dismutase (SOD) and the content of malondialdehyde (MDA) in liver,and the hepatic pathohistological changes following the treatment.

RESULTThe activities of ALT and AST and the MDA content in liver was significantly increased and the activity of SOD was largely inhibited in the animals of modeling group. Following the treatment with AIEP, ALT and AST activities and MDA content were significantly reduced and SOD activity was obviously increased in the mice of treatment group. Furthermore, AIEP could ameliorate the hepatic pathological changes.

CONCLUSIONAIEP have protective effects on acute hepatic injury induced by CCL4 in mice, and are the effect of the liver protecting active sites.

Alanine Transaminase ; metabolism ; Animals ; Aspartate Aminotransferases ; physiology ; Carbon Tetrachloride Poisoning ; drug therapy ; Chemical and Drug Induced Liver Injury ; drug therapy ; Drugs, Chinese Herbal ; therapeutic use ; Liver ; drug effects ; injuries ; metabolism ; Male ; Malondialdehyde ; metabolism ; Mice

OBJECTIVETo observe and compare the protective effect of garlic oil against carbon tetrachloride (CCL)-induced acute liver injury.

METHODSThe experiments include 4 preventive groups and 2 therapeutic groups. In every preventive and therapeutic group, the mice were randomized into 6 groups with 15 each, including one negative control group, one solvent control group, one CCl4 model group and 3 garlic oil groups (25, 50, and 100 mg/kg body weight). Before given a single gavage of CCl4 (80 mg/kg), the mice were pretreated with garlic oil by gavage in preventive group 1 (30 days, once daily), preventive group 2 (5 days, once daily), preventive group 3 (ahead of 2 h, once), preventive group 4 (immediately, once) or the vehicle (corn oil, 10 ml/kg) in solvent control group. In therapeutic groups, the mice were gavaged garlic oil 2 h (once, in therapeutic 1) or for 5 days (once daily, in therapeutic 2) after administration CCl. After 24 h of the last administration, blood was collected and centrifuged at 2500 r/min at 4 degrees C for 10 min, and serum was removed to measure ALT and AST activities. The liver was dissected, weighed to calculate the liver coefficient (relative liver weight). At the same time, the liver samples were studied by histological examinations.

RESULTSCompared with negative group, the liver coefficient and the activities of ALT and AST in serum of model group were increased remarkably (P < 0.01). Compared with CCl model group, the liver coefficient and the activities of ALT and AST in serum were decreased significantly (P < 0.01) by garlic oil dose-dependently in each preventive group. Simultaneously, histological assessment showed that garlic oil effectively alleviated hepatocyte injuries induced by CCl4. Comparing the preventive effects of garlic oil in every group, it was better in preventive group 3 than others. However, all indexes and histological examinations in therapeutic group 1 did not show the difference with those of CCl4 model group. In therapeutic group 2, all indexes recovered after 5 d of CCl4 administration.

CONCLUSIONSGarlic oil can prevent acute liver injury induced by CCl4 and the effect is better in ahead of 2 h group than others.

Alanine Transaminase ; metabolism ; Animals ; Aspartate Aminotransferases ; metabolism ; Carbon Tetrachloride Poisoning ; drug therapy ; prevention & control ; Chemical and Drug Induced Liver Injury ; drug therapy ; prevention & control ; Garlic ; Liver ; metabolism ; Male ; Mice ; Mice, Inbred Strains ; Plant Oils ; administration & dosage ; therapeutic use