Ni Toxicity Research Articles

Low-dose and repeated exposure to nickel leads to bioaccumulation and cellular and metabolic alterations in quails

Nickel (Ni) is a widespread environmental pollutant commonly released into effluent due to industrial activities, the use of fuels, or wastewater disposal. Many studies confirm the toxic effects of this heavy metal. However, there is a lack of knowledge and data on bioaccumulation patterns in tissues as well as cellular and molecular responses following the exposure of living organisms to Ni. In this study, Japanese quails were exposed to low (10 μg/L) and high (2000 μg/L) Ni concentrations in the form of nickel(II) chloride via drinking water. Sub-chronic exposure lasted 30 days while nominal concentrations represented average Ni content in drinking water (low dose) and average Ni levels in highly polluted aquatic environments (high dose). It was revealed that a high dose of Ni was correlated with increased water intake and decreased body weight. Overall, Ni exposure induced the development of microcytic anemia and alterations in measured blood indices. Moreover, Ni exposure impaired immunological activation as seen through the increased number of the white blood cells, increased heterophile/lymphocyte (H/L) ratio, and pronounced thrombocytosis. Ni elicited changes in the albumin, glucose, cholesterol, and triglyceride serum levels in a concentration-dependent manner. Alterations of plasma protein fractions suggested liver functional impairment while high levels of urea and creatinine indicated potential kidney injury. Granulation of heterophiles and an increase in erythroblasts in the bone marrow showed that the hematopoietic tissue was also impacted by Ni toxicity. On average each quail bioaccumulated 5.87 μg of Ni per gram of tissue. Moreover, the distribution and bioaccumulation of Ni in terms of relative concentration were as follows: feathers > kidneys > heart > liver > pectoral muscles. Assessed bioaccumulation levels and associated cellular and metabolic alterations have revealed new multilayer toxicological data that will help in the extrapolation of Ni toxicity in other vertebrates, including humans.

Synergistic mitigation of nickel toxicity in pepper (Capsicum annuum) by nitric oxide and thiourea via regulation of nitrogen metabolism and subcellular nickel distribution.

Nickel (Ni) contamination hinders plant growth and yield. Nitric oxide (NO) and thiourea (Thi) aid plant recovery from heavy metal damage, but their combined effects on pepper (Capsicum annuum ) plant tolerance to Ni stress need more study. Sodium nitroprusside (0.1mM, SNP) and 400mgL-1 Thi, alone and combined, were studied for their impact on pepper growth under Ni toxicity. Ni stress reduces chlorophyll, PSII efficiency and leaf water and sugar content. However, SNP and Thi alleviate these effects by increasing leaf water, proline and sugar content. It also increased the activities of superoxide dismutase, catalase, ascorbate peroxidase and peroxidase. Nickel stress lowered nitrogen assimilation enzymes (nitrate reductase, nitrite reductase, glutamine synthetase, glutamate synthase and glutamate dehydrogenase) and protein content, but increased nitrate, ammonium and amino acid content. SNP and Thi enhanced nitrogen assimilation, increased protein content and improved pepper plant growth and physiological functions during Ni stress. The combined treatment reduced Ni accumulation, increased Ni in leaf cell walls and potentially in root vacuoles, and decreased Ni concentration in cell organelles. It effectively mitigated Ni toxicity to vital organelles, surpassing the effects of SNP or Thi use alone. This study provides valuable insights for addressing heavy metal contamination in agricultural soils and offers potential strategies for sustainable and eco-friendly farming practices.

Soil-Plant-Ni-As: Four-Fold Interactions – Modest Blessing from Total Disguise

As an essential plant nutrient, deficiency of nickel (Ni) can cause metabolic and enzymatic disorder in plants; however an excess amount of this element can also be proven deadly for a plant. To examine the critical level of Ni tolerance two plant species, Kalmi (Ipomoea aquatica) and Red Amaranthus (Amaranthus cruentus) were selected where Red Amaranthus (Amaranthus cruentus) was verified as a hyper accumulator of Ni. In this diverse experimental set up, arsenic (As) was applied with irrigation water and increased doses of Ni was observed to put antagonistic effect on availability as well as plant uptake of As. The results from such a complex and diverse four-fold interaction can be concluded as a little blessing of remediation of As toxicity from a disguise of Ni toxicity.

Citric acid assisted phytoextraction of nickle from soil helps to tolerate oxidative stress and expression profile of NRAMP genes in sunflower at different growth stages.

Soil polluted with Nickel (Ni) adversely affects sunflower growth resulting in reduced yield. Counterbalancing Ni toxicity requires complex molecular, biochemical, and physiological mechanisms at the cellular, tissue, and whole plant levels, which might improve crop productivity. One of the primary adaptations to tolerate Ni toxicity is the enhanced production of antioxidant enzymes and the elevated expression of Ni responsive genes. In this study, biochemical parameters, production of ROS, antioxidants regulation, and expression of NRAMP metal transporter genes were studied under Ni stress in sunflower. There were four soil Ni treatments (0, 50, 100, and 200 mg kg-1 soil), while citric acid (CA, 5 mM kg-1 soil) was applied on the 28th and 58th days of plant growth. The samples for all analyses were obtained on the 30th and 60th day of plant growth, respectively. The results indicated that the concentrations of Ni in roots and shoots were increased with increasing concentrations of Ni at both time intervals. Proline contents, ascorbic acid, protein, and total phenolics were reduced under Ni-stress, but with the application of CA, improvement was witnessed in their contents. The levels of malondialdehyde and hydrogen peroxide were enhanced with the increasing concentration of Ni, and after applying CA, they were reduced. The contents of antioxidants, i.e., catalase, peroxidase, superoxide dismutase, ascorbate peroxidase, dehydroascorbate reductase, and glutathione reductase, were increased at 50 ppm Ni concentration and decreased at higher concentrations of Ni. The application of CA significantly improved antioxidants at all concentrations of Ni. The enhanced expression of NRAMP1 (4, 51 and 81 folds) and NRAMP3 (1.05, 4 and 6 folds) was found at 50, 100 and 200ppm Ni-stress, respectively in 30 days old plants and the same pattern of expression was recorded in 60 days old plants. CA further enhanced the expression at both developmental stages. In conclusion, CA enhances Ni phytoextraction efficiency as well as protect plant against oxidative stress caused by Ni in sunflower.

Nickel toxicity alters growth patterns and induces oxidative stress response in sweetpotato.

Nickel (Ni) contaminated soil is a persistent risk to plant growth and production worldwide. Therefore, to explore the Ni toxicity levels in sweetpotato production areas, we investigated the influence of different Ni treatments (0, 7.5, 15, 30, and 60 mg L-1) for 15 days on phenotype, Ni uptake, relative water content, gas exchange, photosynthetic pigments, oxidative stress, osmolytes, antioxidants, and enzymes of sweetpotato plants. The results presented that Ni at higher levels (30 and 60 mg L-1) substantially reduced growth, biomass, and root morphological traits. The Pearson correlation analysis suggested that Ni toxicity causes oxidative injuries as persistent augmentation of hydrogen peroxide (H2O2) and malonaldehyde (MDA) and reduced RWC, gas exchange, and photosynthetic pigment. Furthermore, this study revealed that sweetpotato could tolerate moderate Ni treatment (up to 15 mg L-1) by reducing oxidative stress. The results also indicated that the increase in the activities of mentioned osmolytes, antioxidants, and enzymes is not sufficient to overcome the higher Ni toxicity. Based on these results, we suggest using low Ni-contaminated soil for better growth of sweetpotato and also could be used as a phytoremediator in moderate Ni-contaminated soil.

Supplementation of nitric oxide and spermidine alleviates the nickel stress-induced damage to growth, chlorophyll metabolism, and photosynthesis by upregulating ascorbate-glutathione and glyoxalase cycle functioning in tomato.

Experiments were conducted to evaluate the role of exogenously applied nitric oxide (NO; 50 µM) and spermidine (Spd; 100 µM) in alleviating the damaging effects of Ni (1 mM NiSO46H2O) toxicity on the growth, chlorophyll metabolism, photosynthesis, and mineral content in tomato. Ni treatment significantly reduced the plant height, dry mass, and the contents of glutamate 1-semialdehyde, δ-amino levulinic acid, prototoporphyrin IX, Mg-prototoporphyrin IX, total chlorophyll, and carotenoids; however, the application of NO and Spd alleviated the decline considerably. Supplementation of NO and Spd mitigated the Ni-induced decline in photosynthesis, gas exchange, and chlorophyll fluorescence parameters. Ni caused oxidative damage, while the application of NO, Spd, and NO+Spd significantly reduced the oxidative stress parameters under normal and Ni toxicity. The application of NO and Spd enhanced the function of the antioxidant system and upregulated the activity of glyoxalase enzymes, reflecting significant reduction of the oxidative effects and methylglyoxal accumulation. Tolerance against Ni was further strengthened by the accumulation of proline and glycine betaine due to NO and Spd application. The decrease in the uptake of essential mineral elements such as N, P, K, and Mg was alleviated by NO and Spd. Hence, individual and combined supplementation of NO and Spd effectively alleviates the damaging effects of Ni on tomato.

Transcriptome analysis of trembling aspen (Populus tremuloides) under nickel stress.

Plants have evolved heavy metal tolerance mechanisms to adapt and cope with nickel (Ni) toxicity. Decrypting whole gene expression of Trembling Aspen (Pinus tremuloides) under nickel stress could elucidate the nickel resistance/tolerance mechanisms. The main objectives of the present research were to 1) characterize the P. tremuloides transcriptome, and 2) compare gene expression dynamics between nickel-resistant and nickel-susceptible P. tremuloides genotypes with Whole Transcriptome (WT) sequencing. Illumina Sequencing generated 27–45 million 2X150 paired-end reads of raw data per sample. The alignment performed with StringTie Software added two groups of transcripts to the draft genome annotation. One group contained 32,677 new isoforms that match to 17,254 genes. The second group contained 17,349 novel transcripts that represent 16,157 novel genes. Overall, 52,987 genes were identified from which 36,770 genes were selected as differently expressed. With the high stringency (two-fold change, FDR value ≤ 0.05 and logFC value ≥1 (upregulated) or ≤ -1 (downregulated), after GSEA analysis and filtering for gene set size, 575 gene sets were upregulated and 146 were downregulated in nickel resistant phenotypes compared to susceptible genotypes. For biological process, genes associated with translation were significantly upregulated while signal transduction and cellular protein process genes were downregulated in resistant compared to susceptible genotypes. For molecular function, there was a significant downregulation of genes associated with DNA binding in resistant compared to susceptible lines. Significant upregulation was observed in genes located in ribosome while downregulation of genes in chloroplast and mitochondrion were preponderant in resistant genotypes compared to susceptible. Hence, from a whole transcriptome level, an upregulation in ribosomal and translation activities was identified as the main response to Ni toxicity in the resistant plants. More importantly, this study revealed that a metal transport protein (Potrs038704g29436 –ATOX1-related copper transport) was among the top upregulated genes in resistant genotypes when compared to susceptible plants. Other identified upregulated genes associated with abiotic stress include genes coding for Dirigent Protein 10, GATA transcription factor, Zinc finger protein, Auxin response factor, Bidirectional sugar transporter, and thiamine thiazole synthase.

The thiol-reductase activity of YUCCA6 enhances nickel heavy metal stress tolerance in Arabidopsis.

Anthropogenic activities cause the leaching of heavy metals into groundwater and their accumulation in soil. Excess levels of heavy metals cause toxicity in plants, inducing the production of reactive oxygen species (ROS) and possible death caused by the resulting oxidative stress. Heavy metal stresses repress auxin biosynthesis and transport, inhibiting plant growth. Here, we investigated whether nickel (Ni) heavy metal toxicity is reduced by exogenous auxin application and whether Ni stress tolerance in Arabidopsis thaliana is mediated by the bifunctional enzyme YUCCA6 (YUC6), which functions as an auxin biosynthetic enzyme and a thiol-reductase (TR). We found that an application of up to 1 µM exogenous indole-3-acetic acid (IAA) reduces Ni stress toxicity. yuc6-1D, a dominant mutant of YUC6 with high auxin levels, was more tolerant of Ni stress than wild-type (WT) plants, despite absorbing significantly more Ni. Treatments of WT plants with YUCASIN, a specific inhibitor of YUC-mediated auxin biosynthesis, increased Ni toxicity; however yuc6-1D was not affected by YUCASIN and remained tolerant of Ni stress. This suggests that rather than the elevated IAA levels in yuc6-1D, the TR activity of YUC6 might be critical for Ni stress tolerance. The loss of TR activity in YUC6 caused by the point-mutation of Cys85 abolished the YUC6-mediated Ni stress tolerance. We also found that the Ni stress–induced ROS accumulation was inhibited in yuc6-1D plants, which consequently also showed reduced oxidative damage. An enzymatic assay and transcriptional analysis revealed that the peroxidase activity and transcription of PEROXIREDOXIN Q were enhanced by Ni stress to a greater level in yuc6-1D than in the WT. These findings imply that despite the need to maintain endogenous IAA levels for basal Ni stress tolerance, the TR activity of YUC6, not the elevated IAA levels, plays the predominant role inNi stress tolerance by lowering Ni-induced oxidative stress.

Nickel toxicity pretreatment attenuates salt stress by activating antioxidative system and ion homeostasis in tomato (Solanum lycopersicon L.): an interplay from mild to severe stress.

Plants antioxidative system is the first line of defense against oxidative stress caused secondarily by toxic ions under salinity. Plants with pre-activated antioxidative system can better adapt to salinity and can result in higher growth and yield. The current experiment was conducted to assess the adaptation of two tomato genotypes (Riogrande and Green Gold) with pre-activated antioxidative enzymes against salt stress. Tomato seedlings were exposed to mild stress (Ni: 0, 15 and 30mgL-1) for three weeks to activate the antioxidative enzymes. The seedlings with pre-activated antioxidative enzymes were then grown under severe stress in hydroponics (0, 75 and 150mMNaCl) and soil (control, 7.5 and 15 dSm-1) to check the adaptation, growth and yield. The results showed that Ni toxicity significantly enhanced activities of antioxidant enzymes (SOD, CAT, APX and POX) in both the genotypes and reduced growth with higher values in genotype Riogrande than Green Gold. The seedlings with pre-activated antioxidant enzymes showed better growth, low Na+ and high K+ uptake and maintained higher antioxidative enzymes activity than non-treated seedlings after four weeks of salt stress treatment in hydroponics. Similarly, the results in soil salinity treatment of the Ni pretreated seedlings showed higher yield characteristics (fruit yield per plant, average fruit weight and fruit diameter) than non-treated seedlings. However, Ni pretreatment had nonsignificant effect on tomato fruit quality characteristics like fruit dry matter percentage, total soluble solids, fruit juice pH and titratable acidity. The genotype Riogrande showed better growth, yield and fruit quality than Green Gold due to higher activity of antioxidant enzymes and better ion homeostasis as a result of Ni pretreatment. The results suggest that pre-activation antioxidant enzymes by Ni treatment proved to be an effective strategy to attenuate salt stress for better growth and yield of tomato plants.

Physiological and Biochemical Responses of Pepper (Capsicum annuum L.) Seedlings to Nickel Toxicity.

Globally, heavy metal pollution of soil has remained a problem for food security and human health, having a significant impact on crop productivity. In agricultural environments, nickel (Ni) is becoming a hazardous element. The present study was performed to characterize the toxicity symptoms of Ni in pepper seedlings exposed to different concentrations of Ni. Four-week-old pepper seedlings were grown under hydroponic conditions using seven Ni concentrations (0, 10, 20, 30, 50, 75, and 100 mg L–1 NiCl2. 6H2O). The Ni toxicity showed symptoms, such as chlorosis of young leaves. Excess Ni reduced growth and biomass production, root morphology, gas exchange elements, pigment molecules, and photosystem function. The growth tolerance index (GTI) was reduced by 88-, 75-, 60-, 45-, 30-, and 19% in plants against 10, 20, 30, 50, 75, and 100 mg L–1 Ni, respectively. Higher Ni concentrations enhanced antioxidant enzyme activity, ROS accumulation, membrane integrity [malondialdehyde (MDA) and electrolyte leakage (EL)], and metabolites (proline, soluble sugars, total phenols, and flavonoids) in pepper leaves. Furthermore, increased Ni supply enhanced the Ni content in pepper’s leaves and roots, but declined nitrogen (N), potassium (K), and phosphorus (P) levels dramatically. The translocation of Ni from root to shoot increased from 0.339 to 0.715 after being treated with 10–100 mg L–1 Ni. The uptake of Ni in roots was reported to be higher than that in shoots. Generally, all Ni levels had a detrimental impact on enzyme activity and led to cell death in pepper seedlings. However, the present investigation revealed that Ni ≥ 30 mg L–1 lead to a deleterious impact on pepper seedlings. In the future, research is needed to further explore the mechanism and gene expression involved in cell death caused by Ni toxicity in pepper plants.

Synergistic Interaction between Symbiotic N2 Fixing Bacteria and Bacillus strains to Improve Growth, Physiological Parameters, Antioxidant Enzymes and Ni Accumulation in Faba Bean Plants (Vicia faba) under Nickel Stress.

Several activities in the agriculture sector lead to the accumulation of Nickel (Ni) in soil. Therefore, effective and economical ways to reduce soil bioavailability of Ni must be identified. Five isolates of Rhizobium leguminosarum biovar Viceae (ICARDA 441, ICARDA 36, ICARDA 39, TAL–1148, and ARC–207) and three bacterial strains (Bacillus subtilis, B. circulance, and B. coagulans) were evaluated for tolerance and biosorption of different levels of Ni (0, 20, 40, 60, and 80 mg L−1). Pot experiments were conducted during the 2019/2020 and 2020/2021 seasons using four inoculation treatments (inoculation with the most tolerant Rhizobium (TAL–1148), inoculation with the most tolerant Rhizobium (TAL–1148) + B. subtilis, inoculation with the most tolerant Rhizobium (TAL–1148) + B. circulance, and inoculation with the most tolerant Rhizobium (TAL–1148) + B. coagulans) under different levels of Ni (0, 200, 400, and 600 mg kg−1), and their effects on growth, physiological characteristics, antioxidant enzymes, and Ni accumulation in faba bean plants (Vicia faba C.V. Nobaria 1) were determined. The results showed that Rhizobium (TAL–1148) and B. subtilis were the most tolerant of Ni. In pot trials, inoculation with the most tolerant Rhizobium TAL–1148 + B. subtilis treatment was shown to be more effective in terms of growth parameters (dry weight of plant, plant height, number of nodules, and N2 content), and this was reflected in physiological characteristics and antioxidant enzymes under 600 mg kg−1 Ni compared to the other treatments in the 2019/2020 season. In the second season, 2020/2021, a similar pattern was observed. Additionally, lower concentrations of Ni were found in faba bean plants (roots and shoots). Therefore, a combination of the most tolerant Rhizobium (TAL–1148) + B. subtilis treatment might be used to reduce Ni toxicity.

Assessing the effects of nickel on, e.g., Medicago sativa L. nodules using multidisciplinary approach.

Industrial wastes and fertilizers can introduce excessive levels of nickel (Ni) into the environment, potentially causing threats to plants, animals, as well as human beings. However, the number of studies on the effects of Ni toxicity on nodules is fairly limited. To address this issue, the effects of increasing Ni concentration on alfalfa nodules were assessed at chemical, biochemical, and transcriptomic levels. For this purpose, plants were grown in soils supplied with Ni (control, 0 mg/kg; C1, 50 mg/kg; C2, 150 mg/kg; C3, 250 mg/kg; and C4, 500 mg/kg) for 90 days. Ni loads in leaves, roots, and nodules were monitored after the exposure period. A set of biochemical biomarkers of oxidative stress was determined in nodules including antioxidants and metal homeostasis as well as lipid peroxidation. Gene expression levels of the main targets involved in oxidative stress and metal homeostasis were assessed. Our data indicated a high concentration of Ni in leaves, roots, and nodules where values reached 25.64 ± 3.04 mg/kg, 83.23 ± 5.16 mg/kg, and 125.71 ± 4.53 mg/kg in dry weight, respectively. Moreover, a significant increase in nodule biomass was observed in plants exposed to C4 in comparison to control treatment and percentage increased by 63%. Then, lipid peroxidation increased with a rate of 95% in nodules exposed to C4. Enzymatic activities were enhanced remarkably, suggesting the occurrence of oxidative stress, with increased superoxide dismutase (SOD), glutathione reductase (GR), and ascorbate peroxidase (APX). Our results showed also a significant upregulation of SOD, GR and APX genes in nodules. Nodule homoglutathione (HGSH) levels increased with the different Ni concentrations, with a remarkable decrease of glutathione S-transferase (GST) activity and glutathione (GSH) content for the highest Ni concentration with 43% and 52% reduction, respectively. The phytochelatin (PC) and metallothionein (MT) concentrations increased in nodules, which implied the triggering of a cellular protection mechanism for coping with Ni toxicity. The results suggested that Ni promotes a drastic oxidative stress in alfalfa nodules, yet the expression of MT and PC to reduce Ni toxicity could be used as Ni stress bioindicators. Our findings provide new insights into the central role of alfalfa nodules in limiting the harmful effects of soil pollution. Therefore, nodules co-expressing antioxidant enzymes may have high phytoremediation potential.

Responses of growth and antioxidative enzymes to different Ni concentrations in castor bean (Ricinus communis)

A pot culture experiment was conducted to investigate the effect of different levels of nickel on growth and biochemical parameters of castor bean (Ricinus communis L.). Castor seedlings were grown in control conditions or in soil amended with 50, 100, 300 and 500 mg kg‑1 of Ni. Plants were harvested after 60 days of sowing. A significant decrease in growth, and concentration of chlorophyll and carotenoids were observed with increasing concentrations of Ni. Leaf proline and malondialdehyde concentration increased considerably in response to Ni application. It was observed that the protein concentration in the leaves of castor plants decreased significantly with the increase in Ni concentrations in soil. An increase in protein content and enzyme activities was observed at increasing Ni concentration in soil. Significant changes in the antioxidative enzyme activities were observed in R. communis treated with varying Ni doses. It was found that with increasing concentrations of Ni in soil, the activity of the enzymes also increased. This suggests that the increase of enzyme activity due to Ni toxicity might play a role in the defence response of R. communis.

Nickel Toxicity Interferes with NO3-/NH4+ Uptake and Nitrogen Metabolic Enzyme Activity in Rice (Oryza sativa L.).

The excessive use of nickel (Ni) in manufacturing and various industries has made Ni a serious pollutant in the past few decades. As a micronutrient, Ni is crucial for plant growth at low concentrations, but at higher concentrations, it can hamper growth. We evaluated the effects of Ni concentrations on nitrate (NO3−) and ammonium (NH4+) concentrations, and nitrogen metabolism enzyme activity in rice seedlings grown in hydroponic systems, using different Ni concentrations. A Ni concentration of 200 μM significantly decreased the NO3− concentration in rice leaves, as well as the activities of nitrate reductase (NR), nitrite reductase (NiR), glutamine synthetase (GS), and glutamate synthetase (GOGAT), respectively, when compared to the control. By contrast, the NH4+ concentration and glutamate dehydrogenase (GDH) activity both increased markedly by 48% and 46%, respectively, compared with the control. Furthermore, the activity of most active aminotransferases, including glutamic pyruvic transaminase (GPT) and glutamic oxaloacetic transaminase (GOT), was inhibited by 48% and 36%, respectively, in comparison with the control. The results indicate that Ni toxicity causes the enzymes involved in N assimilation to desynchronize, ultimately negatively impacting the overall plant growth.

Role of Jasmonic and Salicylic Acid on Enzymatic Changes in the Root of Two Alyssum inflatum Náyr. Populations Exposed to Nickel Toxicity

Phytohormones, including salicylic acid (SA) and jasmonic acid (JA) have the potential to ameliorate plant development and tolerance to deleterious effects of toxic metals like nickel (Ni). Therefore, the current study was carried out to evaluate SA and JA's interactive effect on the root antioxidative response of two Alyssum inflatum Nyár. populations against Ni-toxicity. Two A. inflatum species under different Ni concentrations (0, 100, 200, and 400 μM) were exposed to alone or combined levels of SA (0, 50, and 200 μM) and JA (0, 5, and 10 μM) treatments. Results showed that high Ni concentration (400 μM) reduced roots fresh weight in both populations than in control. However, external application of individual SA and JA or combined SA + JA in higher doses had ameliorated roots biomass by mitigating Ni-toxicity, especially in the NM population, in comparison to 400 μM Ni. Under Ni toxicity, SA and JA, especially their combination, induced high Ni accumulation in plants' roots. Moreover, the application of SA and JA alone, as well as combined SA + JA, was found to be effective in the scavenging of hydrogen peroxide by improving the activity of superoxide dismutase, peroxidase, catalase, and ascorbate peroxidase in both populations under Ni-toxicity. Overall, our results manifest that SA and JA's external use, especially combined SA + JA treatments, ameliorate root biomass and plant tolerance by restricting Ni translocation to the shoot, accumulating in roots, and enhancing antioxidant defense systems.

Response mechanism of psychrotolerant Bacillus cereus D2 towards Ni (II) toxicity and involvement of amino acids in Ni (II) toxicity reduction

The toxic effect of Nickel (Ni (II)) on humans and animals has been previously addressed. Owing to the important application of psychrotolerant bacteria in Ni (II) damage remediation in contamination sites at low temperatures, the response mechanism of psychrotolerant bacteria to Ni (II) toxicity must be elucidated. Therefore, the effect of Ni (II) toxicity on a psychrotolerant Bacillus cereus D2 was studied, showing a way to alleviate the Ni (II) toxicity in strain D2. The results showed that strain D2 growth was completely inhibited at a concentration of 100 mg/L of Ni (II). The main effects of Ni (II) toxicity on strain D2 were membrane damage and reactive oxygen species-dependent oxidative stress. Additionally, Ni (II) toxicity resulted in dysregulation of the cell cycle in strain D2. Furthermore, metabolomic analysis showed that the biosynthesis of amino acids and ABC transporters were significantly affected, and the relative abundance of seven important amino acids changed in a concentration-dependent manner. Addition of 20 mM or 5 mM amino acids to 100 mg/L Ni (II)-treated strain D2 restored its growth. This study provides insights into the way to alleviate the Ni (II) toxicity in strain D2, thus contributing to the development of bioremediation strategies.

Complementary square wave voltammetry and tandem mass spectrometry analysis to identify and detect compensatory genomic changes in nematodes due to nickel (II) exposure

Nickel is a toxic heavy metal that may cause negative health outcomes including cancer upon exposure [1]. Square wave voltammetry was used to assay DNA directly extracted from nickel-exposed nematodes that had originated from either high or low Ni-containing environments in order to assess the role of evolutionary genetics in the Ni toxicity process. Extracted DNA was immobilized on pyrolytic graphite (PG) electrodes following layer by layer (LbL) protocols and then electrochemically oxidized in the presence of Ru(bpy)3+ to generate electrocatalytic oxidative currents at ∼+1.05 V vs. SCE. Both C. elegans and P. pacificus nematodes were utilized, each with a volcanic or cosmopolitan soil source strain. DNA oxidative peak currents (Ip) increased for all nematode strains upon exposure to 50 μg/L Ni2+, but those originating from volcanic soils exhibited significantly (40–50%) lower Ip upon Ni2+ exposure compared to similarly exposed nematodes from cosmopolitan soils. Further SWV analysis was performed on DNA from a series of C. elegans N2xCB4856 recombinant inbred advanced intercross line populations (RIALs). A continuum of Ip magnitude was seen as a function of Ni2+ exposure among the RIAL strains indicating Ni-tolerance is complex and affected by multiple loci. The majority of the DNA from Ni-exposed individual RIAL strain cultures produced an increase in oxidative current in comparison to DNA from analogous Ni-unexposed cultures of the same RIAL strains. Liquid chromatography tandem mass spectrometry (LC-MS/MS) analysis on acid hydrolyzed nematode DNA provided validation of the electrochemical findings. Guanine and oxidatively damaged guanine content were monitored via appropriate m/z mass transitions. Guanine content in all Ni-exposed RIAL DNA was lower, while oxidatively damaged guanine was elevated compared to unexposed nematodes in all but one analyzed RIAL. Combined, the complementary electrochemical and MS/MS data provide evidence that evolutionary genetics leads to genetic protection from environmental toxicants, suggesting a possibility that multiple genes are involved in the protection of the organism from Ni exposure.

Assessment of Ni Toxicity to Fungi and Bacteria in Oil Tainted Soils in Greater Port Harcourt Area, Nigeria


 
 
 Intensified urbanization and industrialization are rapidly triggering the release of pollutants to the environment. This study determined the extent of soil contamination with Nickel (Ni) in oil mining areas and its effect on the levels of Ni tolerance by fungi and bacteria. The total CFUs/g of soil were enumerated after a culture period of 7 days at 28°C and LC50 was determined using probit and regression analysis. The mean values of Ni were 1.38±0.23 in industrial area, 1.41±0.36 ppm in agricultural area and 1.02±0.64 in urban area. The mean values of Total Petroleum Hydrocarbon (TPH) were 4,405.46 ppm in industrial area, 55.65 ppm in agricultural area and 1,304.53 ppm in urban area. Nickel’s peak concentration indicating growth of both fungi and bacteria at 150 ppm. There was significant difference (p ≤ 0.000) in the mean levels of LC50 for fungi among the study sites. There was no significant correlation between the concentration of TPH in soil and LC50 of fungi (r = -0.169) and bacteria (r = 0.042). In conclusion, TPH influenced the levels of fungi and bacteria tolerance to Ni in soils. Moreover, it was observed that LC50 can be a reliable method for monitoring chemically resistant microorganisms directly in the environment to improve the use of microorganisms for the bioremediation of oil contaminated soils and in monitoring of antibiotic resistant microorganisms in natural ecosystems.
 
 

Nickel stress-tolerance in plant-bacterial associations.

Nickel (Ni) is an essential element for plant growth and is a constituent of several metalloenzymes, such as urease, Ni-Fe hydrogenase, Ni-superoxide dismutase. However, in high concentrations, Ni is toxic and hazardous to plants, humans and animals. High levels of Ni inhibit plant germination, reduce chlorophyll content, and cause osmotic imbalance and oxidative stress. Sustainable plant-bacterial native associations are formed under Ni-stress, such as Ni hyperaccumulator plants and rhizobacteria showed tolerance to high levels of Ni. Both partners (plants and bacteria) are capable to reduce the Ni toxicity and developed different mechanisms and strategies which they manifest in plant-bacterial associations. In addition to physical barriers, such as plants cell walls, thick cuticles and trichomes, which reduce the elevated levels of Ni entrance, plants are mitigating the Ni toxicity using their own antioxidant defense mechanisms including enzymes and other antioxidants. Bacteria in its turn effectively protect plants from Ni stress and can be used in phytoremediation. PGPR (plant growth promotion rhizobacteria) possess various mechanisms of biological protection of plants at both whole population and single cell levels. In this review, we highlighted the current understanding of the bacterial induced protective mechanisms in plant-bacterial associations under Ni stress.

Modeling the Bioavailability of Nickel and Zinc to Ceriodaphnia dubia and Neocloeon triangulifer in Toxicity Tests with Natural Waters

We studied biotic ligand model (BLM) predictions of the toxicity of nickel (Ni) and zinc (Zn) in natural waters from Illinois and Minnesota, USA, which had combinations of pH, hardness, and dissolved organic carbon (DOC) more extreme than 99.7% of waters in a nationwide database. We conducted 7-day chronic tests with Ceriodaphnia dubia and 96-hour acute and 14-day chronic tests with Neocloeon triangulifer and estimated median lethal concentrations and 20% effect concentrations for both species. Toxicity of Ni and Zn to both species differed among test waters by factors from 8 (Zn tests with C. dubia) to 35 (Zn tests with N. triangulifer). For both species and metals, tests with Minnesota waters (low pH and hardness, high DOC) showed lower toxicity than Illinois waters (high pH and high hardness, low DOC). Recalibration of the Ni BLM to be more responsive to pH-related changes improved predictions of Ni toxicity, especially for C. dubia. For the Zn BLM, we compared several input data scenarios, which generally had minor effects on model performance scores (MPS). A scenario that included inputs of modeled dissolved inorganic carbon and measured Al and Fe(III) produced the highest MPS values for tests with both C. dubia and N. triangulifer. Overall, the BLM framework successfully modeled variation in toxicity for both Zn and Ni across wide ranges of water chemistry in tests with both standard and novel test organisms. Environ Toxicol Chem 2021;40:3049-3062. © 2021 SETAC. This article has been contributed to by US Government employees and their work is in the public domain in the USA.