Intracellular changes of metal elements by fucoidan extracted from brown seaweed (Cladosiphon okamuranus)

This study was undertaken to elucidate the intracellular changes of metal elements after the administration of fucoidan extracted from Cladosiphon okamuranus. TRL1215 cells (normal rat liver cell line) were treated with 0, 0.1, or 1.0 mg/ml fucoidan and incubated in 5% CO2 at 37 degrees C. The cellular levels of Mg, Al, Fe, and Zn were significantly increased in the 1.0 mg/ml fucoidan-treated cells compared to those of the 0.1 mg/ml fucoidan-treated cells and the control. Next, TRL1215 cells were cultured on Mylar film overnight. At 24 h after 5-bromo-2'-deoxyuridine dosing, 0, 0.1, or 1.0 mg/ml fucoidan was treated for 9 h. The cellular distribution of elements was analyzed using in-air micro-micro-particle induced X-ray emission. The X-ray spectra showed that yields of Al, Mg, and Zn were high in order of the 1.0 mg/ml fucoidan-treated sample, the 0.1 mg/ml fucoidan-treated sample, and the control. Fe yield was mildly increased by fucoidan administration. In fucoidan-treated cells, the focal accumulation of Br was correlated spatially with phosphorous-rich region, suggesting that Br was localized within the nucleus. Al distribution provided a spatial association with Br map. These data suggest that fucoidan increases the accumulations of Al, Mg, Fe, and Zn in normal rat hepatocytes, and fucoidan-binding Al is postulated to be transferred into the nucleus.     

Genotoxic and cytotoxic effects induced by aluminum in the lymphocytes of the common carp (Cyprinus carpio)

Few studies have been made in regard to the effect of aluminum on the molecular and cellular structure and function of aquatic organisms; therefore, in the present report we determined the genotoxic and cytotoxic effects induced by the metal on the lymphocytes of carp (Cyprinus carpio). Three groups of fish were exposed to 0.05, 120, and 239 mg/L of aluminum (Al), respectively, by using Al₂ (SO₄)₃·7H₂O, and another group was included as control. The cells obtained were studied with the comet assay, flow cytometry, and the TUNEL method. With the first method we found a concentration and time dependent, significant increase in the amount of DNA damage induced by Al, and a higher damage when we evaluated the level of oxidized DNA. By applying flow cytometry we established that the metal induced a DNA content increase and ploidy modifications as well as apoptosis and disturbances of the cell cycle progression. With the last method we determined a significant increase in the amount of apoptotic cells, mainly in the 72–96 h period. Our results established that Al caused deleterious DNA and cellular effects in the tested organism, and they suggested the pertinence of evaluating toxicity induced by the metal in organisms living in contaminated water bodies.     

Aluminum neurotoxicity is reduced by dantrolene and dimethyl sulfoxide in cultured rat hippocampal neurons

Cell death was reduced in cultured rat hippocampal cells treated with aluminum chloride by dantrolene and dimethylsulfoxide, indicating aluminum toxicity may be mediated through release of calcium from intracellular stores and oxidative stress. Cell death was reduced to a lesser degree by cycloheximide and actinomycin D, indicating some evidence for apoptosis, however apoptosis did not appear to be a major cause of cell death from aluminum toxicity.     

The use of levoglucosenone and isolevoglucosenone as templates for the construction of C-linked disaccharides

Because of their functionalities (enone, ketone, and acetal) and their bicyclic structure (steric factors), levoglucosenone (1,6-anhydro-3,4-dideoxy-beta-D-glycero-hex-3-enopyran-2-ulose) and isolevoglucosenone (1,6-anhydro-2,3-dideoxy-beta-D-glycero-hex-3-enopyran-4-ulose) are useful templates for the convergent and combinatorial synthesis of (1-->2), (1-->3), and (1-->4)-linked C-disaccharides in reactions combining them with sugar-derived carbaldehydes. Synthetic methods relying on conjugate nucleophilic additions of these enones, their combination with aluminum reagents and aldehydes (Baylis-Hillman reaction) and modified Takai-Hiyama-Nozaki-Kishi couplings of enol triflates derived from them with sugar-derived aldehydes are reviewed. Highly stereoselective methods have thus been developed. These allow the generation of disaccharide mimetics with a high molecular diversity.     

Accumulation of aluminum in rat brain: does it lead to behavioral and electrophysiological changes?

The present study was undertaken to examine possible aluminum (Al) accumulation in the brain of rats and to investigate whether subchronic exposure to the metal leads to behavioral and neurophysiological changes in both treated and control groups. Each of the groups consisted of 10 animals. Aluminum chloride (AlCl₃) at a low (50 mg/kg/d) or high (200 mg/kg/d) dose was applied to male Wistar rats by gavage for 8 wk. Al-free water by gavage was given to the control group throughout the experiment. Behavioral effects were evaluated by open-field (OF) motor activity and by acoustic startle response (ASR). Electrophysiological examination was done by recording spontaneous activity and sensory-evoked potentials from the visual, somatosensory, as well as auditory cortex. The Al content of each whole brain was determined by electrothermal atomic absorption spectrophotometry. Subchronic Al exposure slightly caused some changes in the evoked potentials and electrocorticograms and in the OF and ASR performance, but these results were not statistically significant. The brain Al levels of the control and the low and high dose of Al-exposed groups were measured as 0.717±0.208 μg/g (wet weight), 0.963±0.491 μg/g (wet weight) and 1.816±1.157 μg/g (wet weight), respectively.     

Aluminum Toxicity: A Case Study on Tobacco (<i>Nicotiana tabacum</i> L.)

Aluminum is an abundant metal in the earth’s crust that turns out to be toxic in acidic environments. Many plants are affected by the presence of aluminum at the whole plant level, at the organ level, and at the cellular level. Tobacco as a cash crop (Nicotiana tabacum L.) is a widely cultivated plant worldwide and is also a good model organism for research. Although there are many articles on Al-phytotoxicity in the literature, reviews on a single species that are economically and scientifically important are limited. In this article, we not only provide the biology associated with tobacco Al-toxicity, but also some essential information regarding the effects of this metal on other plant species (even animals). This review provides information on aluminum localization and uptake process by different staining techniques, as well as the effects of its toxicity at different compartment levels and the physiological consequences derived from them. In addition, molecular studies in recent years have reported specific responses to Al toxicity, such as overexpression of various protective proteins. Besides, this review discusses data on various organelle-based responses, cell death, and other mechanisms, data on tobacco plants and other kingdoms relevant to these studies.     

Physiological basis of reduced Al tolerance in ditelosomic lines of Chinese Spring wheat

Aluminum tolerance was assessed in the moderately Al-tolerant wheat (Triticum aestivum L.) cultivar Chinese Spring and a set of ditelosomic lines derived from Chinese Spring. Three ditelosomic lines lacking chromosome arms 4DL, 5AS and 7AS, respectively, exhibited decreased Al tolerance relative to the euploid parent Chinese Spring based on reduced root growth in Al-containing solutions. The physiological basis of the reduced Al tolerance was investigated. Measurements by inductively coupled argon plasma mass spectroscopy of root apical Al accumulation demonstrated that two of these three lines had a decreased ability to exclude Al from the root apex, the site of Al phytotoxicity. As Al-induced malate exudation has been suggested to be an important physiological mechanism of Al tolerance in wheat, this parameter was quantified and malate exudation was shown to be smaller in all three deletion lines compared with Chinese Spring. These results suggest that the decreased Al tolerance in at least two of the three ditelosomic lines is due to the loss of different genes independently influencing a single Al-tolerance mechanism, rather than to the loss of genes encoding alternative Al-tolerance mechanisms. Received: 3 July 2000 / Accepted: 9 August 2000     

Effects of oral aluminum on essential trace elements metabolism during pregnancy

The present study was conducted to assess in rats the effects of oral aluminum (Al) exposure on calcium (Ca), magnesium (Mg), manganese (Mn), copper (Cu), zinc (Zn), and iron (Fe) accumulation and urinary excretion. Three groups of plug-positive Sprague-Dawley (SD) rats were given by gavage 0, 200, and 400 mg/kg/d of Al(OH)₃ on gestational days 1–20. Three groups of nonpregnant female SD rats of the same age received Al(OH)₃ by gavage at the same doses for 20 consecutive days. At the end of the treatment period, 24-h urine samples were collected for analysis of Al and essential elements. Subsequently, all animals were sacrificed and samples of liver, bone, spleen, kidneys, and brain were removed for metal analyses. With some exceptions, the urinary amounts of Al, Mn, and Cu excreted by pregnant animals as well as the urinary levels of Al excreted by nonpregnant rats were higher in the Al-treated groups than in the respective control groups. Although higher Al levels were found in the liver of pregnant rats, the concentrations of Al in the brain of these animals were lower than those found in the same tissues of nonpregnant rats. With regard to the essential elements, tissue accumulation was most affected in pregnant than in nonpregnant animals. In pregnant rats, the hepatic and renal concentrations of Ca, Mg, Mn, Cu, Zn, and Fe, as well as the levels of Ca in bone, and the concentrations of Cu in brain were significantly higher in the Al-exposed groups than in the control group. According to the current results, oral Al exposure during pregnancy can produce significant changes in the tissue distribution of a number of essential elements.     

Quantitative determination of callose in tree roots

The formation of callose in tree roots has been suggested as a physiological indicator of aluminum (Al) toxicity. Quantifying callose in the roots in forest soils, however, is hampered by the presence of autofluorescent materials in the roots that disturb the measurement of callose by fluorescence spectrophotometry. Tannins in the roots cause these measurement problems. Here we report on the measurement of callose in the root apices of European chestnut (Castanea sativa) seedlings collected in an acidified forest soil. The callose was quantified with a modified protocol which included three washing steps with polyvinylpolypyrrolidone (PVPP) before the callose was extracted. This procedure reduced the autofluorescence by about 50%. With the use of water or ethanol alone, callose could be measured in only about 15% of the root samples, whereas with the use of PVPP callose could be determined in 95% of the samples. This improved method could help to evaluate the effects of Al toxicity on tree roots grown in forest soils, where callose is detected as a physiological indicator.     

铝对大白鼠海马所致损害的实验研究

为探讨铝对海马的损害,用３０只健康大白鼠,体重２００～３００克,分为Ａ组（正常对照）１０只,Ｂ组（低铝组饲料中加５００ｍｇ／ｋｇＡｌＣｌ３）１０只,Ｃ组（高铝组饲料中加２５００ｍｇ／ｋｇ／ＡｌＣｌ３）１０只。分别饲养１２个月后,分组断头取脑海马,按组织化学及酶组织化学常规做“铝定性”反应,琥珀酸脱氢酶（ＳＤＨ）、乳酸脱氢酶（ＬＤＨ）、硫胺素焦磷酸酶（ＴＰＰａｓｅ）、镁激活三磷酸腺苷酶（Ｍｇ２＋－ＡＴＰａｓｅ）、胆碱酯酶（ＣｈＥ）测定。按电镜常规做超微结构的观察。结果提示：Ｃ组,海马ＳＤＨ、Ｍｇ２＋－ＡＴＰａｓｅ、ＣｈＥ活性明显减弱（由强阳性（）下降为阳性（＋）,铝反应增强（在海马的神经细胞内强阳性（）;同时海马神经元内线粒体嵴断裂、肿胀、空泡样变,神经纤维髓鞘变性（如不规则卷曲、松散）。说明铝对海马的功能与结构均有损害