AlCl3 Treatment Research Articles

Effects of aluminum toxicity on physiological and leaf chlorophyll fluorescent characteristics of rubber tree seedlings.

Aluminum toxicity is common in tropical acid soils. However, its effects on rubber tree growth and latex production are still unclear. Using potted sand culture seedlings of rubber tree, the effects of different aluminum ion concentrations on physiological and chlorophyll (Chl) fluorescence characteristics were investigated. The results showed that the cell membrane permeability, free proline content, and soluble sugar content were significantly increased, while the relative water content, catalase and peroxidase activities, Chl a content, Chl maximum fluorescence yield, maximum photosynthesis efficiency and potential activity of PSII, photochemical quenching coefficient, non-photochemical quenching coefficient and photosynthetic electron transport rate were significantly decreased when the saplings were subjected to AlCl3 treatments with concentration higher than 200 mmol·L-1. When the AlCl3 concentration was lower than 100 mmol·L-1, the aforementioned parameters did not show any significant variation among different treatments for the entire duration of the experiment. These results indicated that the rubber tree could tolerate some degree of aluminum toxicity. The threshold concentration of aluminum toxicity for rubber tree seedlings would be between 100 to 200 mmol·L-1. When this threshold was exceeded, aluminum toxicity would cause irreversible damage to rubber tree seedlings.

Neuroprotective, antidiabetic and antioxidant effect of Hedera nepalensis and lupeol against STZ + AlCl3 induced rats model.

PurposeThis study was aimed to evaluate the effect of Hedera nepalensis crude extract (HNC) and its isolated compound lupeol on antioxidant defence system, biochemical parameters and behavioural indices of Alzheimer disease generated in diabetic rats.MethodsTo evaluate the effect of the plant extract and lupeol, symptoms of Alzheimer and diabetes were induced in rats by STZ + AlCl3 treatment. Glucose level was measured with glucometer followed by antioxidant and biochemical assessment of the treated and untreated animals. Behavioural response of the rats was determined by Elevated Plus Maze (EPM) test and Morris Water Maze (MWM) test followed by determination of brain neurotransmitters by HPLC.ResultsHNC significantly reduced blood glucose level in a time dependent manner and elevated liver function markers were significantly (P < 0.05) reinstated to normal levels. HNC showed increase in level of catalase (CAT), superoxide dismutase (SOD) and reduced glutathione (GSH). HPLC quantification revealed that HNC treatment led to significant (p < 0.001) elevation in the level of neurotransmitters (dopamine and serotonin) in the midbrain region as compared to Alzheimer control (AC) group. EPM and MWM test showed decrease in cognitive and memory impairment in a rat group treated with HNC as compared to AC group.ConclusionOverall, results showed that H. nepalensis has therapeutic potential for the treatment of diseases like Alzheimer and diabetes. Graphical abstractTherapeutic effect of Hedera nepalensis K. Koch and lupeol against STZ + AICI3 induced diabetic rats model.

Centella Asiatica Extracts Regulates Aluminium Chloride-Induced Neurotoxicity in Rats: Impact on Inflammation, Apoptosis and Biogenic Amine Levels

investigate the therapeutic potential of CA against chronic Aluminium Chloride (AlCl3) exposure induced rats. Wistar albino rats were segregated into four groups: group 1-control rats, group 2-rats received AlCl3 (300 mg/kg body weight, every day orally) for 60 days, rats in group 3-received CA (500 mg/kg body weight, orally) and group 4 rats were initiated with both AlCl3 and CA treatment.

Attenuation of Aluminum-Induced Neurotoxicity by Tannoid Principles of Emblica officinalis in Wistar Rats

Introduction: In our earlier studies, we reported the neuroprotective effect of tannoid principles of Emblica officinalis (EoT) against aluminum chloride (AlCl3)-induced neurotoxicity in the hippocampus and cortex of rats. The present study is focused on the efficacy of EoT in the mitigation of AlCl3-induced toxicity in the cerebellum. Materials and Methods: Rats were randomly divided into four groups and treated with AlCl3 (100 mg/kg, b.w. i.p.), EoT (100 mg/kg, b.w. oral), and simultaneously with AlCl3 and EoT daily for 60 days. Results: AlCl3 treatment altered the body weight, brain and cerebellum weight, Al levels, acetylcholinesterase activity, and the expression of apoptotic markers. Treatment with EoT attenuated these physiological, biochemical, and molecular indices. Conclusion: The results of the present study strengthen the fact that the nutritional supplement of EoT in AlCl3-treated rats might improve the adverse effects by its pharmacological properties.

Cadmium Disrupts Subcellular Organelles, Including Chloroplasts, Resulting in Melatonin Induction in Plants.

Cadmium is a well-known elicitor of melatonin synthesis in plants, including rice. However, the mechanisms by which cadmium induces melatonin induction remain elusive. To investigate whether cadmium influences physical integrities in subcellular organelles, we treated tobacco leaves with either CdCl2 or AlCl3 and monitored the structures of subcellular organelles—such as chloroplasts, mitochondria, and the endoplasmic reticulum (ER)—using confocal microscopic analysis. Unlike AlCl3 treatment, CdCl2 (0.5 mM) treatment significantly disrupted chloroplasts, mitochondria, and ER. In theory, the disruption of chloroplasts enabled chloroplast-expressed serotonin N-acetyltransferase (SNAT) to encounter serotonin in the cytoplasm, leading to the synthesis of N-acetylserotonin followed by melatonin synthesis. In fact, the disruption of chloroplasts by cadmium, not by aluminum, gave rise to a huge induction of melatonin in rice leaves, which suggests that cadmium-treated chloroplast disruption plays an important role in inducing melatonin in plants by removing physical barriers, such as chloroplast double membranes, allowing SNAT to gain access to the serotonin substrate enriched in the cytoplasm.

Energetics of Excitatory and Inhibitory Neurotransmission in Aluminum Chloride Model of Alzheimer's Disease: Reversal of Behavioral and Metabolic Deficits by Rasa Sindoor.

Alzheimer’s disease (AD) is an age-related neurodegenerative disorder, characterized by progressive loss of cognitive functions and memory. Excessive intake of aluminum chloride in drinking water is associated with amyloid plaques and neurofibrillary tangles in the brain, which are the hallmark of AD. We have evaluated brain energy metabolism in aluminum chloride (AlCl3) mouse model of AD. In addition, effectiveness of Rasa Sindoor (RS), a formulation used in Indian Ayurvedic medicine, for alleviation of symptoms of AD was evaluated. Mice were administered AlCl3 (40 mg/kg) intraperitoneally once a day for 60 days. The memory of mice was measured using Morris Water Maze test. The 13C labeling of brain amino acids was measured ex vivo in tissue extracts using 1H-[13C]-NMR spectroscopy with timed infusion of [1,6-13C2]glucose. The 13C turnover of brain amino acids was analyzed using a three-compartment metabolic model to derive the neurotransmitter cycling and TCA cycle rates associated with glutamatergic and GABAergic pathways. Exposure of AlCl3 led to reduction in memory of mice. The glutamatergic and GABAergic neurotransmitter cycling and glucose oxidation were found to be reduced in the cerebral cortex, hippocampus, and striatum following chronic AlCl3 treatment. The perturbation in metabolic rates was highest in the cerebral cortex. However, reduction in metabolic fluxes was higher in hippocampus and striatum following one month post AlCl3 treatment. Most interestingly, oral administration of RS (2 g/kg) restored memory as well as the energetics of neurotransmission in mice exposed to AlCl3. These data suggest therapeutic potential of RS to manage cognitive functions and memory in preclinical AD.

Fas- and Mitochondria-Mediated Signaling Pathway Involved in Osteoblast Apoptosis Induced by AlCl3.

Aluminum (Al) is known to induce apoptosis of osteoblasts (OBs). However, the mechanism is not yet established. To investigate the apoptotic mechanism of OBs induced by aluminum trichloride (AlCl3), the primary OBs from the craniums of fetal Wistar rats were exposed to 0mg/mL (control group, CG), 0.06mg/mL (low-dose group, LG), 0.12mg/mL (mid-dose group, MG), and 0.24mg/mL (high-dose group, HG) AlCl3 for 24h, respectively. We observed that AlCl3 induced OB apoptosis with the appearance of apoptotic morphology and increase of apoptosis rate. Additionally, AlCl3 treatment activated mitochondrial-mediated signaling pathway, accompanied by mitochondrial membrane potential (ΔΨm) depolarization, release of cytochrome c from the mitochondria to the cytoplasm, as well as survival signal-related factor caspase-9 and caspase-3 activation. AlCl3 exposure also activated Fas/Fas ligand signaling pathway, presented as Fas, Fas ligand, and Fas-associated death domain expression enhancement and caspase-8 activation, as well as the hydrolysis of Bid to truncated Bid, suggesting that the Fas-mediated signaling pathway might aggravate mitochondria-mediated OB apoptosis through hydrolyzing Bid. Furthermore, AlCl3 exposure inhibited Bcl-2 protein expression and increased the expressions of Bax, Bak, and Bim in varying degrees. These results indicated that AlCl3 exposure induced OB apoptosis through activating Fas- and mitochondria-mediated signaling pathway and disrupted B-cell lymphoma-2 family proteins.

Protective Effects of Açai in Combination with Vitamin C against Aluminum-Induced Toxicity in Rat Liver

Aluminum is associated with the pathogenesis of several diseases. Açai has recently emerged as a natural source of antioxidants. The present study was conducted to evaluate the protective effect of Açai in combination with vitamin C against the aluminum chloride induced toxicity. Seventy rats were divided into 7 groups:- Group (GP) 1: control group, GP 2: treated with AlCl3, GP 3: treated with Açai, GP 4: treated with vitamin C, GP 5: treated with AlCl3 and Açai , GP 6: treated with AlCl3 and vitamin C, GP 7: treated with AlCl3, Açai and vitamin C. After 4 weeks, blood and liver specimens were collected to evaluate biochemical alterations and hepatic antioxidant and inflammatory parameters. AlCl3 treatment decreased liver enzymes (alanine aminotransferase, aspartate amino transferase, alkaline phosphatase), tumor necrosis factor-α and IL-6 while hepatic malondialdehyde was elevated. In contrast, hepatic glutathione, super oxide dismutase, catalase were decreased. Açai and vitamin C treatment improved the adverse effects induced by AlCl3, while co-administration with vitamin C promoted the action of açai on hepatic damage and antioxidant parameters. Açai showed a protective effect against AlCl3 induced toxicity, particularly in combination with vitamin C.

Evaluation of Aluminum Chloride As an Effective Short-Term Solution for Reducing Odor - Causing Volatile Fatty Acids in Duck Litter

ABSTRACT This study evaluated the effects of aluminum chloride (AlCl3) on pH and volatile fatty acid levels in duck litter over the course of a three-week experimental period. Ninety one-day-old Pekin ducks (45 males and 45 females) were distributed into three treatments with three replicates each (10 ducks per replicate) using a completely randomized design. Two treatments were top-dressing duck litter with thin layers (1-2 cm) of 50 g or 100 g of AlCl3 per kg of litter, respectively; the control group received no litter treatment. Although no significant differences in propionic acid levels (p>0.05) were observed in any of the treatments, overall pH values for the 50 g and 100 g AlCl3 treatments were both lower (p<0.05) than those of the control group. Additionally, the two AlCl3 treatments revealed a corresponding influence (p<0.05) on acetic acid levels during the last two weeks of the experimental period. These results indicate that aluminum chloride amendments (at a suggested rate of 100 g per kg of duck litter) are potentially useful in lowering the pH of duck litter, thereby decreasing acetic acid production as an indicator of odor emissions.

Aluminum effects on embryo suspensor polytene chromosomes of Phaseolus coccineus L

Aluminum (Al) represents a widespread environmental pollutant, with severe toxic impacts on plants. In this study, we documented for the first time the structural and functional responses induced by two concentrations of AlCl3 (10−2 M and 10−1 M) in the polytene chromosomes that characterize the chromatin organization in the embryo suspensor cells of Phaseolus coccineus. Polytene chromosomes showed signs of dose-dependent genotoxicity following AlCl3 treatments with a significant increase in both chromatin stickiness and chromatin fragmentation. Polytene chromosomes specifically reacted to AlCl3 also in terms of DNA and RNA puffing activity: with respect to the control, the treatments promoted ex-novo and/or inhibited puff formation along chromosome arms, suggesting a fine modulation of the differential genome activity in response to the treatments. The nuclei of suspensors from control and treated seeds showed nucleoli mainly arranged by more than one NOR-bearing chromosome. In addition, AlCl3 treatments affected the frequency of nucleoli organized by singular organizer chromosomes, with an increase in the frequencies of nucleoli organized by chromosome II and a reduction in the frequencies of those organized by chromosomes I or V. These results confirm that, also in our system, nucleolus may react as stress response organelle.

Aluminum chloride elicitation (amendment) improves callus biomass growth and reserpine yield in Rauvolfia serpentina leaf callus

The biotechnological approach of exploiting cell culture elicitation (amendment) offers an attractive alternative strategy to overcome the limited availability of biologically active and medicinally important secondary metabolites. The present study investigated the influence of abiotic aluminum chloride (AlCl3) elicitation on alkaloid yield in Rauvolfia serpentina. This metallic ion was used to enhance the biosynthesis of reserpine in leaf-derived callus, cultured in 1.0 mg l−1 BAP + 0.5 mg l−1 IAA amended Murashige and Skoog (MS) medium and this study revealed the increased yield of reserpine in cultivated tissues. This enhanced yield could help in minimizing the indiscriminate harvest of endangered flora for natural alkaloid extraction. The elicitor’s impact on callus biomass, alteration of biochemical attributes and reserpine yield at 0.05 mM (A1), 0.10 mM (A2), 0.15 mM (A3) and 0.20 mM (A4) was evaluated at periodic intervals. Maximum callus biomass was observed in 0.15 mM AlCl3 amended medium with a highest fresh weight of 1.24 g and dry weight of 0.14 g at day 6. To understand the role of AlCl3 in plant defense mechanism, various antioxidant enzymes i.e. superoxide dismutase (SOD), catalase (CAT) and ascorbate peroxidase (APX) activities were assayed in in vitro cultivated calli with or without AlCl3 treatment. The above enzymes activities increased linearly with increasing AlCl3 level, i.e. 5.10 enzyme unit (EU) min−1 mg−1 protein SOD, 3.93 EU min−1 mg−1 protein CAT and 0.83 EU min−1 mg−1 protein APX, all being maximum at A4 treatment. The yield of reserpine was quantified in callus tissues by using HPTLC method, indicating that the reserpine synthesis was enhanced with increasing elicitor treatment up to A3 and maximum being at 0.15 mM AlCl3 amended medium (0.129 mg g−1 DW). Higher elicitation level (0.20 mM) had a very little influence on callus biomass and reserpine synthesis. Besides, the role of genes encoding pyroline-5-carboxylate synthetase (P5CS) and tryptophan decarboxylase (TDC), which participate in reserpine biosynthetic pathway is also discussed.

Aluminum chloride caused liver dysfunction and mitochondrial energy metabolism disorder in rat

Aluminum (Al) is known to exert hepatotoxicity. However, the mechanisms mostly are unclear. Liver is a metabolism organ that maintains the energy level and structural stability of body, mitochondria are the main sites of energy metabolism, thus, we hypothesized that mitochondrial energy metabolism disorder contributes to liver dysfunction in aluminum chloride (AlCl3) treatment rat. To verify the hypothesis, forty male Wistar rats were randomly allocated and orally exposed to 0, 64mg/kg, 128mg/kg and 256mg/kg body weight AlCl3 in drinking water for 120days, respectively. We found that AlCl3 exposure reduced the electron transport chain complexes I–V activities and adenosine triphosphate (ATP) level, as well as disturbed mitochondrial DNA transcript, presenting as the inhibited mRNA expressions of NADH dehydrogenase 1, NADH dehydrogenase 2, cytochrome b, cytochrome c oxidase subunit 1, cytochrome c oxidase subunit 3 and ATP synthase 6, indicating that AlCl3 exposure disturbs the mitochondrial energy metabolism, and it caused an increase in liver enzymes (Aspartate aminotransferase and Alanine aminotransferase) and histopathological lesions. Additionally, we found that reactive oxygen species accumulation and decreased superoxide dismutase activity in mitochondria, and increased 8-Hydroxydeoxyguanosine levels in mitochondrial DNA, demonstrating AlCl3 exposure promotes mitochondrial oxidative stress, which may be a contributing factor to mitochondrial energy metabolism disorder and liver dysfunction. The study displayed that mitochondria are the potential target of liver damage induced by AlCl3, providing considerable direction for the prevention and clinical intervention of liver diseases.

Tannoid principles of Emblica officinalis attenuated aluminum chloride induced apoptosis by suppressing oxidative stress and tau pathology via Akt/GSK-3βsignaling pathway

Ethnopharmacological relevanceFruits of Phyllanthus emblica Linn. or Emblica officinalis Gaertn. (Phyllanthaceae) are used in Ayurveda, Siddha, Unani, Arabic, Tibetan and various other folk medicinal systems to promote intelligence and memory. Recent study from our lab indicated the neuroprotective effect of tannoids principles of Emblica officinalis (EoT) against memory loss caused by aluminum chloride (AlCl3) intoxication through attenuating acetylcholine esterase activity and the expression of amyloid β protein biosynthesis related markers. However the molecular mechanism of EoT has not yet been fully elucidated. Aim of the studyThe aim of the present study was to further investigate the neuroprotective mechanisms of EoT against AlCl3-induced cognitive deficits, tau hyperphosphorylation, oxidative stress and apoptosis. Materials and methodsRats were treated with AlCl3 for 60 days to induce biochemical and physiological abnormalities similar to AD patients. AD rats were treated with EoT (100mg/kg., bw. oral) for 60 days. For the examination of neuroprotective effect of EoT, behavior analysis, biochemical estimations and western blot were performed in the hippocampus and cortex of control, EoT treated and untreated AD rats. ResultsIntraperitoneal injections of AlCl3 (100mg/kg., b.w.) for 60 days enhanced the learning and memory deficits, levels of TBARS and diminished the levels of reduced glutathione and activities of enzymatic antioxidants as compared to control group. Moreover toxicity of AlCl3 is accompanied by the enhanced expressions of Bax, caspases-3,-9, cytosolic cytochrome c (cyto c), and pTau along with diminished expressions of Bcl-2, mitochondrial cyto c, pGSK-3β and pAkt. Coadministration of EoT nullified the cognitive deficits, biochemical abnormalities and apoptosis induced by AlCl3 treatment. Moreover EoT prevents tau hyperphosphorylation by targeting the GSK-3β/Akt signaling pathway. ConclusionsThis study confirms that EoT would be used as a potential drug candidate for AD and other tau pathology-related neuronal degenerative diseases.

Caspase-like proteases regulate aluminum-induced programmed cell death in peanut

Recent evidence has proved that caspase protease activities are detected in both mammals and plants during programmed cell death (PCD). The characteristics and functions of caspase-like proteases play important roles in understanding the mechanisms of PCD in plants. In this work, we report firstly the involvement of caspase-like protease activities and effects in aluminum (Al) stress in two contrasting peanut genotypes. Caspase-like activities in the root tip cells of ‘Zhonghua 2’ (Al-sensitive) and ‘99-1507’ (Al-tolerant) were detected using synthetic caspase substrates during Al-triggered PCD. Caspase-1-, -2-, -3-, -4-, -5-, -6-, -8- and -9-like proteases were found in peanut root tip cells. VDQQDase (caspase-2-like) and WEHD (caspase-5-like) were the first detected in the plants, and almost all of the caspase-like proteases were activated during Al-induced PCD, especially caspase-3-like and caspase-1-like, which was higher in ‘Zhonghua 2’ than in ‘99-1507’. The highest activity levels of caspase-3- and caspase-1-like proteases occurred 8 and 4 h after 100 µM Al treatment, respectively. Compared with 100 µM AlCl3 treatment alone, specific caspase-3 protease inhibitor Ac-DEVD-CHO inhibited the increase of caspase-3-like protease activity, Al content, Hsr203j expression, cell death and DNA fragmentation, and the decrease in root growth induced by 100 µM AlCl3 treatment, but it was more obvious in ‘Zhonghua 2’ than in ‘99-1507’. In conclusion, there were different caspase-like proteases in root tips of peanut, and caspase-3-like protease was a crucial executioner in Al-induced PCD. Its effects in the ‘Zhonghua 2’ genotype were higher than in ‘99-1507’. An improved model of the mechanism of Al-induced PCD and Al tolerance differences in different genotypes is proposed.

Effects of Metal Oxyhydroxide Coatings on Photoanode in Quantum Dot Sensitized Solar Cells

Exploring facile modifications on photoanode to suppress charge recombination at photoanode/electrolyte interfaces is an efficient way to improve the performance of quantum dot sensitized solar cells (QDSCs). Herein, a series of metal oxyhydroxide gels have been overcoated on CdSeTe QD sensitized photoanodes via a hydrolysis and condensation process from the corresponding metal chloride (NbCl5, ZrOCl2, SnCl4, FeCl3, AlCl3, CoCl2, CuCl2, MgCl2, and ZnCl2) aqueous solutions, and their effects on the photovoltaic performance are systematically investigated. Photovoltaic measurement results indicate that the NbCl5 and ZrOCl2 modifications offer a remarkable enhancement in photovoltaic performance, especially in photovoltage. The SnCl4 AlCl3, MgCl2, and ZnCl2 treatments give a negligible influence, and the FeCl3, CuCl2, and CoCl2 treatments present a negative effect on the performance. DFT calculations suggest that different metal oxyhydroxide coatings bring forward distinct densities of empty states at the su...

Effects of aluminum on the reduction of neural stem cells, proliferating cells, and differentiating neuroblasts in the dentate gyrus of D-galactose-treated mice via increasing oxidative stress.

Aluminum (Al) accumulation increases with aging, and long-term exposure to Al is regarded as a risk factor for Alzheimer's disease. In this study, we investigated the effects of Al and/or D-galactose on neural stem cells, proliferating cells, differentiating neuroblasts, and mature neurons in the hippocampal dentate gyrus. AlCl3 (40 mg/kg/day) was intraperitoneally administered to C57BL/6J mice for 4 weeks. In addition, vehicle (physiological saline) or D-galactose (100 mg/kg) was subcutaneously injected to these mice immediately after AlCl3 treatment. Neural stem cells, proliferating cells, differentiating neuroblasts, and mature neurons were detected using the relevant marker for each cell type, including nestin, Ki67, doublecortin, and NeuN, respectively, via immunohistochemistry. Subchronic (4 weeks) exposure to Al in mice reduced neural stem cells, proliferating cells, and differentiating neuroblasts without causing any changes to mature neurons. This Al-induced reduction effect was exacerbated in D-galactose-treated mice compared to vehicle-treated adult mice. Moreover, exposure to Al enhanced lipid peroxidation in the hippocampus and expression of antioxidants such as Cu, Zn- and Mn-superoxide dismutase in D-galactose-treated mice. These results suggest that Al accelerates the reduction of neural stem cells, proliferating cells, and differentiating neuroblasts in D-galactose-treated mice via oxidative stress, without inducing loss in mature neurons.

Aluminum trichloride impairs bone and downregulates Wnt/β-catenin signaling pathway in young growing rats

Aluminum (Al) can accumulate in bone and cause bone diseases. Few studies have investigated molecular mechanism of Al-induced bone diseases. Thus, in this study, rats were orally exposed to 0 (control group) and 0.4 g/L aluminum trichloride (AlCl3) (treatment group) for 30, 60, 90 or 120 days, respectively. The Al content of femora and serum, bone histological structure, bone mineral density (BMD) of the distal and proximal femoral metaphysis and Wnt/β-catenin signaling pathway (the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5) in rat femora were determined on day 30, 60, 90 or 120, respectively. The results showed that the Al contents of femora and serum were increased, the BMD of the distal and proximal femoral metaphysis were decreased, the femora histological structure were disrupted, the mRNA expressions of Wnt3a, Fzd2, LRP-5, β-catenin, Tcf4, cyclin D1 and c-Myc, the protein levels of Wnt3a and β-catenin, the activities of Fzd2 and LRP-5 were all decreased in the treatment group compared with the control group with time prolonged. These results indicated that AlCl3 impaired femora by inhibiting the Wnt/β-catenin signaling pathway in young growing rats.

Water deficit and aluminum interactive effects on generation of reactive oxygen species and responses of antioxidative enzymes in the seedlings of two rice cultivars differing in stress tolerance.

Aluminum (Al) is a major constraint to crop productivity in acid soils, whereas water deficit severely limits crop production in arid and semi-arid regions of the world. The objective of the present study was to examine the effects of both stresses, Al excess and water deficit, individually and in combination on the production of the reactive oxygen species (ROS) superoxide anion (O2˙(-)), hydrogen peroxide (H2O2), hydroxyl radical, and lipid peroxidation and the activity of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and guaiacol peroxidase (GPX) in the seedlings of two rice (Oryza sativa L.) cvs. Malviya-36 (sensitive to water deficit and Al) and Vandana (tolerant to water deficit and Al). When 15-day grown seedlings were exposed to water deficit (created with 15% polyethylene glycol, PEG-6000) or Al (1 mM AlCl3) treatment or both treatments together for 24-72 h, the lengths and fresh weights of root/shoot declined in the seedlings of the sensitive cultivar, whereas in the tolerant seedlings, either little or insignificant decline in these parameters was observed due to the treatments. Biochemical determinations and histochemical studies revealed that under a similar level of water deficit, Al, or combined treatment, seedlings of sensitive cultivar showed a higher level of production of O2˙(-), H2O2, hydroxyl radical, and lipid peroxides compared to the tolerant seedlings. Seedlings of tolerant cultivars, both in roots and shoots, had constitutively higher activity levels of antioxidative enzymes SOD, CAT, and GPX and showed a greater increase in activity under water deficit or Al treatment alone or in combination compared to the similarly treated seedlings of sensitive cultivar. Our results suggest that a lower constitutive level of ROS and a high antioxidative enzyme capacity are associated with tolerance to both water deficit and Al excess in rice seedlings.

Cloning and Expression Analysis of Tolerance to Aluminum-toxicity Candidate Gene GmSTOP1 in Soybean

Aluminum toxicity is one of the major factors that limits the growth and production of crops in acid soils. AtSTOP1 transcription factor can regulate the expression of genes related to aluminum-toxicity tolerance mechanisms, which plays an important role in aluminum-toxicity tolerance in Arabidopsis. To study the expression features of the STOP1-like gene in soybean, we cloned a STOP1 gene located on chromosome 16 from the aluminum-toxicity tolerant soybean cultivar (Kefeng-1) using RT-PCR, and designated as GmSTOP1. The length of GmSTOP1 coding DNA sequence was 1566 bp, which encoded 521 amino acid residues. Diverse cis-acting promoter elements involved in hormone, heat and stress responses were discovered in the 1500 第 12期 丛亚辉等: 大豆耐铝毒候选基因 GmSTOP1的克隆与表达分析 1803 bp upstream region of GmSTOP1, such as ABRE, HSE, TC-rich repeats, and other elements. Protein structure prediction showed that it did not have any signal-peptide or transmembrane region, but contained four conservative Cys-2-His-2 zinc-finger domains. Phylogenetic analysis demonstrated that GmSTOP1 was similar to the putative STOP1-like protein from Phaseolus vulgaris. Results of subcellular localization showed that GmSTOP1 protein is located in the cell nucleus. The transcripts of GmSTOP1 were detected in all organs tested including root, shoot apical meristem, stem, leaf, flower, pod and seed, with the highest level in seed. GmSTOP1 was up-regulated in soybean roots by 25 μmol L AlCl3 treatment, and reached the highest relative expression level at 24 hours, which was about 9.2 times of the level in control (0 μmol L AlCl3). In addition, Real-time PCR analysis showed that the expression of GmSTOP1 in soybean leaf and root was also up-regulated by ABA, NaCl, and PEG, respectively. These results indicated that GmSTOP1 might participate in soybean response to abiotic stresses including aluminum-toxicity, high salinity and osmosis stress, which provides the basis for further studying the functions of GmSTOP1.

Protective Effect of Centella asiatica against Aluminium-Induced Neurotoxicity in Cerebral Cortex, Striatum, Hypothalamus and Hippocampus of Rat Brain- Histopathological, and Biochemical Approach

Aluminum (Al) is a potent environmental neurotoxin, which is involved in the progression of neurodegenerative processes. Remarkable biological and medicinal properties of Centella asiatica (CA) are well known in last few decades. Therefore, the present study has been designed to explore the neuroprotective effect of CA on chronic aluminium chloride (AlCl3) exposure induced neurotoxicity in rat brain regions (cerebral cortex, striatum, hypothalamus and hippocampus). Wistar albino rats were segregated into four groups: group 1-control rats, group 2- rats received AlCl3 (300 mg/kg body weight, every day orally) for 60 days, rats in group 3-received CA (500 mg/kg body weight, orally) and group 4 rats were initiated with both AlCl3 and CA treatment. Administration of AlCl3 developed behavioral deficits, triggered lipid peroxidation (LPO), compromised acetylcholine esterase (AChE) activity, and reduced the levels of superoxide dismutase (SOD), catalase (CAT), reduced glutathione (GSH) and glutathione-S-transferase (GST) and caused histologic aberrations. AlCl3–induced alterations in the activities of SOD, CAT, GSH and GST, levels of LPO, activity of AChE, behavioral deficits and histologic aberrations were attenuated on treatment with CA. Results of the study demonstrate neuroprotective potential of CA against AlCl3- induced oxidative damage and cognitive dysfunction.