Morin applied in speciation of aluminium in natural waters and biological samples by reversed-phase high-performance liquid chromatography with fluorescence detection.

A reversed-phase high-performance liquid chromatographic method with fluorescence detection for the determination of labile monomeric aluminium has been developed through pre-column complexation using morin as the analytical reagent. The highly fluorescent aluminium-morin complex (excitation wavelength 418 nm, emission wavelength 490 nm) was separated on a Spherisorb ODS 2 column with an eluent consisting of 30% methanol and 70% water (pH 1.0 with perchloric acid). The most remarkable point of this protocol was that only the most toxic aluminium species, that is, free aqua-aluminium ion and its monomeric hydroxo complex ions, selectively respond among various aluminium complexes. This strategy has been successfully applied to direct fractionation of the toxic aluminium in natural waters and biological samples without any pretreatment.

Neurotransmitter dopamine applied in electrochemical determination of aluminum in drinking waters and biological samples.

It was demonstrated that the decrease of the differential pulse voltammetric (DPV) anodic peak current of dopamine (3,4-dihydroxyphenylethylamine, DA) was linear with the increase of aluminum (Al) concentration. Under optimum experimental conditions (pH 4.6, 1.2 x 10(-3) M DA, and 0.04 M NaAc-HAc buffer solution), the linear range is 4.0 x 10(-7)-8.0 x 10(-5) M, the detection limit is 1.4 x 10(-7) M, and the relative standard deviation for 4 x 10(-5) M Al(III) is 3.5% (n=8). Many foreign species, especially some low-molecule-weight biological molecules, were chosen for interference testing. The proposed method was applied to the determination of Al in biological samples such as synthetic renal dialysate, Ringer's solution, human blood, cerebrospinal fluid of a patient, and urine of a diabetic patient. The corresponding recoveries were generally between 95 and 105%. The basic principle of the method was determined by examining Al complexed with DA. This results in the blockage of the electroactive sites on DA, followed eventually by the reduction of the electrochemical response of DA. This result was verified by examining the behavior of DA, both in the presence and absence of Al, using electrochemical, UV-Vis, Raman, and (13)C NMR spectroscopic methods.

Aluminium speciation in cerebrospinal fluid of acutely aluminium-intoxicated dialysis patients before and after desferrioxamine treatment; a step in the understanding of the element's neurotoxicity.

BACKGROUND: The association between aluminium and dialysis encephalopathy and deterioration of the neurological state during desferrioxamine treatment of dialysis patients is well established. At present little is known about the speciation and the mechanisms underlying the element's neurotoxicity. METHODS: Aluminium speciation was performed in cerebrospinal fluid samples of acutely aluminium-intoxicated dialysis patients using a recently developed high-performance liquid chromatographic/electrothermal atomic absorption spectrometric hybrid method. RESULTS: Baseline cerebrospinal fluid aluminium levels of samples taken shortly after the intoxication were low but elevated (5.0 +/- 2.0 micrograms/l, n = 3) as compared to subjects with normal renal function (< 1 microgram/l). In contrast to the situation noted in serum and to the iron speciation in cerebrospinal fluid, aluminium was not bound to transferrin but appeared as two distinct compounds, the main fraction eluting at the elution volume of aluminium-citrate/silicate. The second compound was not identified. Forty-four hours after desferrioxamine administration the cerebrospinal fluid aluminium levels had increased up to a concentration of 10.3 +/- 2.5 micrograms/l (n = 3). This was accompanied by a change in the speciation profile with aluminium appearing at the elution volume of aluminoxamine. CONCLUSIONS: Our findings may contribute to a better understanding of the neurotoxic effects of aluminium and its desferrioxamine chelate in dialysis patients.

[Toxic aluminum encephalopathy. Predominant involvement of the limbic system on MRI]. / Encéphalopathie toxique à l'aluminium. Atteinte prédominante du système limbique en IRM.

Two patients underwent acoustic schwannoma surgery by transmastoid approach. Petrous bone defect was filled in with aluminium-containing bone cement (Ionocem). A pseudomeningocele by CSF accumulation in subcutaneous temporoparietal area appeared after the procedure and, in subsequent weeks, encephalopathy with confusion and seizures. MRI showed cerebral involvement with herpes-like disposition. Temporal stereotactic biopsy in a case did not confirm viral encephalitis but disclosed cellular accumulation of lipofucsin and particles highly suggestive of aluminum-inclusions. Aluminium's levels in blood and CSF of both patients were very high and confirm the brain's toxic involvement. Aluminium's toxicity would be advocated in patients with neurologic disorders who have undergone maxillofacial or skull bone-cementoplasty by an aluminum-containing biomaterial, if this cement is in contact with CSF.

Hepatic and cerebrospinal fluid accumulation of aluminium and bismuth in volunteers taking short course anti-ulcer therapy.

To investigate the possible absorption and deposition of bismuth or aluminium from agents used in the treatment of peptic ulcers, we have measured levels of bismuth and aluminium in the liver tissue of 15 patients undergoing elective liver biopsy and in the cerebrospinal fluid (CSF) of 15 patients undergoing elective myelography after administration of standard therapeutic doses of tripotassium dicitrato bismuthate (TBS), sucralfate or aluminium hydroxide for 1 month. Aliquots of liver or CSF were separated and levels of both aluminium and bismuth were assayed in each sample by atomic absorption spectrophotometry. The group who received TBS had significantly higher liver bismuth levels than the other two treatment groups, but there was no significant difference in CSF bismuth levels among the three groups. There was no significant difference in either liver or CSF aluminium levels among the three treatment groups. We conclude that tissue accumulation of bismuth may occur after short-course therapy with colloidal bismuth, although there is no evidence of CNS accumulation of bismuth in the present study.

[Aluminum, hypothetic cause of Alzheimer disease]. / L'aluminium, cause hypothétique de la maladie d'Alzheimer.

A great deal of research has focused on aluminium as a putative causative factor in Alzheimer's disease. We measured by atomic absorption spectrophotometry aluminium levels in blood, urine and cerebrospinal fluid from 15 patients with Alzheimer's disease, compared with 20 control individuals. There were no statistically significant differences between the two groups. This suggests that aluminium is not a causative factor for Alzheimer's disease.

Kinetics of aluminum in rats. IV: Blood and cerebrospinal fluid kinetics.

Aluminum causes central nervous system (CNS) toxicities in both humans and various animal species. Although blood aluminum concentrations are monitored in the clinic, very little is known regarding the relationship between such concentrations and corresponding CNS aluminum content. As a first step in that direction, this study was undertaken to simultaneously determine blood and CSF kinetics of this element. Following intravenous injection of aluminum (1 mg/kg), there was a rapid (within 30 min, post injection) increase in CSF aluminum; peak concentrations (38-45 ng/ml) were achieved between 2-3 h. While peak blood aluminum concentrations increased about 58-fold from the pre-dose value (from 256 +/- 120 to 14,730 +/- 388 ng/ml), corresponding increases in CSF aluminum were only about 20-fold. Blood and CSF aluminum concentrations declined monoexponentially with half-lives of 2.77 and 3.45 h, respectively (P < 0.05). Results from these showed that blood and CSF compartments achieve equilibrium and indicated the feasibility of determining brain aluminum content using blood concentrations.

Aluminum-induced acute cholinergic neurotoxicity in rat.

In the present study the acute effect of intravenous aluminum chloride (1 mg/kg) on choline acetyltransferase (ChAT) and acetylcholinesterase (AChE) activities of rats was investigated. Aluminum was found to cross the blood-brain barrier (BBB) as indicated by the detection of aluminum in the cerebrospinal fluid (CSF) 30 min after femoral vein injection. Two hours following aluminum injection, ChAT activity in the basal forebrain and hippocampus was significantly reduced by 30% and 22%, respectively, whereas no change was observed in the caudate nuclei. On the other hand, AChE activity was significantly increased by 45% in the caudate nuclei, whereas little change was observed in other brain areas. This report demonstrates that rapid transport of Al across the BBB, and the acute nature of Al neurotoxicity in rats.

Determination of aluminum in biological fluids by furnace atomic absorption spectrophotometry.

Detailed procedures were developed for the furnace atomic absorption spectrophotometry (FAAS) determination of aluminum (Al) in serum, urine, cerebrospinal fluid (CSF), and proportionated dialysate. Of particular note were the use of Mg (NO3)2.6H2O as a matrix modifier and the employment of the standard additions routine in analysis. The accuracy of the method(s) used is supported by work with assayed controls and by recovery studies. The use of a "clean room" was shown to be unnecessary. Normal serum, urine, and CSF Al ranges observed were 4.8-8.9, 5.1-9.1, and 1.0-5.8 micrograms L-1 respectively.

Cerebrospinal fluid aluminum levels following deferoxamine.

Deferoxamine is widely used in the diagnosis and treatment of aluminum toxicity and has a characteristic combination of side effects, including a poorly defined worsening of existing neurologic symptoms. However, to date, no measurement of cerebrospinal fluid (CSF) aluminum concentrations after deferoxamine exist. We report the case of a patient who developed acute neurological deterioration in conjunction with sepsis and elevated serum aluminum levels shortly after renal transplantation. Simultaneous values for blood and CSF aluminum were measured in response to deferoxamine and hemodialysis. The increase in CSF aluminum levels appears to parallel that seen in serum after deferoxamine. We hypothesize that this elevation in CSF aluminum may account for the observed neurologic deterioration after deferoxamine and postulate various pathophysiologic mechanisms that might be involved.

Role of aluminium in sporadic motor neuron disease.

In an attempt to ascertain the role of aluminium in sporadic motor neuron disease (MND), trace metals were estimated in blood, plasma and cerebrospinal fluid (CSF) of 38 patients of sporadic MND and 30 controls by direct current plasma emission spectrophotometry. CSF aluminium levels (20.76 +/- 4.38 micrograms/dl) were significantly higher (P less than 0.05) in those patients of MND who presented as progressive bulbar palsy (PBP) as compared to the other subtypes of MND (amyotrophic lateral sclerosis = 7.71 +/- 2.01 micrograms/dl; progressive muscular atrophy = 10.01 +/- 2.41 micrograms/dl) and controls (11.63 +/- 2.82 micrograms/dl). Aluminium may be important in the etiopathogenesis of a subgroup of sporadic MND.

[Function of the blood-cerebrospinal fluid barrier and selected biochemical cerebrospinal fluid components in senile dementias of various types]. / Blut-Liquor-Schrankenfunktion und ausgewählte biochemische Liquor-komponenten bei Altersdemenzen verschiedenen Typs.

Some selected CSF and serum components were determined in demental patients classified by the Hachinski test into vascular and primary-degenerative groups. As for the vascular group, the frequency distribution of the serum/CSF albumin ratios characterizing the barrier function corresponds to that of controls, in primary-degenerative cases, however, it is shifted to higher values. In vascular dementia higher CSF LAP activities pointing to actual cell damaging processes in the CNS were found. The concentrations of lactate and some trace metals in CSF and serum are not suitable for differential diagnostic purposes.

Spinal fluid aluminum levels in patients with Alzheimer disease.

Spinal fluid from 180 male patients was examined for aluminum levels. Values were coordinated for age and protein determinations. In addition, values were listed according to the patient's diagnosis. Although in most instances no correlation could be made, 10 patients with Alzheimer disease showed significantly low levels of aluminum.

[Estimation of aluminium in biological fluids by atomic absorption spectrophotometry in a graphite oven (author's transl)]. / Dosage de l'aluminium dans les liquides biologiques par spectrophotométrie d'absorption atomique en four graphite.

The possibilities of use of a graphite oven type HGA 74 (Perkin Elmer) for the estimation of aluminium in biological fluids by atomic absorption spectrophotometry are described, with a special study of the stages of drying, mineralisation, atomisation, flow of inert gas, requirement for correction of non-specific absorption, etc. Under fixed experimental conditions, the limit of sensitivity (absorption 1%) was 2.28.10.(-11) grams and the linearity was good up to 100 microgram/l. This method of analysis by direct treatment of the samples required only small volumes of the latter and reduces the risk of contamination.