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Aluminum chloride was tested for its effect on primary T-dependent humoral immune response. The administration of aluminum chloride in the genotoxic dose (0.04 M) caused in mice a profound immunosuppressive effect accompanied by diminished thymic and splenic cellularity. The findings suggest that aluminum chloride possesses marked immunotoxic properties.
Aluminum (Al) compounds are widely used in drugs and food additives but the toxicity of such compounds is not known in detail except in patients with renal insufficiency (J. W. Coburn and A. C. Alfrey, 1986, Kidney Int. 29, Suppl. 18). In this experiment, toxicity of ingested Al was investigated in relation to nutritional conditions in normal rats having no renal insufficiency. Sucrose, lactose, milk, casein and soy-protein diets were prepared. As the Al source, aluminum chloride (AlCl3) was added to these diets at the level of 2000 micrograms/g (ppm). Male weanling Wistar rats were fed for 67 days without any Al effect on body weight gain. After a half-day starvation they were terminated. The significance of difference resulting from Al treatment was statistically tested between rats consuming diet with or without added Al. Serum Al concentrations did not exceed 20 ng/ml in any of the groups. Tibia Al concentration doubled in rats consuming added Al in every diet but lactose. Liver Al concentration increased significantly in the Sucrose, Milk, and Casein groups compared to each Control group consuming diet without addition of Al. No lactose effect on Al accumulation was observed. With Al treatment, anemia and hypophosphatemia were not observed, but a decrease in tibia weight was observed with every diet. Aluminum-dependent decreases in serum triglyceride (TG) concentration were also observed in all dietary groups, without any effect on serum cholesterol or phospholipid (P-lipid) concentrations.(ABSTRACT TRUNCATED AT 250 WORDS)
Aluminum (Al) has been said to associate with the Alzheimer's-like neurodegeneration in humans. One of the proposed mechanisms for the action of Al is that excess Al might interfere with trace metal metabolism. In this study, the levels of Ca, Mg, Cu, and Zn in blood, liver, and different regions of the brain (separated into the cortex, hippocampus, cerebellum, and brainstem) were measured in mice after daily oral administration of AICI3 (100 mg/kg body weight) for 2 mo. It was found that upon prolonged oral administration of AI, serum Al level was elevated significantly. There was no marked change in serum Ca, Mg, Zn, or Cu content. In the liver, Al content was not increased but there was a significant elevation in Cu and Zn content compared to control animals, probably due to the prolonged administration of the acidic salt solution. In brain, there was a significant twofold increase in Al in the hippocampus and a significant decrease in Al in the cortex. In addition to regional changes in AI content, Zn content in the hippocampus and increased Cu content in the hippocampus, cortex, and brainstem were significantly reduced. Data demonstrated that Al could alter Zn and Cu homeostasis in selected brain regions. The possible relation between Al and neuronal cell injury was discussed.
Aluminum subhalides of the type Al(22)X(20).12L (X = Cl, Br; L = THF, THP) are the only known representatives of polyhedral aluminum subhalides and exhibit interesting multicenter bonding properties. Herein, we report on the synthesis and structural investigation of the first chlorides of this type. Additional investigations applying solid-state (27)Al NMR (MAS), XPS (of Al(4)Cp(4) and Al(22)X(20).12L), and quantum chemical calculations shed more light upon the structure of the molecules and possible Al modifications.
Aluminum and bisulfite salts inhibit the growth of several fungi and bacteria, and their application effectively controls potato soft rot caused by Erwinia carotovora. In an effort to understand their inhibitory action, ultrastructural changes in Erwinia carotovora subsp. atroseptica after exposure (0 to 20 min) to different concentrations (0.05, 0.1, and 0.2 M) of these salts were examined by using transmission electron microscopy. Plasma membrane integrity was evaluated by using the SYTOX Green fluorochrome that penetrates only cells with altered membranes. Bacteria exposed to all aluminum chloride concentrations, especially 0.2 M, exhibited loosening of the cell walls, cell wall rupture, cytoplasmic aggregation, and an absence of extracellular vesicles. Sodium metabisulfite caused mainly a retraction of plasma membrane and cellular voids which were more pronounced with increasing concentration. Bacterial mortality was closely associated with SYTOX stain absorption when bacteria were exposed to either a high concentration (0.2 M) of aluminum chloride or prolonged exposure (20 min) to 0.05 M aluminum chloride or to a pH of 2.5. Bacteria exposed to lower concentrations of aluminum chloride (0.05 and 0.1 M) for 10 min or less, or to metabisulfite at all concentrations, did not exhibit significant stain absorption, suggesting that no membrane damage occurred or it was too weak to allow the penetration of the stain into the cell. While mortality caused by aluminum chloride involves membrane damage and subsequent cytoplasmic aggregation, sulfite exerts its effect intracellularly; it is transported across the membrane by free diffusion of molecular SO2 with little damage to the cellular membrane.
OBJECTIVE: To study the effect of aluminum chloride on motor and species-typical behaviors in mice. METHODS: Male ICR mice were administered with drinking double distilled water only containing AlCl(3) (10, 50, 300 mg x kg(-1) x d(-1)), and control group with drinking double distilled water only for 100 days. Spontaneous activity test, grip strength, beam traversal, tightrope task, food hoarding, and nest construction were used to study the effect of chloride aluminum on motor and species-typical behaviors in mice. RESULTS: The frequencies of spontaneous activity in low dose group, medium dose group and high dose group [(81.53 +/- 8.97), (71.67 +/- 8.37), (66.73 +/- 6.96) times respectively] were lower than that in control [(106.46 +/- 8.21) times] (P < 0.01), and were negatively correlated with doses (r(s) = -0.42, P < 0.01). Grip strength scores in medium dose group (19.19 +/- 1.48) and high dose group (13.36 +/- 1.46) respectively were lower than that in control (24.31 +/- 1.43) (P < 0.05, P < 0.01). Food hoarding was greater in high dose group [96.10 (90.20-99.00) g] than that in control group [84.00 (78.00-90.00) g (P < 0.05)]. The rest of parameters were of no statistical significance. CONCLUSION: Subchronic exposure to AlCl(3) in mice may diminish motor activity and grip strength, but motor coordination was not impaired; alteration in food hoarding suggests damage to hippocampus cell.
Various aluminum salts were evaluated for in vitro and in vivo antimicrobial activity and ability to bind with serum proteins (astrigency) with the object of finding a colorless substance to substitute for carbol-fuchsin solution (Castellani paint) in the treatment of symptomatic interdigital athlete's foot. Aluminum chlorohydrate was more powerful in killing bacteria and fungi than aluminum acetate and aluminum chloride. However, aluminum chloride showed pronounced astringency and was the only compound to bring about rapid resolution of the signs and symptoms of athlete's foot in open-ended clinical trials. This salt promptly controls odor, pruritus, and maceration. The beneficial effect depends largely on drying the surface, not killing organisms. A solution of 30% aluminum chloride was found to be equlvalent to carbol-fuchsin solution in effectively treating symptomatic athlete's foot.
Aluminum chloride injected into the brains of developing rabbits produced profound neurofibrillary changes to neurons of spinal cord and cerebrum similar to those produced in adult rabbits, along with a variety of clinical symptoms with the exception of seizures. Approximately half of the rabbits survived for more than three weeks, and many survived for several months. Many rabbits with large numbers of neurofibrillary changes had no clinical signs and symptoms. The dynamics and topography of the neurofibrillary changes induced by aluminum chloride are described over a period of several months. Many neurofibrillary tangles were seen in neurons of spinal cord and cerebrum up to 60 days after injection of aluminum chloride. There was no obvious correlation between the degree of neurofibrillary changes and the severity of the clinical signs and symptoms. Animals examined at 85 and 100 days after injection of aluminum chloride had fewer neurofibrillary tangles of none at all, and apparently they had recovered from the neurofibrillary changes. This chronic animal model will allow better investigations of the biochemistry and pathology of neurofibrillary changes, and it will enable behavioral studies to be performed in animals with neurofibrillary changes.
Phosphorus (P) runoff from fields fertilized with swine (Sus scrofa domesticus) manure may contribute to eutrophication. The objective of this study was to evaluate the effect of aluminum sulfate (alum) and aluminum chloride applications to swine manure on P runoff from small plots cropped to tall fescue (Festuca arundinacea Shreb.). There were six treatments in this study: (i) unfertilized control plots, (ii) untreated manure, (iii) manure with alum at 215 mg Al L(-1), (iv) manure with aluminum chloride at 215 mg Al L(-1), (v) manure with alum at 430 mg Al L(-1), and (vi) manure with aluminum chloride at 430 mg Al L(-1). Manure application rates were equivalent to approximately 125 kg N ha(-1). Alum and aluminum chloride additions lowered soluble reactive phosphorus (SRP) levels from about 130 mg P L(-1) to approximately 30 mg P L(-1) at low rates. At high rates, SRP levels in swine manure were around 1 mg P L(-1). Soluble reactive P concentrations in runoff were 5.50, 3.66, 3.00, 0.87, 0.87, and 0.55 mg P L(-1), for normal manure, low alum, low aluminum chloride, high alum, high aluminum chloride, and unfertilized control plots, respectively. Hence, high alum and aluminum chloride reduced SRP concentrations in runoff by 84% and were not statistically different from SRP concentrations in runoff from unfertilized control plots. These data indicate that treating swine manure with alum or aluminum chloride could result in significant reductions in nonpoint-source P runoff.
BACKGROUND: In the past few years, dermatologists have begun to use aluminum chloride (Drysol) as a hemostatic agent for minor surgical procedures. An unusual histiocytic reaction was noted in biopsies of skin previously treated with aluminum chloride. This reaction consisted of a proliferation of histiocytic cells that contained prominent basophilic cytoplasmic granules. OBJECTIVE: To determine the cause of this reaction and the nature of the basophilic granular material within the histiocytic cells. METHODS: Four cases are presented in which re-excised tissue previously treated with aluminum chloride were examined with special histochemistry staining and roentgen diffraction studies. RESULTS: The granules of these histiocytes stained positively with the aluminon stain, a stain specific for aluminum, although no aluminum was found using the less sensitive roentgen diffraction studies. CONCLUSION: These studies support the concept that aluminum chloride can cause a proliferative histiocytic reaction when used as a topical cauterizing agent.
AIM: To investigate the effect of melatonin on learning and memory impairment in mice induced by aluminum chloride and its possible mechanism. METHODS: Mice were treated with intracerebroventricular (icv) injection of 2 microL 5% aluminum chloride solution, once a day for 5 d. At the same time, the mice were given intraperitoneally melatonin 0.6, 3 and 15 mg.kg-1, once a day for 14 d. The passive avoidance of the mice was assessed by step-through test on day 15 after the last icv injection, and then the place navigation and spatial probe ability by Morris water maze were tested. After the spatial probe test, the activities of total superoxide dismutase (T-SOD), CuZn superoxide dismutase (CuZn-SOD), glutathione peroxidase (GSH-Px) and the content of malondialdehyde (MDA) in the cerebral cortex and hippocampus of mice brain were determined. RESULTS: Melatonin ameliorated significantly the impairment of passive avoidance memory, the place navigation and spatial probe ability of mice induced by aluminum chloride. Melatonin was found to prevent significantly the decline of T-SOD, CuZn-SOD and GSH-Px activities, the increase of MDA content in the cortex and hippocampus of mouse brain induced by aluminum chloride. CONCLUSION: The results suggest that melatonin improves significantly the learning and memory impairment in mice induced by aluminum chloride, and this effect may be attributed to its antioxidation.
Studies have previously demonstrated that sucralfate possesses intrinsic antibacterial activity. This study was designed to indirectly assess whether aluminum is the active antibacterial component of sucralfate and to further evaluate factors that may influence this agent's antibacterial activity. Utilizing an in vitro model, the antibacterial activity of sucralfate, an equivalent quantity of aluminum in the form of aluminum chloride, and a control were compared. In addition, the influences of bacterial species (Enterobacter cloacae and Pseudomonas aeruginosa), time (0-24 h) and environmental pH (3,5,7) on the agents' antibacterial activities were evaluated. Equivalent quantities of aluminum, as either sucralfate or aluminum chloride, were added to two of three flasks containing approximately 10(5) cfu/ml of bacteria in pH-adjusted simulated gastric fluid. The third flask served as a control. Samples were obtained over 24 h, diluted and subcultured onto agar plates. The experiments demonstrated that bacterial growth was influenced by pH, time and treatment (aluminum chloride or sucralfate). Regardless of pH or bacterial species, bacterial death occurred within 20 min following the addition of aluminum chloride. In contrast, bacterial death following the addition of sucralfate was more variable and appeared to be pH dependent. In conclusion, sucralfate and aluminum chloride both possess antibacterial activity, even at pH values that normally support bacterial growth in gastric fluid. Although differences in the antibacterial activity of the two agents may in part be related to drug-induced changes in pH, these differences also support data suggesting that aluminum release from sucralfate is incomplete and is dependent on pH.
A randomized double-blind bilateral study of twenty-five patients with acne vulgaris showed that eight weeks' treatment with 6.25 percent aluminum chloride in anhydrous alcohol gave better results than alcohol alone (p = 0.1). Improvements were recorded with both 6.25 percent aluminum chloride in anhydrous alcohol and with placebo, but 6.25 percent aluminum chloride in anhydrous alcohol proved better after four weeks' treatment. The effect on acne of 6.25 percent aluminum chloride in anhydrous alcohol is probably due to the disinfectant and antiperspirant action of aluminum chloride whereas the effect of placebo can be assigned to the sebostatic action of alcohol. The result of this study confirms previous results of open uncontrolled studies.
Soaking retraction cord in an aluminum chloride solution before placing into gingival sulci does not lessen the cord's ability to absorb fluid. Black silk suture is clinically ineffective and should be replaced with a dark, size 0 impregnated retraction cord.
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Aluminum chloride (2.48 X 10(-4) to 1.24 X 10(-3) M) inhibits spontaneous motility of ascending colon of the rat. Resting tension was not affected. At concentrations between 2.07 X 10(-5) to 1.24 X 10(-3) M it inhibited in a dose-dependent manner the contractions induced by maximal doses of acetylcholine. Higher doses produced a very marked inhibition that was attributable to acidification of the medium. The inhibiting effect was more intense when the incubation medium contained an excess of calcium (3.6 and 4.3 mM) or theobromine (10(-4) and 10(-3) M). This inhibiting effect tended to be smaller in the presence of low calcium (0.6 and 1.0 mM) or verapamil (3 X 10(-8) and 10(-7) M).
The monthly intracisternal inoculation of aluminum chloride (AlCl3) to young adult New Zealand white rabbits induces motor neuron degeneration marked by intraneuronal neurofilamentous aggregates similar to that observed in amyotrophic lateral sclerosis (ALS). However, in contrast to ALS, this process occurs in the experimental paradigm in the absence of a glial response. In addition, whereas ALS is a fatal disorder, the cessation of aluminum exposure leads to both clinical and neuropathological recovery. Because microglia can influence neuronal regeneration, we have examined the effect of both acute and chronic aluminum exposure on microglial activation in vivo. We have studied microglial morphology in young adult New Zealand white rabbits receiving either single (1000 microg) or repeated sublethal (100 microg monthly) intracisternal inoculums of AlCl3. In addition, rabbits receiving 1000 microg AlCl3 inoculums were studied following an unilateral sciatic axotomy 48 h prior to the AlCl3 exposure. Our studies demonstrate that microglial activation in vivo is inhibited by AlCl3 exposure, and that a correlation exists between the extent of microglia suppression and the potential for recovery. This suggests that microglial activation is an important determinant of neuronal injury.
The experiment reported here, gave the following answers to the questions asked (see introduction): a. Water with 30 ppm F gave deleterious effects on wethers. A considerable difference was observed as compared to animals given about 1 ppm F in their water, see Table IV. b. The toxicity was slightly less from bore hole water containing 30 ppm F, as compared to Nairobi tap water with added fluorine to 30 ppm F. The difference in toxicity may be due to the very high content of minerals in the bore hole water, see Table I. c. More fluorine was excreted in faeces when aluminum chloride was added to the diet, as compared to animals which did not receive aluminum chloride. Aluminum chloride had no alleviating effect on fluorosis, but apparently decreased gut absorption of fluorine and also reduced fluorine retention in the bones, se Table VII. Under the conditions of this experiment, toxic levels of fluorine were considerable lower than the quoted safe levels in the literature.