Effects of ZnSO4-induced peripheral anosmia on zebrafish behavior and physiology.

Olfaction plays a key role in modulating behavioral and physiological responses of various animal species, including fishes. Olfactory deficits can be induced in fish experimentally, and utilized to examine the role of olfaction in their normal and pathological behaviors. Here, we examine whether experimental anosmia, evoked by ZnSO4 in adult zebrafish can be associated with behavioral and/or physiological responses. We show that experimental ZnSO4-induced anosmia caused acute, but not prolonged, anxiogenic-like effects on zebrafish behavior tested in the novel tank test. The procedure also elevated whole-body cortisol levels in zebrafish. Moreover, ZnSO4 treatment, but not sham, produced damage to olfactory epithelium, inducing overt basal cell vacuolization and intercellular edema. The loss of olfaction, assessed by the fish food preference behavior in the aquatic Y-maze, was present 1h, but not 24h, after the treatment. Collectively, this suggests that transient experimental anosmia by ZnSO4 modulates zebrafish behavior and olfaction, which can be used to evoke and assess their stress-related anxiety-like states.

Pharmacological effects of Ibuprofen on learning and memory, muscarinic receptors gene expression and APP isoforms level in pre-frontal cortex of AlCl3-induced toxicity mouse model.

UNLABELLED: Aluminium metal (Al) has been implicated in the etiology of many neurodegenerative diseases, most commonly the Alzheimer's disease (AD). Al causes biochemical defects by affecting the neurotransmitters level, causes conformational changes in amyloid ß protein and increases amyloid accumulation in brain. AIM: This study was aimed at evaluating neuroprotective effect of Ibuprofen (IBU) (25 mg/kg/day for 12 days) in AlCl3-induced (150 mg/kg/day for 12 days) toxicity. METHODS: Treated mice were subjected to learning and memory tests. Cholinergic muscarinic receptors (mAChR; M1-M5) and APP isoforms (APP695, APP770 and APP common) gene expression were carried out from the pre-frontal cortex area. RESULTS: Profound effect on learning and memory was observed in IBU treated group along with enhanced expression of M1 mAChR (0.40 ± 0.03; p < 0.01) compared to AlCl3-induced toxicity group (0.05 ± 0.02). Fear memory was improved in IBU treated group (89.68 ± 2.58, p < 0.01) as compared to AlCl3-induced toxicity group (54.58 ± 8.21). Discrimination index in social novelty test in IBU treated group was improved (81.13 ± 8.71; p < 0.05), compared to AlCl3-induced toxicity group (46.28 ± 5.55). Similarly, recognition memory of IBU treated group in novel object recognition test (NOB) was retained (66.85 ± 5.60; p < 0.05) as compared to AlCl3-induced toxicity group (33.06 ± 11.80). CONCLUSION: IBU demonstrated memory enhancing effect, however, its effect on the APP isoforms expression in pre-frontal cortex needs further studies.

Odors from proximal species reverse the stress-decreased neurogenesis via main olfactory processing.

Unconditioned foot shock followed by restraint in water was used as a stress regimen to induce decreases in neurogenesis in mouse dentate gyrus (DG). Presence of conspecific odors has been known to reverse the stress-induced decrease in DG neurogenesis. In this study, we found that the conspecific odors did not produce these protective effects in mice whose MOE was impaired by nasal zinc sulfate lavage. Moreover, we observed that the presence of odors from rats, hamsters, and guinea pigs throughout the stress procedure reversed the stress-induced decrease in cell proliferation and neurogenesis in mouse dentate gyrus, while these odors alone did not affect mouse dentate cell proliferation or neurogenesis. In contrast, the presence of rabbit, sugar glider, hedgehog, beetle odors did not affect cell proliferation, neurogenesis, the stress-decreased cell proliferation or neurogenesis in DG. Finally, the presence of fox urine odors decreased mouse dentate cell proliferation and neurogenesis but did not affect the stress-induced decrease in cell proliferation or neurogenesis. Taken together, we conclude that olfactory processing via activation of sensory neurons in MOE is responsible for the conspecific odor-produced protective effect against the stress-decreased cell proliferation and neurogenesis. Phylogenetic distances of the odor-generating species and mice might contribute to the odors' protective effects against the stress-induced decreases in cell proliferation and neurogenesis.

Dynamic oxidoreductive potential of astringent retraction agents.

The aim of this study was to evaluate the dynamics of the cytotoxicity of gingival margin retraction astringents based on aluminium chloride, aluminium sulphate, and ferric sulphate (solutions and gels) in human fibroblasts isolated from gingiva. The cytocompatibility of ten astringent-based chemical retraction agents: Gingiva Liquid, Alustin, Racestypine, Orbat sensitive, Astringedent®, Alustat, Hemostat, Racécord, Gel cord and ViscoStat®, in dilutions of 1 : 10 and 1 : 20, with human gingival fibroblasts was investigated. The MTT assay was performed to determine oxidoreductive mitochondrial function after 3, 5, 10 min and 24 h of incubation. Cell viability was determined according to the chemical group, concentration, exposure time, and the clinical form of the gingival retraction agents. Ferric sulphate- based agents were the most cytotoxic, followed by aluminium chloride and aluminium sulphate. The form of the astrigents influenced cell viability. The evaluated astringents may have cytotoxic potential for gingival margin tissues under clinical conditions.

Aluminium-induced DNA damage and adaptive response to genotoxic stress in plant cells are mediated through reactive oxygen intermediates.

Experiments employing growing root cells of Allium cepa were conducted with a view to elucidate the role of reactive oxygen intermediates (ROI) in aluminium (Al)-induced DNA damage, cell death and adaptive response to genotoxic challenge imposed by ethyl methanesulphonate (EMS) or methyl mercuric chloride (MMCl). In a first set of experiments, root cells in planta were treated with Al at high concentrations (200-800 microM) for 3 h without or with pre-treatments of dihydroxybenzene disulphonic acid (Tiron) and dimethylthiourea (DMTU) for 2 h that trap O(2)(.-)and hydrogen peroxide (H(2)O(2)), respectively. At the end of treatments, generation of O(2)(.-) and H(2)O(2), cell death and DNA damage were determined. In a second set of experiments, root cells in planta were conditioned by Al at low concentrations (5 or 10 microM) for 2 h and after a 2 h intertreatment interval challenged by MMCl or EMS for 3 h without or with a pre-treatment of Tiron or DMTU. Conditioning treatments, in addition, included two oxidative agents viz rose bengal and H(2)O(2) for comparison. Following treatments, root cells in planta were allowed to recover in tap water. Genotoxicity and DNA damage were evaluated by micronucleus (MN), chromosome aberration (CA) or spindle aberration (SA) and comet assays at different hours (0-30 h) of recovery. The results demonstrated that whereas Al at high concentrations induced DNA damage and cell death, in low concentrations induced adaptive response conferring genomic protection from genotoxic challenge imposed by MMCl, EMS and Al. Pre-treatments of Tiron and DMTU prevented Al-induced DNA damage, cell death, as well as genotoxic adaptation to MMCl and EMS, significantly. The findings underscored the biphasic (hormetic) mode of action of Al that at high doses induced DNA damage and at low non-toxic doses conferred genomic protection, both of which were mediated through ROI but perhaps involving different networks.

The effects of ingested aluminium on brain cytochrome oxidase activity / Efectos de la ingestión de aluminio sobre la actividad de la oxidasa citocrómica del cerebro

Aluminium has a unique combination of physical and chemical properties which has enabled man to put this metal to very wide and varied use. However, prolonged exposure to aluminium ions may lead to adverse health effects. In this study, we evaluated the effects of dietary aluminium on the protein composition and the intrinsic activity of cytochrome oxidase (COX) for brain mitochondria. New Zealand white rabbits were maintained on a diet of commercial rabbit pellets and distilled water for a period of 12 weeks. For the experimental group, AlCl3, 330mg/kg/L was added to the drinking water. When compared to the control, mitochondria isolated from the brains of the AlCl3 fed rabbits showed no change in Km but an approximate 35% decrease in both the low and high affinity Vmax values. Also, whereas the protein composition of the mitochondria from both sources appeared to be normal, isolation of highly purified COX proved to be difficult and for the AICI3 fed rabbits, a number of the enzyme's low molecular weight subunits were absent. These results appear to confirm a relationship between long term aluminium consumption and low brain COX activity; they further suggest that an altered COX structure may be the cause of the low enzymic activity.

El aluminio posee una combinación única de las propiedades físicas y químicas que ha permitido al ser humano hacer un uso amplio y variado de este metal. Sin embargo, un número de estudios recientes, sugiere que la exposición prolongada a los iones de aluminio puede tener efectos nocivos sobre la salud. En el presente estudio, evaluamos los efectos del aluminio dietético sobre la composición proteínica y la actividad intrínseca de la oxidasa citocrómica (COX) para la mitocondria cerebral. Conejos blancos de Nueva Zelanda, fueron mantenidos con una dieta de alimento para conejos y agua destilada por un período de 12 semanas. Para el grupo experimental AlCl3, 330mg/kg/L fueron añadidos al agua potable. En comparación con el grupo de control, las mitocondrias aisladas de los cerebros de los conejos alimentados con AlCl3 no mostraron cambios en Km pero hubo una disminución de aproximadamente 35% tanto en los valores Vmax de baja y alta afinidad. Por otro lado, mientras que la composición proteica de las mitocondrias de ambas fuentes parecía ser normal, resultó difícil aislar el COX altamente purificado y un número de enzimas de subunidades de bajo peso molecular MMMM estuvieron ausentes. Estos resultados parecen confirmar una relación entre el consumo de aluminio a largo plazo y la baja actividad del COX del cerebro. Asimismo, sugieren que una alteración de la estructura del COX puede ser la causa de una baja actividad enzimática.

The effects of ingested aluminium on brain cytochrome oxidase activity.

Aluminium has a unique combination of physical and chemical properties which has enabled man to put this metal to very wide and varied use. However prolonged exposure to aluminium ions may lead to adverse health effects. In this study, we evaluated the effects of dietary aluminium on the protein composition and the intrinsic activity of cytochrome oxidase (COX) for brain mitochondria. New Zealand white rabbits were maintained on a diet of commercial rabbit pellets and distilled water for a period of 12 weeks. For the experimental group, AlCl3, 330 mg/kg/L was added to the drinking water. When compared to the control, mitochondria isolated from the brains of the AICl3 fed rabbits showed no change in Km but an approximate 35% decrease in both the low and high affinity Vmax values. Also, whereas the protein composition of the mitochondria from both sources appeared to be normal, isolation of highly purified COX proved to be difficult and for the AlCl3 fed rabbits, a number of the enzyme's low molecular weight subunits were absent. These results appear to confirm a relationship between long term aluminium consumption and low brain COX activity; they further suggest that an altered COX structure may be the cause of the low enzymic activity.

Male pheromone-stimulated neurogenesis in the adult female brain: possible role in mating behavior.

The regulation of female reproductive behaviors may involve memories of male pheromone signatures, formed in part by neural circuitry involving the olfactory bulb and hippocampus. These neural structures are the principal sites of adult neurogenesis; however, previous studies point to their independent regulation by sensory and physiological stimuli. Here we report that the pheromones of dominant (but not subordinate) males stimulate neuronal production in both the olfactory bulb and hippocampus of female mice, which are independently mediated by prolactin and luteinizing hormone, respectively. Neurogenesis induced by dominant-male pheromones correlates with a female preference for dominant males over subordinate males, whereas blocking neurogenesis with the mitotic inhibitor cytosine arabinoside eliminated this preference. These results suggest that male pheromones are involved in regulating neurogenesis in both the olfactory bulb and hippocampus, which may be important for female reproductive success.

[Set up of in vitro methods able to detect the safety of astringent liquids]. / Messa a punto di metodi in vitro per la valutazione dell'innocuità dei liquidi astringenti.

AIM: Most of dental operators agree about a gengival retraction impregnated cord in order to obtain an accurate and overwide dental impression. Hemostatic agents allow the formation of the primary coagulum that determines/causes the retraction of gum connective. Sometimes these astringent liquids cause local inflammation reaction as reported in literature. Aim of this work was the evaluation of the cytotoxic and inflammatory action of the most common astringent liquid on human gum primary cells by in vitro tests. METHODS: For this purpose primary cultures of normal human oral keratinocytes were established, following used either as monolayer or as reconstituted model. All dental preparations were dissolved in CEC medium, diluted to the designed concentrations and applied to the cultured cells. The cytotoxicity was determined by using MTT test, able to evaluate the succinate dehydrogenase activity and therefore the cell viability. Control cultures were treated with CED alone, whereas sodium dodecyl sulphate (SDS) was used as a positive control. Furthermore, the inflammatory response, determined by measuring TNF-alpha and IFN-gamma release, was evaluated on a reconstituted multilayer human oral epidermis model. RESULTS: All agents tested showed a dose-dependent increase in the cytotoxicity to normal human gingival keratinocytes over the dose range examined. In particular the results obtained suggest the higher toxicity of the Astringedent X compound. CONCLUSION: The results obtained from the present studies not only provide useful estimates of relative toxicities of these preparations to human oral mucose, but also can be useful as a standard for cytotoxic and inflammatory assessment of newly developed dental preparations to be topically applied to the oral mucosa. It is important to note, however, that the interpolation of these findings to in vivo conditions remains to be done.

Repeatability of the submitochondrial particle assay.

A study assessing the intralaboratory precision of the in vitro submitochondrial particle (SMP) electron transfer (ETr) and reverse electron transfer (RET) assays was undertaken using the standard reference toxicants, pentachlorophenol (PCP), sodium dodecyl sulfate (SDS), and zinc sulfate 7-hydrate (ZnSO4 7H2O). One to three trials of each assay were manually conducted daily for at least 5 days with each toxicant using commercially available sources of particles and reagents. Composite coefficients of variation (CVs) for the ETr assay ranged from 20.6% for ZnSO4 to 29.3% for PCP (n > or = 15). Composite CVs for the RET assay ranged from 6.5% for SDS to 16.5% for PCP (n > or = 15). Comparison of intralaboratory results with in-house and published data demonstrates that the precision of both of these SMP assays is comparable to that of the more common in vivo, whole-organism bacterial, invertebrate, and fish toxicity tests.

Aluminum chloride induces retinal changes in the rat.

We studied rat retinal changes due to aluminum (Al) toxicosis with a transmission electron microscope (TEM) and an energy dispersive X-ray analyzer (EDXA). Normal 4-week-old Wistar Kyoto rats were divided randomly into Al toxicosis and control groups. The Al toxicosis group was injected ip with 0.3 ml of 4% aluminum chloride (AlCl3) per day every day for 16 weeks. The retina was examined with a TEM and EDXA at 8, 12, and 16 weeks after starting injections with AlCl3. There was a statistically significant increase in the serum Al concentration in the Al toxicosis group (p < 0.001). We observed prominent pathologic changes at 16 weeks after the first injections. Thin retinal pigment epithelium (RPE), and disappearance of the photoreceptor outer and inner segments and nuclei were observed. There were high-density irregular granules in the outer and inner plexiform layers and in the inner nuclear layer. We found dense granules in the cells, which remained between the RPE and the inner nuclear layer. EDXA detected Al in the high-density irregular granules in these areas. Al injected ip caused accumulation of Al in the rat retina and the destruction of photoreceptor cells. These findings indicate that Al is toxic to the retina.

Gingival inflammatory response induced by chemical retraction agents in beagle dogs.

PURPOSE: The aim of this in vivo study on dogs was to investigate and compare the inflammatory potential of four different retraction agents on the gingival connective tissue. MATERIALS AND METHODS: All procedures on eight beagle dogs were performed under general anesthesia: taking oral hygiene measures, placing retraction cords medicated with four chemical agents into the gingival sulci, and taking tissue biopsies. The specimens were evaluated after a 10-minute exposure to chemical agents. The inflammatory response of the connective tissue underlying the sulcular and junctional epithelium triggered by retraction agents was assessed quantitatively. Microscopic images of tissue specimens were morphometrically analyzed using a computer-assisted morphometric method. RESULTS: The most intense inflammatory response in the connective tissue underlying the sulcular epithelium was triggered by astringent retraction agents--Racestyptine in specimens taken after 1 day and 1 week and Rastringent after 1 day (P < .05). Tetrahydrozoline-sympathomimetic vasoconstrictor (Visine) was found to have the lowest inflammatory potential. Retraction chemicals produced no significant effects on the connective tissue subjacent to the junctional epithelium. The ratio of the connective tissue area to that of the inflammatory infiltrate showed that 25% aluminum chloride (Racestyptine) was the most aggressive and tetrahydrozoline the least aggressive retraction agent used. CONCLUSION: All the retraction chemicals tested increased the infiltration with inflammatory cells in gingival connective tissue.

Age-related effect of aluminium on the catalase activities of the brains of two species of poikilothermic vertebrates.

BACKGROUND: Although aluminium (Al) has been implicated in various neuropathological states with aging due to its involvement in neurotoxicity, the exact role of the metal ion is still unclear. OBJECTIVE: The aim of the present study is to ascertain whether the antioxidant enzymes of the brain protecting from oxidative damages which accumulate with aging are regulated by Al in an age-dependent manner. METHOD: The inhibitory effect of Al on the catalase activity of brain homogenates of two species of poikilothermic vertebrates was studied in vitro using a spectrophotometric method. RESULTS: At a final concentration of 666 microM, the metal ion inhibited the enzyme activity of the brain in both species. In fish brain the degree of inhibition was not age-dependent. On the other hand, the rate of inhibition increased between young and middle-aged lizards followed by a decline in the old counterparts. CONCLUSION: Al inhibits catalase activity but this effect may not be a major contributing factor in the aging of the brain in the two species capable of maintaining their antioxidant capacity until old age.

Viability of fibroblasts in cell culture after treatment with different chemical retraction agents.

Prior to fixed prosthodontic impression procedures, temporary horizontal retraction of the free gingival tissue should be accomplished apically to the preparation finishing line. The mechanical-chemical method using cotton retraction cords of various sizes impregnated with various retraction chemicals is the most commonly employed retraction technique. Most retraction agents have pH values from 0.8 to 0.3, and are therefore hazardous to the cut dentine and periodontal tissues. Sympathomimetic vasoconstrictors introduced recently have a pH of 5.6, and are free of systemic side-effects. The present study using the dye exclusion test, colony forming ability test and colorimetric assay was undertaken to evaluate cytotoxic effects of four chemical retraction agents on cultured V-79 fibroblasts, and the dependence of cytotoxicity on the agent concentration and time of exposure. Original concentrations of retraction agents produced stronger cytotoxic effects than dilutions of 1:1 and 1:10. The most aggressive agent, 25% aluminium chloride, took only 1 min to damage all cell cultures. The proportion of cells damaged after 10 min of exposure to tetrahydrozoline was 60%, which was significantly less compared with other chemicals tested. With the colony forming ability test using retraction agents diluted to 1:10 the greatest number of colonies emerged in samples treated with tetrahydrozoline (statistical significance: P < 0.01). The colorimetric assay showed equal cytotoxic effects for 25% aluminium sulphate and tetrahydrozoline. The colorimetric test used in the study has proved an ergonomic, accurate and reliable test for cytotoxicity determination.

Effects of aluminum on the neurotoxicity of primary cultured neurons and on the aggregation of beta-amyloid protein.

Recent epidemiological, neuropathological, and biochemical studies have suggested a possible link between the neurotoxicity of aluminum and the pathogenesis of Alzheimer's disease. However, this relationship remains controversial. To investigate detailed characteristics of neurotoxicity of aluminum, we used primary cultured neurons of rat cerebral cortex as an in vitro model system for the observation of morphological changes induced by chronic exposure to aluminum. Although the exposure to aluminum chloride (10-100 microM) for 1 week did not cause marked neuronal death, degeneration of neuritic processes and accumulation of tau protein and beta-amyloid protein appeared after chronic exposure to 50 microM aluminum chloride for more than 3 weeks. We also investigated the polymerization of beta-amyloid protein in vitro using the immunoblotting technique. We thus found that aluminum induced conformational changes in beta-amyloid protein and enhanced its aggregation in vitro. The aggregated beta-amyloid protein was dissolved by the addition of desferrioxamine, a chelator of aluminum. The aggregated beta-amyloid protein pre-incubated with aluminum formed fibrillar deposits on the surface of cultured neurons.

Vasopressin reverses aluminum-induced impairment of synaptic plasticity in the rat dentate gyrus in vivo.

Aluminum (Al), an important neurotoxin, contributes to a variety of cognitive dysfunction and mental diseases. Previous studies have demonstrated that Al impairs hippocampal long-term potentiation (LTP) in vitro and in vivo. In the present study, both LTP and LTD (long-term depression) were recorded in the same animal to investigate the Al-induced impairment of synaptic plasticity. Another aim of the present research was to verify whether the impairment of synaptic plasticity induced by Al could be reversed by vasopressin (VP) treatment. Neonatal Wistar rats were exposed to Al from parturition through adulthood (pre- and post-weaning) by the drinking of 0.3% aluminum chloride (AlCl(3)) solution. The input-output (I/O) function, paired-pulse reaction (PPR), excitatory postsynaptic potential (EPSP) and population spike (PS) amplitude were measured in the dentate gyrus (DG) of adult rats (60-90 days) in response to stimulation applied to the lateral perforant path. The results showed: (1) Al reduced the amplitudes of both EPSP LTP (control: 132+/-7%, n=7; Al-exposed: 115+/-10%, n=8, P<0.05) and PS LTP (control: 242+/-18%, n=7; Al-exposed: 136+/-7%, n=8, P<0.01) significantly. The amplitudes of EPSP LTD (control: 82+/-6%, n=7; Al-exposed: 92+/-7%, n=8, P<0.05) and PS LTD (control: 81+/-4%, n=7; Al-exposed: 98+/-5%, n=8, P<0.05) were also decreased by Al treatment. The Al-induced impairments of PS LTP and PS LTD were more serious than that of EPSP LTP and EPSP LTD. (2) In control rats, VP had an increase in the PS LTP amplitude (control: 242+/-18%, n=7; control+VP: 358+/-23%, n=6, P<0.01), while it had no significant effects on PS LTD (control: 81+/-4%, n=7; control+VP: 76+/-7%, n=6, P>0.05). (3) In Al-exposed rats, VP had a significant increase in the amplitudes of both PS LTP (Al-exposed: 136+/-7%, n=8, Al-exposed+VP: 255+/-16%, n=6, P<0.01) and PS LTD (Al-exposed: 98+/-5%, n=8; Al-exposed+VP: 81+/-6%, n=6, P<0.05). After the application of VP, the range of synaptic plasticity (PS LTP+PS LTD) in Al-exposed rats increased from 38% to 174%, which surpassed that in control rats (161%). It was suggested that VP could reverse Al-induced impairment of synaptic plasticity and might be an effective medicine to cure Al-induced neurological disorders.

Mitochondrial cytochrome c oxidase subunit III is selectively down-regulated by aluminum exposure in PC12S cells.

Aluminum (Al) has been implicated in several neurological diseases including dialysis dementia and Alzheimer's disease (AD). One possible mechanism of Al neurotoxicity could involve alteration of mitochondrial gene expression. We exposed PC12 cells to 0.1-100 microM AlCl3 for 6h at pH 7.4. Internalized Al, measured by atomic absorption spectrometry, was linearly proportional to the extracellular Al concentration. Northern blot analyses showed that cytochrome c oxidase subunit III (COX III) mRNA was significantly reduced by 70% after addition of 1 microM AlCl3. Higher concentrations of AlCl3 did not show a significant further effect. These results suggest that Al neurotoxicity involves a specific impairment of cytochrome c oxidase.

Motor neuronal death in sporadic amyotrophic lateral sclerosis (ALS) is not apoptotic. A comparative study of ALS and chronic aluminium chloride neurotoxicity in New Zealand white rabbits.

Whether diseased motor neurones in sporadic amyotrophic lateral sclerosis (ALS) die via apoptosis is unknown. Because this relates primarily to difficulties in utilizing post-mortem tissue from end-stage disease, motor neurone degeneration in ALS spinal cord was compared with that of a model of a chronic motor neurone degeneration. Degenerating motor neurones in ALS, identified by ubiquitin immunoreactivity, did not demonstrate the morphological characteristics of apoptosis and were not c-Jun immunoreactive or TUNEL positive. A temporal analysis of spinal motor neurone death in the chronic AlCl3 neurotoxicity model of motor neurone degeneration was also undertaken. AlCl3 was administered intracisternally every 4 weeks and, at intervals of 51, 107, 156 and 267 days, evidence of apoptosis was sought by morphology, TUNEL hybridization or DNA laddering. Double-labelling immunostudies were also performed with antibodies to either c-Jun, ubiquitin or high molecular weight neurofilament (NFH) with TUNEL hybridization. Although significant neurone loss was evident, apoptosis was not found. These studies demonstrate a lack of apoptosis in ALS spinal motor neurones and suggest that this observation does not relate to the utilization of post-mortem tissue in which apoptotic neurones may have been lost.

Effects of aluminum chloride on normal and uremic adult male rats. Tissue distribution, brain choline acetyltransferase activity, and some biological variables.

Normal and uremic adult male rats were given a daily ip injection of 20 mg Al (Al chloride)/kg for 14 d. The results indicate that Al induces a significant decrease in food ingestion, weight gain, and total protein concentration in the plasma. Compared with control animals, very high increases in Al levels were found in plasma and hepatic homogenates (about 36 and 19 times, respectively). In the brain homogenates, the Al increases were lower (about 23%). The brain cholineacetyltransferase activity was reduced: 10.6 and 14.9% in normal and uremic rats, respectively. The nephrectomy and the food restriction did not affect the total protein concentrations in plasma and the cerebral cholineacetyltransferase activity. Both were only found to be reduced in the rats treated by Al chloride.