Toxic boost: Acute, reversible neurotoxicity after ingestion of methylcyclopentadienyl manganese tricarbonyl (MMT) mistaken for an energy drink.

Methylcyclopentadienyl manganese tricarbonyl (MMT) is an organometallic compound used as a gasoline additive for its antiknock properties. Human ingestion of MMT has not previously been reported. We present the case of a 54-year-old man who developed seizures and altered mental status after drinking 12 oz. of MMT-containing NOS Octane Booster Racing Formula. Due to label similarities, he mistook this for the NOS High Performance energy drink. The patient was intubated due to persistent seizures despite benzodiazepine treatment and admitted to the intensive care unit. He had two further seizures while intubated, but he was successfully extubated on the 4th day post-ingestion. He was confused and ataxic following extubation, but one day later his symptoms resolved and he was discharged without further incident. This case highlights the importance of responsible labeling of consumables. It is important for clinicians and poison centers to report any such instances to the United States Food and Drug Administration.

The Toxic Effects of Ethylene Glycol Tetraacetate Acid, Ferrum Lek and Methanol on the Glutathione System: correction Options.

Objectives: The purpose of this study was to measure the level of lipid peroxidation and investigate the response of the glutathione system to toxic doses of ethylene glycol tetraacetate acid (EGTA), Ferrum Lek, methanol, and Depakine (valproate sodium). Methods: This study focused on analyzing the toxic effects of EGTA, Ferrum Lek and methanol on lipid peroxidation processes and glutathione levels in animals. The study involved 375 outbred adult mice, of both sexes, weighing 28-31 g, and 100 outbred rats, weighing 180-200 g. Results: After 14 days of valproate sodium/ademethionine treatment, the GR (glutathione reductase) activity in experimental animals continued to be higher than in controls. Using EGTA enhanced glutathione reductase and glutathione S transferase activities in the liver and kidney. The activity of glutathione peroxidase, however, increased only in the kidney (2.1-fold, p ≤ 0.001), while in the liver, a 31% drop was observed (p ≤ 0.05). The 15-mg and 30-mg doses of Ferrum Lek caused the liver level of thiobarbituric acid reactive substances to grow 3- and 3.5-fold, respectively (p ≤ 0.001). Conclusion: The results of the study indicate that poisoning affected practically all components of the glutathione system. The oxidative stress was likely to result from an increased generation of reactive oxygen species against the background of inhibited antioxidant protection.

Bismuth Subsalicylate Coagulopathy in a Patient with Chronic Liver Disease.

Bismuth subsalicylate (BSS) is the active ingredient in over-the-counter antacid and antidiarrheal medications. Coagulopathy in the setting of acetylsalicylic acid toxicity is well documented but not in setting of bismuth subsalicylate overuse. We present a case report of coagulopathy from BSS poisoning in a patient with underlying cirrhosis. The patient's high prothrombin time suggests inhibition of vitamin K-dependent coagulation factors. The patient had decreased factor V activity, which is responsible for converting prothrombin to thrombin. Patients with cirrhosis often have hypoprothrombinemia which may be exacerbated by salicylate-induced coagulopathy. Given the widespread use of BSS products, physicians should recognize coagulopathy as a possible manifestation of toxicity especially in patients with underlying liver disease.

Utilization of plasmapheresis in the management of bismuth intoxication with acute renal failure.

A 34-year-old female patient who ingested 2400 mg bismuth subcitrate in a suicide attempt was brought to the emergency department. She had mild encephalopathy and acute renal failure on admission. One session of plasmapheresis was performed to remove bismuth, and needed three sessions of hemodialysis and was discharged on the 24th day of hospitalization with the recovery of the renal function.

Heavy Metal-Induced Systemic Dysfunction Attenuated by Tannic Acid.

Lead toxicity is a major public health concern. This study was designed to investigate the effects of oral administration of tannic acid (TA) on lead acetate (LA)-induced oxidative stress in rat liver and kidney. Rats were treated with 50 mg/kg body weight of TA against LA-induced oxidative stress 3 times/week for 2 weeks. At a rate of 50 mg/kg of body weight, LA was given intraperitoneally 3 times/week for 2 weeks. Results show significantly elevated levels of oxidative stress markers observed in LA-treated rats, whereas significant depletion in the activity of nonenzymatic and enzymatic antioxidants as well as histological changes were observed in LA-treated rat liver and kidney. TA treatment significantly attenuated the altered levels of oxidative stress biomarkers for nonenzymatic and enzymatic antioxidants. We demonstrated that TA exhibits potent antioxidant and protected against oxidative damage in rat liver and kidney induced by LA treatment. These findings were further supported by histopathological findings in liver and kidney showing that TA protected tissue from the deleterious effects of LA treatment. These outcomes suggest that the consumption of TA may confer a protective effect against lead intoxication through its antioxidative effect.

[Observation on both Na(+)-K+ Atpase activity and expression of Na(+)-K+ AtPase alpha1 mRNA in lung tissues of rats acute poisoned with nickel carbonyl].

OBJECTIVE: To examine the change of Na(+)-K+ ATPase activity and the expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues of rats poisoned by nickel carbonyl and to discuss the mechanism of lung injury. METHODS: One hundred seventy healthy rats (85 male and 85 female) were exposed by inhalation of 20,135 and 250 mg/m3 nickel carbonyl for 30 min. Rats poisoned by chlorine gas with a concentration 250 mg/m3 served as positive group and healthy SD rats served as no-treatment negative group. The rats were euthanized on 1, 2, 3 and 7 d after the administration of nickel carbonyl or chlorine gas. In various treatment groups, Na(+)-K+ ATPase activity was studied by colorimetric method and the expressions of Na(+)-K+ ATPase alpha1 mRNA were determined by RT-PCR. RESULTS: Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung tissues decreased in all treatment groups and chlorine gas-poisoned group, especially it was obvious decreased on the 2ed and 3rd day (P < 0.05). CONCLUSION: Nickel carbonyl could induce lung damage and decrease Na(+)-K+ ATPase activity and expressions of Na(+)-K+ ATPase alpha1 mRNA in lung.

Health effects of persistent organic pollutants: the challenge for the Pacific Basin and for the world.

Persistent organic pollutants include some organo-metals, such as methylmercury; lipophilic halogenated organics, such as dioxins, polychlorinated biphenyls, chlorinated pesticides, and polybrominated flame retardants; and perfluorinated compounds used as repellants. These compounds are resistant to degradation both in the environment and in the human body and tend to bioaccumulate within the food chain. Persistent organic pollutants cause a variety of adverse health effects, including cancer, immune system suppression, decrements in cognitive and neurobehavioral function, disruption of sex steroid and thyroid function, and at least some of them increase the risk of chronic diseases, such as hypertension, cardiovascular disease, and diabetes. Some compounds are byproducts of industry and combustion. Although the manufacture and use of most man-made chemicals has been reduced in recent years, the levels currently present in the population are still associated with an elevated risk of human disease. Others are still manufactured and used. These are dangerous chemicals that have contaminated even areas remote from the industrialized world, such as the polar regions.

[The curative effects of different drugs on liver cell damage of rats induced by acute nickel carbonyl poisoning].

OBJECTIVE: To assess the curative effects of different drugs on liver cell damage of rats induced by acute nickel carbonyl poisoning. METHODS: In present study 220 SD rats were divided into control group (10 rats), carbonyl nickel group (10 rats), 20 mg/kg methylprednisolone group (40 rats), 100 mg/kg DDC group (40 rats), 10 µmol/kg sodium selenite group (40 rats), 0.25 ml shenfuhuiyangtang group (40 rats) and 20 mg/kg methylprednisolone with 100 mg/kg DDC group (40 rats). All rats except for control group inhaled passively 250 mg/m(3) carbonyl nickel for 30 minutes. At 4h and 30h after exposure, the drugs were given intraperitoneally to the rats. On the 3rd and 7th days after exposure, the liver samples were taken from 10 rats each group. The DNA damage of liver cells was detected using comet assay, the ultrastructure changes in liver cells were examined under an electronmicroscope. RESULTS: Compared to carbonyl nickel group, the tail lengths of liver cells in 5 groups administrated at 4 h or 30 h and tested on the 3rd or 7th day after exposure decreased significantly (P < 0.05). Compared to the control group, the tail lengths of liver cells in sodium selenite and shenfuhuiyangtang groups administrated at 4h after exposure or sodium selenite, shenfuhuiyangtang and methylprednisolone with DDC groups administrated at 30h after exposure increased significantly (P < 0.05 or P < 0.01), when tested on the 3rd day after exposure. Except from methylprednisolone sub-group administrated at 4h and tested on the 7th day after exposure, the tail lengths of liver cells in other groups administrated at 4 h or 30 h and tested on the 7th day after exposure increased significantly (P < 0.05). Compared to carbonyl nickel group, the Olive moment of liver cells in 5 groups administrated at 4 h or 30 h tested on the 3rd or 7th day after exposure decreased significantly (P < 0.05 or P < 0.01). Compared to the control group, the Olive moment of liver cells in following groups (selenite and shenfuhuiyangtang groups administrated at 4 h or 30 h and tested on the 3rd or 7th day after exposure, DDC group administrated at 4 h or 30 h and tested on the 7th day after exposure, DDC group administrated at 30h and tested on the 3rd day after exposure, and methylprednisolone with DDC group administrated at 30 h and tested on the 7th day after exposure) increased significantly (P < 0.05 or P < 0.01). As compared with carbonyl nickel group, the ultrastructure observation indicated that the nucleus and other organelles of liver cells in methylprednisolone, DDC and methylprednisolone with DDC groups administrated at 4h and tested on the 3rd day were access to normal levels. CONCLUSION: The results of present study showed that methylprednisolone, DDC and methylprednisolone with DDC could improve obviously the repair of rat liver cell damage induced by acute carbonyl nickel poisoning, and the curative effects of early treatment were better than those of later treatment.

Organoarsenicals. Uptake, metabolism, and toxicity.

Arsenic is categorized by the WHO as the most significant environmental contaminant of drinking water due to the prevalence of geogenic contamination of groundwaters. Arsenic and the compounds which it forms are considered to be carcinogenic. The mechanism of toxicity and in particular of carcinogenicity of arsenic is still not well understood. The complexity originates from the fact that arsenic can form a rich variety of species, which show a wide variability in their toxicological behavior. The process of biomethylation was for many years regarded as a detoxification process; however, more recent research has indicated that the reverse is in fact the case. In this book chapter we give a summary of the current state of knowledge on the toxicities and toxicological mechanisms of organoarsenic species in order to evaluate the role and significance of these regarding their adverse effects on human health.

[Cases of nickel carbonyl acute poisoning at major petrochemical enterprises].

Follow-up of patients with nickel carbonyl acute poisoning varying in severity revealed a pathologic trend--functional and organic disorders of nervous system with asthenic vegetative, asthenic organic dysfunctions, toxic encephalopathy, bronchopulmonary diseases (toxic bronchitis with subsequent pneumosclerosis), toxic myocardium dystrophy, hepatobiliary system affection--toxic hepatopathy.

[Acid-base state of blood in pregnant rats after application of lead acetate].

It was shown that the increase of lead content in the blood, liver, placenta of female rats, rat embryo and embryo's liver (by 80.4; 30.9; 26.8; 18.2 and 22.7%, respectively) of rats poisoned by lead causes pH decrease in blood, reduction of HCO3- concentration, content of general CO2, level of pCO2 and pO2, that evidences for development of subcompensated metabolic acidosis. It was determined, that the poisoning of pregnant rats causes deep metabolic acidosis and hypoxia in their organisms that can result in the prenatal death of fetus.

Lithium toxicity from an Internet dietary supplement.

INTRODUCTION: The widespread availability of medications and herbal products on the Internet has increased the potential for poisonings. We are reporting a case of mild, acute lithium toxicity occurring after the intentional misuse of a lithium-containing "dietary supplement" (Find Serenity Now) obtained over the Internet. CASE REPORT: An 18-year-old woman presented to our emergency department (ED) after ingesting 18 tablets of Find Serenity Now; each tablet contained, according to the listing, 120 mg of lithium orotate [3.83 mg of elemental lithium per 100 mg of (organic) lithium orotate compared to 18.8 mg of elemental lithium per 100 mg of (inorganic) lithium carbonate]. The patient complained of nausea and reported one episode of emesis. Her examination revealed normal vital signs. The only finding was a mild tremor without rigidity. Almost 90 minutes after the ingestion, her serum lithium level was 0.31 mEq/L, a urine drug screen was negative, and an electrocardiogram (ECG) showed a normal sinus rhythm. The patient received intravenous fluids and an anti-emetic; one hour later, her repeat serum lithium level was 0.40 mEq/L. After 3 hours of observation, nausea and tremor were resolved, and she was subsequently transferred to a psychiatric hospital for further care. Prior human and animal data have shown similar pharmacokinetics and shared clinical effects of these lithium salts. DISCUSSION: Over-the-Internet dietary supplements may contain ingredients capable of causing toxicity in overdose. Chronic lithium toxicity from ingestion of this product is also of theoretical concern.