Persistent mercury hot spot in Central Europe and Skalka Dam reservoir as a long-term mercury trap.

This study aimed to evaluate the relevance of the floodplain pollution sinks of the legacy mercury (Hg) hot spot in Kössein-Röslau river system (east Bavaria, Germany) for further mobilisation and fluvial transport of mercury in suspended particulate matter (SPM), as an important transport medium of Hg in aquatic systems. The channel belt fluvial erosion as the secondary pollution pathway was also considered. The hot spot has originated from the production of Hg compounds such as C2H5HgCN and C6H5HgCl in Chemical Factory Marktredwitz, and even more than 30 years after the factory abandonment, the Kössein and the Röslau rivers still export polluted fine grained SPM (median 25-35 µm) with mean annual concentrations of 17.4 mg/kg. SPM sampling was performed by floating samplers, supported by floodplain drill cores and by recent channel sediments manually collected along the polluted rivers further. Based on long-term monitoring data set from state enterprise Povodí Ohre, fish in the Skalka Reservoir have had Hg concentrations in their muscles up to 6 mg/kg for at least the last 14 years, exceeding the European maximal limit of 0.5 mg/Hg/kg. In addition, the Hg inventory in the Kössein-Röslau river stretches was therefore calculated; it produced an estimate of ca. 21 t Hg in a 22-km-long channel belt, prone to fluvial remobilisation during floods. Although a major portion of the fluvially transported Hg has yet been trapped by the Skalka Reservoir, the Hg content in the SPM exported farther downstream still varies between 2 and 10 mg/kg Hg. Due to the considerable Hg inventory in the Kössein-Röslau rivers, an improvement will not occur downstream unless specific measures target the secondary pollution mechanism(s).

Cognitive sequelae of methanol poisoning involve executive dysfunction and memory impairment in cross-sectional and long-term perspective.

Methanol poisoning leads to lesions in the basal ganglia and subcortical white matter, as well as to demyelination and atrophy of the optic nerve. However, information regarding cognitive deficits in a large methanol sample is lacking. The principal aim of the present study was to identify the cognitive sequelae of methanol poisoning and their morphological correlates. A sample of 50 patients (METH; age 48 ± 13 years), 3-8 months after methanol poisoning, and 57 control subjects (CS; age 49 ± 13 years) were administered a neuropsychological battery. Forty-six patients were followed in 2 years' perspective. Patients additionally underwent 1.5T magnetic resonance imaging (MRI). Three biochemical and toxicological metabolic markers and a questionnaire regarding alcohol abuse facilitated the classification of 24 patients with methanol poisoning without alcohol abuse (METHna) and 22 patients with methanol poisoning and alcohol abuse (METHa). All groups were compared to a control group of similar size, and matched for age, education, premorbid intelligence level, global cognitive performance, and level of depressive symptoms. Using hierarchical multiple regression we found significant differences between METH and CS, especially in executive and memory domains. METHa showed a similar pattern of cognitive impairment with generally more severe executive dysfunction. Moreover, all METH patients with extensive involvement on brain MRI (lesions in ≥2 anatomical regions) had a more severe cognitive impairment. From a longitudinal perspective, we did not find any changes in their cognitive functioning after 2 years' follow-up. Our findings suggest that methanol poisoning is associated with executive dysfunction and explicit memory impairment, supposedly due to basal ganglia dysfunction and disruption of frontostriatal circuitry proportional to the number of brain lesions, and that these changes are persistent after 2 years' follow-up.

Markers of oxidative damage of nucleic acids and proteins among workers exposed to TiO2 (nano) particles.

OBJECTIVE: The use of nanotechnology is growing enormously and occupational physicians have an increasing interest in evaluating potential hazards and finding biomarkers of effect in workers exposed to nanoparticles. METHODS: A study was carried out with 36 workers exposed to (nano)TiO2 pigment and 45 controls. Condensate (EBC) titanium and markers of oxidation of nucleic acids (including 8-hydroxy-2-deoxyguanosine (8-OHdG), 8-hydroxyguanosine (8-OHG), 5-hydroxymethyl uracil (5-OHMeU)) and proteins (such as o-tyrosine (o-Tyr), 3-chlorotyrosine (3-ClTyr) and 3-nitrotyrosine (3-NOTyr)) were analysed from samples of their exhaled breath. RESULTS: In the production workshops, the median total mass 2012 and 2013 TiO2 concentrations were 0.65 and 0.40 mg/m(3), respectively. The median numbers of concentrations measured by the scanning mobility particle sizer (SMPS) and aerodynamic particle sizer (APS) were 1.98 × 10(4) and 2.32 × 10(4) particles/cm(3), respectively; and about 80% of those particles were smaller than 100 nm in diameter. In the research workspace, lower aerosol concentrations (0.16 mg/m(3) and 1.32 × 10(4) particles/cm(3)) were found. Titanium in the EBC was significantly higher in production workers (p<0.001) than in research workers and unexposed controls. Accordingly, most EBC oxidative stress markers, including in the preshift samples, were higher in production workers than in the two other groups. Multiple regression analysis confirmed an association between the production of TiO2 and the levels of studied biomarkers. CONCLUSIONS: The concentration of titanium in EBC may serve as a direct exposure marker in workers producing TiO2 pigment; the markers of oxidative stress reflect the local biological effect of (nano)TiO2 in the respiratory tract of the exposed workers.

Supplemented creatine induces changes in human metabolism of thiocompounds and one- and two-carbon units.

The administration of creatine (5 g/day for one month) to 11 young active sportsmen affected their urinary excretion of creatine, creatinine, and thiodiglycolic acid (TDGA) as well as blood levels of homocysteine, vitamin B12 and folates. The probands were divided into four groups, according to the amount of creatine found in urine, and of folates and vitamin B12 determined in blood. The changes of folates and vitamin B12 were mutually reciprocal. Each group utilized CR as donor of one- and two-carbon (1C and 2C) units by means of homocysteine (HoCySH), folates, and vitamin B12, in different metabolic pathways. In 10 men the creatine administration was accompanied by an increase of HoCySH level in blood, while in the last man, with accidentally discovered hyperhomocysteinemia, the HoCySH level dropped by 50%. Differences between initial and terminal TDGA levels indicate that creatine affects equilibria of redox processes. Creatinine excretion into urine changed in the dependence on the extent of metabolic disturbances.

Diagnostic significance of urinary thiodiglycolic acid as a possible tool for studying the role of vitamins B12 and folates in the metabolism of thiolic substances.

We have found that the determination of thiodiglycolic acid (TDGA) in urine may help to characterize metabolic imbalance of substances participating in methionine synthesis, which leads to hyperhomocystinuria. From the metabolic scheme, based on a proper combination of known facts, we attempted to theoretically explain and to demonstrate the possibilities of TDGA formation via different ways of homocysteine transformation. This scheme was used in evaluating the results obtained by testing urine of a woman suffering from impaired function of methionine synthase reductase (CblE type of homocystinuria). The amount of TDGA excreted in her morning urine was very sensitive to the changes in her treatment based upon a combination of N5-formyl tetrahydrofolate, betaine and vitamin B12. Vitamin B12 given in the evening either alone or together with betaine increased the TDGA excretion in the morning urine up to ten times. On the other hand, in the absence of vitamin B12, betaine in combination with N5-formyl tetrahydrofolate hindered the appearance of TDGA in the morning urine. Generally, the determination of TDGA in urine of an appropriately pretreated patient may indicate the degree of success of the treatment.

Survey of Amanita phalloides poisoning: clinical findings and follow-up evaluation.

The aim of our study was to evaluate the severity of hepatic and kidney damage with a focus on their reversibility, and to analyze the prognostic factors following Amanita phalloides poisoning based on calls made to the Czech Toxicological Information Centre. A variety of clinical and laboratory parameters were collected. Student's t-test and Fisher's test were used for statistical analysis. Amanita phalloides poisoning was verified in 34 cases (5 children, 29 adults). The following findings emerged: vomiting (76%), diarrhea (62%), hepatic failure (24%), and renal failure (11%). Two patients died on the fifth day after mushroom ingestion. In 18 patients, all serum levels normalized by the time of discharge; in 10 patients up to 7.3 months on average after discharge. Five patients did not comply with follow-up. Renal damage persisted in only one patient, 19 months after discharge. In conclusion, the interval to recovery from hepatic and renal damage by the time of discharge depended on a decrease in the prothrombin index and an increase in serum transaminase and bilirubin levels. Recovery was favorable in all subjects who survived the acute phase of poisoning, except in one patient with a solitary kidney.

Ethylene glycol poisoning in the Czech Republic (2000-2002).

BACKGROUND: The objective of the study was to evaluate the severity of kidney damage retrospectively and to analyze prognostic factors following ethylene glycol (EG) poisonings. METHODS: Data concerning the clinical course of patients with EG poisoning between 2000 and 2002 were analyzed. The chi2 test, Student's t test, Fisher's test and the calculation of linear correlation coefficients were used for statistical analysis. RESULTS: Thirty-three discharge records were obtained. Three patients died, and 11 patients developed acute renal failure (mean maximum serum creatinine level 618 micromol/l). Upon discharge, serum creatinine levels were still elevated in 10 patients. In all but 1 patient, renal function completely normalized within 20 months after intoxication. CONCLUSION: Adult men are the most endangered segment of the population. The most important prognostic factors are the ingested dose and early antidotal treatment. EG toxic kidney damage is reversible.

Detection of bioactive surfactants in aqueous solutions on the basis of H2O2-voltammetry.

The voltammetric determination of surfactants at the hanging mercury drop electrode in aqueous solutions is described, based on the shift of the peak potential deltaEp or the increase of the peak height deltaip of the electroreduction of hydrogen peroxide or of the second oxygen reduction step, with increasing concentration of surfactants. Although the selectivity of this method is rather limited, it could be utilized, e.g., for monitoring the absence (or presence) or for the determination of the contents of specified surfactants by comparing the obtained deltaip (deltaEp) signal with the reference state of the system or with that of a selected reference surface active substance. As model surfactants n-octanol, tetrabutylammonium chloride and sodium dodecylbenzenesulfonate were used, the regular adsorption behavior of which is well known. The method was successfully applied to control the presence of a commercial detergent in water for rinsing bottles for infusion solutions.

A single major-gene defect underlying cardiac conotruncal malformations interferes with myocardial growth during embryonic development: studies in the CTD line of keeshond dogs.

The common forms of isolated congenital heart disease are usually not inherited in a Mendelian pattern, and most are considered multifactorial threshold traits. A large subset consisting of a group of malformations of the ventricular outflow region, termed "conotruncal defects" (CTDs), include subarterial ventricular septal defects, tetralogy of Fallot, and persistent truncus arteriosus. Similar aggregations of CTDs have been reported in human families and in the keeshond breed of dog. The results of our early breeding experiments utilizing noninbred keeshonds were not consistent with any hypothesis of a fully penetrant monogenic inheritance. Here we report a recent series of genetic and embryologic studies conducted after more than 10 generations of selective inbred matings between affected-CTD-line dogs. The results are now consistent with a defect at a single autosomal locus, the Mendelian pattern of transmission having been obscured prior to selective inbreeding by genetic background. On the basis of morphometric embryologic studies, the mutant CTD allele causes conotruncal malformations in homozygous animals by interfering with myocardial growth in the conotruncus during the critical window when the conotruncal cushions fuse to form the conotruncal septum.