Accidental ingestion of methyl ethyl ketone peroxide: N-acetylcysteine treatment and toxicological analysis.

INTRODUCTION: Methyl ethyl ketone peroxide (MEKP) is a highly toxic product which promotes tissue damage by uncontrolled free radical production. CASE REPORT: A man accidentally ingested 110 ml of MEKP (37%) at his workplace after mistaking it with a bottle of water. A loading dose of N-acetylcysteine (NAC) and subsequent maintenance doses were applied at the hospital for three consecutive days. Biochemical and hematological parameters showed significant alterations. Tracheal intubation, gastric lavage and hemodialysis were not performed. Methyl ethyl ketone (MEK) and MEKP were detected in EDTA-blood samples by GC-FID and LC-QTOF/MS respectively. An endoscopy exam identified tissue damage. The patient was admitted to the hospital for 10 days. No sequelae were reported after the MEKP poisoning. Oral administration of NAC was successful as an antidote without another approach. CONCLUSIONS: Although NAC treatment was successful, supervision after the hospitalization period was required according to the prognosis. Workplace conditions promoted anosmia, explaining the accident. MEKP and MEK were successfully detected in blood samples even with less-than-ideal storage conditions. Knowledge of MEKP dangerousness and good work practices can prevent accidental MEKP poisoning.

Silicon Reverses Lipid Peroxidation but not Acetylcholinesterase Activity Induced by Long-Term Exposure to Low Aluminum Levels in Rat Brain Regions.

Aluminum (Al) is the most widely distributed metal in the environment and is extensively used in daily life leading to easy exposure to human beings. Besides not having a recognized physiological role, Al may produce adverse effects through the interaction with the cholinergic system contributing to oxidative stress. The present study evaluated, in similar conditions of parenteral nutrition, whether the reaction of silicon (SiO2) with Al(3+) to form hydroxyaluminosilicates (HAS) reduces its bioavailability and toxicity through intraperitoneal administrations of 0.5 mg Al/kg/day and/or 2 mg Si/kg/day in Wistar rats. Al and Si concentrations were determined in rat brain tissue and serum. Acetylcholinesterase (AChE) activity and lipid peroxidation (LPO) were analyzed in the cerebellum, cortex, hippocampus, striatum, hypothalamus, and blood. An increase in the Al concentration was verified in the Al + Si group in the brain. All the groups demonstrated enhanced Si compared to the control animals. Al(3+) increased LPO measured by thiobarbituric acid reactive substances (TBARS) in cerebellum and hippocampus, whereas SiO2 reduced it when compared with the control group. An increase of AChE activity was observed in the Al-treated group in the cerebellum whereas a decrease of this enzyme activity was observed in the cortex and hippocampus in the Al and Al + Si groups. Al and Si concentrations increased in rat serum; however, no effect was observed in blood TBARS levels and AChE activity. SiO2 showed a protective effect in the hippocampus and cerebellum against cellular damage caused by Al(3+)-induced lipid peroxidation. Thus, SiO2 may be considered an important protector in LPO induced by Al(3+).

Presence of synthetic pharmaceuticals as adulterants in slimming phytotherapeutic formulations and their analytical determination.

Obesity that is associated with a high consumption of slimming substances is considered a public health problem around the world. In this context, the increasing consumption of phytotherapeutic formulations as alternative obesity treatments has revealed the presence of synthetic pharmaceuticals as adulterants. The illegally added adulterants are frequently anorexic, anxiolytic, and antidepressant pharmaceuticals. This review aims to describe the analytical methodologies utilized for the determination of adulterants in slimming phytotherapeutic formulations. Furthermore, this review describes some important adulteration cases, which occurred mainly in Europe, Asia, Brazil, and the USA.

A new method for the simultaneous determination of 1,4-benzodiazepines and amfepramone as adulterants in phytotherapeutic formulations by voltammetry.

The use of synthetic pharmaceuticals in phytotherapeutics can be defined as an illegal practice, since these compounds are normally present as non-declared compounds in the phytotherapeutical formulations. This work aims to show the development of an analytical method based on adsorptive cathodic stripping voltammetry (AdCSV) for the simultaneous determination of 1,4-benzodiazepines and amfepramone. The developed method was used to measure seven benzodiazepines (clonazepam, flurazepam, alprazolam, midazolam, medazepam, chlordiazepoxide, and diazepam) and amfepramone in slimming formulations that have been commercialized in Brazil. This method permits the screening of adulterant classes in a single voltammetric run by using a hanging mercury drop electrode as a working electrode and Ringer buffer (pH 10.0) as a supporting electrolyte. Recovery values ranging from 92.0% to 117.0% demonstrate the reliability of the method in the determination of adulterants in real samples. Among the 12 samples studied by the proposed method, 4 were demonstrated to be adulterated by 1,4-benzodiazepines.

Cerebellar thiol status and motor deficit after lactational exposure to methylmercury.

This study examined the exclusive contribution of methylmercury (MeHg) exposure through maternal milk on biochemical parameters related to the thiol status (glutathione (GSH) levels, glutathione peroxidase (GPx) and glutathione reductase (GR) activities) in the cerebellums of suckling mice. The same biochemical parameters were also evaluated in the cerebellums of mothers, which were submitted to a direct oral exposure to MeHg (10 mg/L in drinking water). With regard to the relationship between cerebellar function and motor activity, the presence of signs of motor impairment was also evaluated in the offspring exposed to MeHg during lactation. After the treatment (at weaning period), the pups lactationally exposed to MeHg showed increased levels of mercury in the cerebellum compared to pups in the control group and a significant impairment in the motor performance in the rotarod apparatus. In addition, these pups showed decreased levels of GSH in the cerebellum compared to pups in the control group. In dams, MeHg significantly increased the levels of cerebellar GSH and the activities of cerebellar GR. However, this was not observed in pups. This study indicates that (1) the exposure of lactating mice to MeHg causes significant impairments in motor performance in the offspring which may be related to a decrease in the cerebellar thiol status and (2) the increased GSH levels and GR activity, observed only in the cerebellums of MeHg-exposed dams, could represent compensatory pathophysiologic responses to the oxidative effects of MeHg toward endogenous GSH.