Activation of stress reactions in the dinophyte microalga Prorocentrum cordatum as a consequence of the toxic effect of ZnO nanoparticles and zinc sulfate.

According to the results of the experimental study, the main regularities of changes in morphological, structural-functional and fluorescent indices of P. cordatum were established when zinc oxide nanoparticles ZnO NPs (0.3-6.4 mg L-1) and Zn in form of salt (0.09-0.4 mg L-1) were added to the medium. The studied pollutants have cytotoxic (growth inhibition, development of oxidative stress, destruction of cytoplasmic organelles, disorganization of mitochondria) and genotoxic (changes in the morphology of nuclei, chromatin condensation) effects on microalgae, affecting almost all aspects of cell functioning. Despite the similar mechanism of action of zinc sulfate and ZnO NPs on P. cordatum cells, the negative effect of ZnO NPs is also due to the inhibition of photosynthetic activity of cells (significant decrease in the maximum quantum yield of photosynthesis and electron transport rate), reduction of chlorophyll concentration from 3.5 to 1.8 pg cell-1, as well as mechanical effect on cells: deformation and damage of cell membranes, aggregation of NPs on the cell surface. Apoptosis-like signs of cell death upon exposure to zinc sulfate and ZnO NPs were identified by flow cytometry and laser scanning confocal microscopy methods: changes in cell morphology, cytoplasm retraction, development of oxidative stress, deformation of nuclei, and disorganization of mitochondria. It was shown that the first signs of cell apoptosis appear at 0.02 mg L-1 Zn and 0.6 mg L-1 ZnO NPs after 72 h of exposure. At higher concentrations of pollutants, a dose-dependent decrease in algal enzymatic activity (up to 5 times relative to control) and mitochondrial membrane potential (up to 4 times relative to control), and an increase in the production of reactive oxygen species (up to 4-5 times relative to control) were observed. The results of the presented study contribute to the disclosure of fundamental mechanisms of toxic effects of pollutants and prediction of ways of phototrophic microorganisms reaction to this impact.

Unraveling the effects of zinc sulfate nanoparticles and potassium fertilizers on quality of maize and associated health risks in Cd contaminated soils under different moisture regimes.

This study investigated the interactive effects of zinc sulfate nanoparticles (ZnSO4 NPs) and potassium fertilizers (SOP and MOP) on growth and quality of maize (Zea mays L.) under different moisture regimes in cadmium contaminated soils. It seeks to identify how these two different sources of nutrients interact to improve the quality of maize grains and fodder production to ensure food safety and food security under abiotic stresses. The experiment was conducted in a greenhouse under two moisture regimes including M1 (non-limiting regime, 20-30 %) and M2 (water-limiting, 10-15 %) at Cd contamination of 20 mg kg-1. The results showed that ZnSO4 NPs combined with potassium fertilizers significantly increased the growth and proximate composition of maize in Cd contaminated soil. Moreover, applied amendments significantly alleviated the stress induced in maize by improving the growth. The greatest increase in maize growth and quality was observed when ZnSO4 NPs were applied in combination with SOP (K2SO4). The results also showed that the interactive effects of ZnSO4 NPs and potassium fertilizers significantly affected the Cd bioavailability in soil and concentration in plants. It was observed that MOP (KCl) enhanced the Cd bioavailability in soil due to presence of Cl anion. In addition, the application of ZnSO4 NPs combined with SOP fertilizer reduced the concentration of Cd in maize grain and shoot, and significantly reduced the probable health risks to humans and cattle. It suggested that this strategy could help to reduce Cd exposure through food consumption and therefore ensure food safety. Our findings suggest that ZnSO4 NPs and SOP can be used synergistically to improve maize crop production and development of agricultural practices in areas affected by Cd contamination. Moreover, by understanding the interactive effects of these two sources of nutrients, this research could help in the management of areas affected by heavy metals contamination. ENVIRONMENTAL IMPLICATION: The application of zinc and potassium fertilizers can increase the biomass of maize, minimize abiotic stresses, and improve the nutritional value of the crop in Cd contaminated soils; this is particularly true when zinc sulfate nanoparticles and sulfate of potash (K2SO4) are used in conjunction. This form of fertilizer management can lead to a greater, more sustainable yield of maize under contaminated soils, which could have a major impact on global food supply. Remediation coupled with agro-production (RCA) not only improves the effectiveness of the process but will also encourage farmers to take part in soil remediation by easy management.

Toxicity assessment of zinc sulfate: A commonly used compound.

Because zinc sulfate (ZnSO4) is widely used in many fields such as biomedicine, electronics, and chemistry, it is important to evaluate its toxic effects. In this study, the cyto-genotoxic effects of ZnSO4 on meristematic cells in the root tip of Allium cepa L. were investigated. After calculating the effective concentration (EC50 = 70 ppm) of ZnSO4, A. cepa root tip cells were suspended for 24, 48, 72, and 96 h in solutions of 35 ppm (EC50/2), 70 ppm (EC50), and 140 ppm (EC50 × 2) concentrations. Using the counts of dividing cells, the mitotic index (MI) was calculated. Chromosome aberration index (CAI) was determined from percentages of abnormal cells. When the obtained data were statistically evaluated, it was determined that all application concentrations caused a significant decrease in MI and an increase in CAI compared to the control group (distilled water). It was concluded that increased ZnSO4 dose concentrations and exposure times caused cytotoxicity and genotoxicity in the root cells of A. cepa L.

Sulfated polysaccharides of some seaweeds exhibit neuroprotection via mitigation of oxidative stress, cholinergic dysfunction and inhibition of Zn - induced neuronal damage in HT-22 cells.

BACKGROUND: Sulfated polysaccharides from marine algae are known to possess antioxidative activities, however, their therapeutic role in metal-induced neurodegeneration has not been explored. In this study, the neuroprotective potentials of sulfated polysaccharides isolated from Ecklonia maxima (PKPM), Gelidium pristoides (PMNP), Ulva lactuca (PULV), Ulva rigida (PURL) and Gracilaria gracilis (PGCL) against Zn-induced neurodegeneration in rats' hippocampal neuronal cells (HT-22) were assessed. METHODS: Cells were cultured and maintained at 37 °C. Control cells did not contain Zinc sulphate (ZnSO4) while other experimental groups contain Zn (50 µM) alone or in combination with sulfated polysaccharides (0.4 or 0.8 mg/mL). Cell viability was assessed using MTT assay while apoptotic assay was also determined using acridine orange and ethidium bromide staining technique. Oxidative stress parameters (superoxide dismutase and catalase activities, glutathione and nitric oxide levels) and acetylcholinesterase activity were also assessed in neuronal cells treated with or without Zn. RESULTS: Zn significantly reduced cell viability to about 50%. However, sulfated polysaccharides improved cell viability to about 95%. The sulfated polysaccharides also prevented late apoptosis and necrosis triggered by Zn. Furthermore, superoxide dismutase and catalase activities including glutathione content were significantly low in cells induced with Zn. Treatment with sulfated polysaccharides triggered a significant increase in antioxidant enzymes and glutathione content as well as a decrease in the activity of acetylcholinesterase in cells treated with Zn. CONCLUSION: PKPM, PGCL, PURL, PULV and PMNP exhibit neuroprotective effects against neuronal damage induced by Zn and this may be attributed to inhibition of apoptosis, oxidative damage and acetylcholinesterase activity. These polysaccharides may be good therapeutic agents to protect neuronal cells against Zn - induced pathological processes associated with Alzheimer's disease.

Biodistribution and acute toxicity of cadmium-free quantum dots with different surface functional groups in mice following intratracheal inhalation.

Indium phosphide/zinc sulfate (InP/ZnS) quantum dots (QDs) are presumed to be less hazardous than those that contain cadmium. However, the toxicological profile has not been established. The present study investigated the acute toxicity of InP/ZnS QDs with different surface modifications (COOH, NH2, and OH) in mice after pulmonary aerosol inhalation. InP/ZnS QDs were able to pass through the blood-gas barrier and enter the circulation, and subsequently accumulated in major organs. No obvious changes were observed in the body weight or major organ coefficients. Red blood cell counts and platelet-related indicators were in the normal range, but the proportion of white blood cells was altered. The InP/ZnS QDs caused varying degrees of changes in some serum markers, but no histopathological abnormalities related to InP/ZnS QDs treatment was observed in major organs except that hyperemia in alveolar septa was found in lung sections. These results suggested that the effects of respiratory exposure to InP/ZnS QDs on the lungs need to be fully considered in future biomedical application although the overall toxicity of quantum dots is relatively low.

Reversible olfactory dysfunction impaired learning and memory with impaired hippocampal synaptic plasticity and increased corticosterone release in mice.

Olfactory dysfunction is related with various neurodegenerative and neuropsychiatric disorders such as Alzheimer's disease and Parkinson's disease, which show impaired cognitive functions. However, the effects of olfactory dysfunction on hippocampal dependent learning and memory remain elusive. In this study, mice were treated with intranasal zinc sulfate (ZnSO4) infusion which resulted in a complete but reversible loss of olfactory function. Olfaction was totally destroyed even 1 week after zinc sulfate treatment, but partially recovered 4 weeks later. We found learning and memory in Y-maze and fear conditioning were not affected by ZnSO4 1 week after the treatment, but learning and memory were severely destroyed 4 weeks later. Electrophysiology results showed impaired hippocampal long-term potentiation and long-term depression 4 weeks after the olfaction dysfunction, while only long-term depression was impaired 1 week after the treatment. Western blot showed that the expression and phosphorylation of GluA1 in zinc group did not show any increase after fear conditioning as the control mice. Serum corticosterone release was increased in olfactory deficit mice at baseline and after acute stress when tested 3, 10 and 20 days after the olfactory dysfunction. All these results indicated that reversible olfactory dysfunction elicited impaired hippocampal function in mice. The higher corticosterone release after olfactory deficiency might serve as an underling mechanism.

Type 3 adenylyl cyclase in the MOE is involved in learning and memory in mice.

Although olfactory dysfunction is related to learning and memory impairment, the causal relationship between main olfactory epithelium (MOE) disruption and learning and memory is still unknown. The present study aimed to establish whether MOE disruption causes learning and memory impairment and whether the expression of type 3 adenylyl cyclas (AC3) in the MOE is related to learning and memory. First, the buried food test was carried out to confirm that MOE function was disrupted in mice treated with nasal instillation of zinc sulfate (ZnSO4 mice), and mice with specific knockdown of AC3 in the MOE by CRISPR/Cas9 technology (AC3KD/MOE mice). Then, behavioural tasks associated with learning and memory were administered. ZnSO4 mice and AC3KD/MOE mice showed impairments in learning and memory tests, including the novel object recognition test, the step-down passive avoidance test, the Morris water maze test, and the Y-maze test. Our data demonstrate that MOE disruption caused by nasal exposure to ZnSO4 or specific knockdown of AC3 in the MOE resulted in learning and memory impairment, and they further demonstrate that the expression of AC3 in the MOE plays a major role in learning and memory.

Effects of three zinc-containing sunscreens on development of purple sea urchin (Strongylocentrotus purpuratus) embryos.

The growing popularity of physical sunscreens will lead to an increased release of ingredients from zinc oxide (ZnO) sunscreens into marine environments. Though zinc (Zn) is a necessary micronutrient in the ocean, greater than natural Zn concentrations may be released into marine environments by use of sunscreens. The extent of the consequences of this addition of Zn to the ocean are not fully understood. We investigated the effects of materials released by ZnO- sunscreens on the development of California purple sea urchin, Strongylocentrotus purpuratus. Embryos incubated in various concentrations of Zn (0.01, 0.05, 0.1, 0.5, and 1 mg/L), the sources of which included zinc-containing compounds: ZnO and zinc sulfate (ZnSO4); and ZnO sunscreens: All Good, Badger, and Raw Elements brands. Based on EC50 values, ZnO-containing sunscreens were slightly, but not significantly, more toxic than ZnO and ZnSO4, suggesting that sunscreens may release additional unknown materials that are detrimental to sea urchin embryo development. All concentrations of Zn-exposure resulted in significant malformations (skeletal abnormality, stage arrest, axis determination disruption), which were identified using light and fluorescence confocal microscopy. The concentration of Zn2+ internalized by the developing embryos correlated positively with the concentration of Zn in seawater. Additionally, exposure to both ZnO sunscreens and ZnO and ZnSO4 at 1 mg/L Zn, significantly increased calcein-AM (CAM) accumulation, indicating decreased multidrug resistant (MDR) transporter activity. This is one of the first studies documenting ZnO-containing sunscreens release high concentrations of Zn that are internalized by and have detrimental effects on aquatic organisms.

The influence of surface waters on the bioavailability and toxicity of zinc oxide nanoparticles in freshwater mussels.

The release of engineered nanoparticles in the aquatic environment could pose a threat to the biota. The purpose of the study was to examine the influence of surface water characteristics on zinc oxide nanoparticles (nZnO) and ZnS04 toxicity to the freshwater mussel Dreissena polymorpha. Mussels were exposed to an equivalent concentration of 25 µg/L Zn as either nZnO or ZnSO4 for 96 h at 15 °C in 4 types of surface waters: green water (high conductivity and pH with low natural organic matter content), brown water (low conductivity and pH with high natural organic matter content), diluted municipal effluent (high conductivity and pH with high urban organic matter content) and aquarium water (treated green water with organic matter removed). After the exposure period, mussels were analyzed for air-time survival, total and labile Zn levels in tissues, lipid metabolism (phospholipase A2, triglycerides levels) and oxidative stress (glutathione S-transferase, arachidonate cyclooxygenase, lipid peroxidation). The data revealed that mussels exposed to ZnSO4 in controlled aquarium water accumulated more total and labile Zn tissues, decreased oxidative stress and triglycerides and increased air time survival. While nZnO had few effects in aquarium water, oxidative stress was enhanced and total Zn in tissues were decreased in brown water and diluted municipal effluent and triglycerides were higher in nZn-exposed mussels in brown water. Air-time survival was decreased in mussels kept in green water and nZnO. It was also decreased in mussels exposed to ZnSO4 in green water and diluted municipal effluent. In conclusion, the fate and toxic effects of Zn could be influenced by both the chemical form (nanoparticles or ionic Zn) and surface water properties in freshwater mussels.

Comparative toxicity of organic, inorganic and nanoparticulate zinc following dietary exposure to common carp (Cyprinus carpio).

This study was carried out to compare the dietary toxicity of organic zinc (Zn-proteinate, Bioplex Zn®), mineral zinc (ZnSO4), and nanoparticulate zinc (ZnO-NPs) on the basis of some biological responses including growth performance and whole-body proximate composition, and antioxidant enzymes, as well as their accumulative affinity to target organs. These Zn sources with the nominal concentrations of 0, 30, 100, and 500 mg kg-1 diet were added to a basal diet. Juvenile common carp (n = 400; weight of 25.3 ±â€¯2.7 g) were fed with the diets for 56 days. ZnSO4 significantly reduced condition factor (CF) at 500 mg kg-1 diet. The highest activity of superoxide dismutase (SOD) and alkaline phosphatase (ALP) was observed in the plasma of the animals received 500 mg kg-1 diet of all experimental Zn sources. However, this concentration of ZnO-NPs significantly increased the activity of SOD when compared to the respective amount of ZnSO4 and Zn-proteinate. Catalase (CAT) showed a zinc-concentration decreasing activity; the minimum activity was observed in the fish group treated with the diet containing 500 mg kg-1 ZnSO4. Digestive, muscular, and integumentary systems demonstrated the following tissue zinc burden: liver > muscle > bone > posterior intestine ≈ skin > anterior intestine, for ZnO-NPs; liver > muscle ≈ bone ≈ posterior intestine ≈ skin > anterior intestine, for Zn-proteinate; and liver > muscle ≈ bone ≈ skin > posterior intestine ≈ anterior intestine, for ZnSO4. Based on accumulative affinity, taken together, ZnO-NPs displayed the highest affinity to all of the analyzed target organs, and also intestinal Zn accumulation suggested that the gut tissue has the lowest rendering ability against ZnO-NPs in compare to ZnSO4 and Zn-proteinate.

Effects of zinc oxide nanoparticles and zinc sulfate on the testis of common carp, Cyprinus carpio.

The present study analyzed the effects of zinc oxide nanoparticles (ZnO-NPs) and zinc sulfate (ZnSO4) in the testis of six-month-old common carp Cyprinus carpio exposed to three different doses, viz., 10, 50, and 100 µg/L for 21 days. Characterization of ZnO-NPs was done after sonication, the size and shape of ZnO-NPs were determined as ∼20-30 nm spherical structure measured zeta potential of +26.0 mV. After treatment, determination of zinc (Zn) concentration in the testes revealed desired impact of the exposure. Expression of several transcription factors and few steroidogenic enzyme genes in the treated testis showed significant downregulation than the control. Measurement of oxidative stress-related enzymes such as catalase, superoxide dismutase, and glutathione-S-transferase revealed substantial elevation in the testis of treated groups when compared to control. Histological analysis of testis exhibited dose-related response, defective lumen, and slow progression of spermatogenesis. Exposure of both the forms of Zn on TM3 Leydig cell culture displayed loss of adhesion, clumping with decreased viability, and a significant increase in the apoptotic cells. In addition, comet and intracellular reactive oxygen species (ROS) assays authenticated DNA damage upon treatment with a significant increase in ROS. Histological analysis after treatment withdrawal showed revival of testis in carp to rescue the effect. Thus, the present report highlights the adverse effect of Zn on the testis function in common carp as well as evident drastically toxic in in vitro cultures.

Transient Anosmia Induces Depressive-like and Anxiolytic-like Behavior and Reduces Amygdalar Corticotropin-Releasing Hormone in a ZnSO4-Induced Mouse Model.

Olfactory loss is known to affect both mood and quality of life. Transient anosmia was induced in mice to study the resulting changes in mood, behavior, and on a molecular level. Transient anosmia was induced by a single intranasal instillation of ZnSO4 in BALB/c mice. Hematoxylin and eosin (HE) staining, and potato chip finding test were performed to confirm olfactory loss. Tail suspension, forced swim, and splash tests were performed to evaluate depression-related behavior; while the open field, and elevated plus maze tests were used to evaluate anxiety-related behavior. The mRNA levels of amygdalar corticotropin-releasing hormone (CRH) and hypothalamic glucocorticoid receptor (GR) were quantified using real-time PCR to confirm relevant molecular change. Olfactory loss was confirmed 1-2.5 weeks after induction, and this loss was subsequently reversed over time. The results of the behavioral tests indicated increased depression-like and reduced anxiety-like behavior at week 1. Accordingly, PCR data identified decreased amygdalar CRH expression at week 1. These results suggest that transient anosmia induces both depressive and anxiolytic behavior as a result of decreased amygdalar CRH in a mouse model of anosmia.

Zn2+ induced molecular responses associated with oxidative stress, DNA damage and histopathological lesions in liver and kidney of the fish, Channa punctatus (Bloch, 1793).

Zn2+ is essential for normal physiological functioning of all organisms in small quantities, but when its concentration enhances in surrounding environment it acts as a toxicant to organisms. Common sources of Zn2+ pollution are electroplating, alloying, mining, and allied industrial operations. The present study aims to assess the biochemical, histopathological and genotoxicological implications under Zn2+ intoxication along with its accumulation patterns in prime biotransformation sites-liver and kidney, of a bottom feeder fish, Channa punctatus. Fish were chronically exposed to two different concentrations of Zn2+i.e., 5mg/L (permissible limit, T1) and 10mg/L (twice the permissible limit, T2). Simultaneous control was maintained. A significant (p<0.05) increment in Zn2+ bioaccumulation, antioxidant enzymes activities of SOD, CAT and GR and induction in micronuclei frequencies along with the significant (p<0.05) decrement in total protein and GSH were observed in all the exposed groups after 28 d. Altered biochemical parameters coupled with enhanced induction in micronuclei and accumulation of Zn2+ in liver and kidney of fish can be regarded as sensitive biomarkers of Zn2+ induced toxicological manifestations and thus, they may be effectively utilized for reliable ecotoxicological biomonitoring of aquatic regimes polluted with Zn2+.

Chronic High Dose Zinc Supplementation Induces Visceral Adipose Tissue Hypertrophy without Altering Body Weight in Mice.

The trace element zinc plays an important role in human life. Zinc deficiency impairs growth, reproduction, metabolism and immunity in both human and animals. Thus, zinc supplementation is recommended in daily life. However, the effect of long-term chronic zinc supplementation on adipose homeostasis has not been well elucidated. In the current study, mice were supplemented with zinc sulfate in the drinking water for 20 weeks. The results suggested that chronic zinc supplementation impaired systemic glucose clearance after exogenous insulin or glucose challenges, as compared to the control mice. Further study revealed that chronic zinc supplementation made no difference to body weight, but increased visceral adipose tissue weight and adipocyte size. In addition, gene expression of leptin and IL6 in the visceral adipose tissue of zinc-supplemented mice were higher than those of control mice. Moreover, serum level of leptin of the zinc-supplemented mice was twice as high as that of the control mice. Besides, phosphorylation level of AKT T308 was attenuated in the perirenal adipose tissue of zinc-supplemented mice. In comparison, the expression of macrophage marker genes and lipogenic genes were not affected by chronic zinc supplementation, but the protein levels of FAS and SCD1 decreased or tended to decrease in the perirenal adipose tissue of zinc-supplemented mice, as compared to the control mice. Our findings suggest that chronic high dose zinc supplementation induces visceral adipose tissue hypertrophy and impairs AKT signaling in perirenal adipose tissue.

COMPLEX HEAVY METAL SALTS' EFFECT ON GANGLION NUCLEI NEURONS MORPHOLOGICAL FUNCTIONS IN ADULT MALE RATS' CEREBELLAR CORTEX.

In order to analyze the dynamics of morphological and morphometric nuclear rearrangements of cortical cerebellar Purkinje cells under prolonged exposure (for 90 days) on the body of copper sulfate, zinc and iron experiment was conducted on 48 white adult male rats weighing 200-250g, aged 5 -8 months. We used anatomic, morphometric, statistical and common methods of micro anatomical research method. It was found that the combined effect of copper sulfate, zinc and iron on the body has nuclear device ganglion neurons in the cerebellar cortex sufficiently expressive toxicity, which affects the state of neurons. The degree of morphological rearrangements in the nuclear unit is in direct proportion to the duration of the experiment. In the nuclei of ganglion neurons develop nonspecific changes of polymorphic nature, which is reversible in the early stages of experience and irreversible, mainly necrobiotic character (chromatolysis, pycnosis and reksis) in most of the neurons within a timeline.

Using the Slug Mucosal Irritation Assay to Investigate the Tolerability of Tablet Excipients on Human Skin in the Context of the Use of a Nipple Shield Delivery System.

PURPOSE: Neonates are particularly challenging to treat. A novel patented drug delivery device containing a rapidly disintegrating tablet held within a modified nipple shield (NSDS) was designed to deliver medication to infants during breastfeeding. However concerns exist around dermatological nipple tolerability with no pharmaceutical safety assessment guidance to study local tissue tolerance of the nipple and the areola. This is the first Slug Mucosal Irritation (SMI) study to evaluate irritancy potential of GRAS excipients commonly used to manufacture rapidly disintegrating immediate release solid oral dosage form METHODS: Zinc sulphate selected as the antidiarrheal model drug that reduces infant mortality, was blended with functional excipients at traditional levels [microcrystalline cellulose, sodium starch glycolate, croscarmellose sodium, magnesium stearate]. Slugs were exposed to blends slurried in human breast milk to assess their stinging, itching or burning potential, using objective values such as mucus production to categorize irritation potency RESULTS: Presently an in vivo assay, previously validated for prediction of ocular and nasal irritation, was used as an alternative to vertebrate models to anticipate the potential maternal dermatological tolerability issues to NSDS tablet components. The excipients did not elicit irritancy. However, mild irritancy was observed when zinc sulphate was present in blends. CONCLUSION: These promising good tolerability results support the continued investigation of these excipients within NSDS rapidly disintegrating tablet formulations. Topical local tolerance effects being almost entirely limited to irritation, the slug assay potentially adds to the existing preformulation toolbox, and may sit in between the in vitro and existing in vivo assays.

Phenotypic and biochemical alterations in relation to MT2 gene expression in Plantago ovata Forsk under zinc stress.

Plantago ovata Forsk is an annual herb with immense medicinal importance, the seed and husk of which is used in the treatment of chronic constipation, irritable bowel syndrome, diarrhea since ancient times. Zinc, an essential metal, is required by plants as they form important components of zinc finger proteins and also aid in synthesis of photosynthetic pigments such as chlorophyll. However, in excess amount Zn causes chlorosis of leaf and shoot tissues and generate reactive oxygen species. The present study is aimed at investigating the changes in expression levels of MT2 gene in Plantago ovata under zinc stress. Data show up to 1.66 fold increase in expression of PoMT2 in 1000 µM ZnSO4·7H2O treated sample. Our study also describes alteration of MT2 gene expressions in Plantago ovata as observed through Real time PCR (qPCR) done by [Formula: see text] method. In this study we have observed an upregulation (or induction) in the PoMT2 gene expression level in 500 and 800 µM ZnSO4·7H2O treated samples but found saturation on further increasing the dose to 1000 µM of ZnSO4·7H2O. Determination of the phenotypic and biochemical changes in Plantago ovata due to exposure to zinc stress of concentrations 500, 800 and 1000 µM revealed oxidative stress. The enhanced expression of MT2 gene in Plantago ovata has a correlation with the increased total antioxidant activity and increased DPPH radical scavenging activity.

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

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

Comparative Analysis of Transcriptional Profile Changes in Larval Zebrafish Exposed to Zinc Oxide Nanoparticles and Zinc Sulfate.

Many studies of the toxic effects of zinc oxide nanoparticles (ZnO NPs) in aquatic organisms have been performed because of increasing ZnO NP use. However, the toxicological pathways are not understood. In this study, ZnO NPs were found to be more toxic than ZnSO4 to zebrafish larvae, but ZnO NP toxicity did not involve transcript alterations. Biological processes affected by ZnO NPs and ZnSO4 were investigated by performing ingenuity pathway analysis on differently expressed genes in larvae exposed to sub-lethal ZnO NP and ZnSO4 concentrations. We identified upregulated and downregulated differently expressed genes in fish exposed to ZnO NPs and ZnSO4, and found that ZnO NPs slightly induced cell differentiation and pathways associated with the immune system and activated several key genes involved in cancer cell signaling. The results may be key to predicting and elucidating the mechanisms involved in ZnO NP and ZnSO4 toxicity in zebrafish larvae.

Chronic toxicity effects of ZnSO4 and ZnO nanoparticles in Daphnia magna.

The chronic toxicity of ZnSO4 and ZnO nanoparticles has been studied in Daphnia magna also considering the life cycle parameters beyond the standard 21-day exposure time. Specimens have been individually followed until the natural end of their life, and some of them sampled for microscopic analyses at 48h, 9 and 21 days. Despite the low level of exposure (0.3mg Zn/L), ultrastructural analyses of the midgut epithelial cells revealed efficient internalization of nanoparticles between 48h and 9d, and translocation to other tissues as well. At 21d, the most affected fields have been recorded for both compounds; in particular samples exposed to ZnO nanoparticles showed swelling of mitochondria, while those exposed to ZnSO4 had a great number of autophagy vacuoles. The life cycle parameters resulted altered as well, with a significant inhibition of reproduction in both groups, when compared to controls. After the 21-day exposure, some interesting results were obtained: animals, previously exposed to nanoZnO at low concentrations, showed a complete recovery of the full reproduction potential, while those previously exposed to ZnSO4 presented a dose-dependent and compound-specific reduction in lifespan. Based on the results from the present research and the effects of the same chemicals at higher doses, it can be concluded that the soluble form plays a key role in ZnO nanoparticle cytotoxicity, and that the nanoparticulate form is able to locally increase the amount of Zn inside the cell, even within the ovary. It's worth noting that ZnO nanoparticles have been internalized despite the very low concentration used: this raises concern about the possible environmental implications which may derive from their use, and which in turn must be carefully considered.