Ameliorative Effects of Selenium in ZnO NP-Induced Oxidative Stress and Hematological Alterations in Catla catla.

Various applications of zinc oxide nanoparticles (ZnO NPs) can increase pollution in aquatic environments. Consequently, pollution can cause toxicity in fish as indicated by oxidative stress, hematotoxicity, and changes in gill and liver histology. Selenium is known for its antioxidant potential in scavenging the free radicals generated during ZnO NP-induced oxidative stress. This study tested the ameliorative role of selenium against ZnO NP-induced toxicity in freshwater fish Catla catla. Four groups of replicated fish, representing control, selenium-treated, ZnO NP-treated, and ZnO NPs+selenium-treated, were used in this study. The ZnO NPs (40 mg l-1) were given to fish in water whereas selenium (50 µg kg-1) was given as sodium selenite in feed. After 28 days of exposure, the fish specimens were processed to collect samples of blood, gills, and liver. The results demonstrated that the consumption of selenium containing feeds protected the C. catla from ZnO NP-induced toxicity and oxidative stress. The use of selenium containing feeds appeared to have reduced the contents of glutathione S-transferase (GST) and glutathione reduced (GSH), and increased the level of catalase (CAT) and superoxide dismutase (SOD). Furthermore, the consumption of selenium in feeds improved the hematological parameters in ZnO NP-treated fish. This study suggests that dietary selenium might be able to ameliorate ZnO NP-induced toxicity in fish.

Potential Role of L-Arginine and Vitamin E Against Bone Loss Induced by Nano-Zinc Oxide in Rats.

The purpose of this study was to illustrate the effects of zinc oxide nanoparticles (ZnO-NPs) administration on bone turnover and bone resorbing agents in rats and how L-arginine (L-arg) or vitamin E (vit E) co-administrations might affect them. Fasting rats were randomly divided into four groups (n = 10): G1-normal healthy animals; G2-ZnO-NPs-exposed rats (600 mg/kg-1/day-1); G3-ZnO-NPs-exposed rats co-administrated L-arg (200 mg/kg-1/day-1); G4-ZnO-NPs-exposed rats co-administrated vit E (200 mg/kg-1/day-1). The ingredients were orally administered daily. The body weight and food consumption of rats were recorded during the administration period and the experiment continued for three consecutive weeks. The results demonstrated that ZnO-NPs administration induced bone loss in rats as manifested by reduced activity of bone alkaline phosphatase (B-ALP) and increased level of C-terminal peptide type I collagen (CTx). The increase of inflammatory markers, tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) by ZnO-NPs suggests that deleterious effects of ZnO-NPs on bone turnover were, in part, due to inflammation. Confirming to this suggestion, both L-arg and vit E reduced TNF-α and IL-6 levels and consequently decreased bone resorption as indicated by reduced serum CTx level. This study proved that ZnO-NPs can induce bone turnover, which may be reduced by L-arg or vit.E co-administration, partly by anti-inflammatory mechanism.

The effects of baicalein or baicalin on the colloidal stability of ZnO nanoparticles (NPs) and toxicity of NPs to Caco-2 cells.

Recent study suggested that the presence of phytochemicals in food could interact with nanoparticles (NPs) and consequently reduce the toxicity of NPs, which has been attributed to the antioxidant properties of phytochemicals. In this study, we investigated the interactions between ZnO NPs and two flavonoids baicalein (Ba) or baicalin (Bn) as well as the influence of the interactions on the toxicity of ZnO NPs to Caco-2 cells. The antioxidant properties of Ba and Bn were confirmed by 1,1-diphenyl-2-picrylhydrazyl (DPPH) and 2'-azino-bis(3-ethylbenzothiazoline-6-sulphonic acid) (ABTS) assays, with Ba being stronger. However, the presence of Ba or Bn did not significantly affect cytotoxicity, intracellular superoxide or release of inflammatory cytokines of Caco-2 cells after ZnO NP exposure. When Ba was present, the cellular viability of Caco-2 cells after exposure to ZnO NPs was slightly increased, associated with a modest decrease of intracellular Zn ions, but these effects were not statistically different. Ba was more effective than Bn at changing the hydrodynamic sizes, Zeta potential and UV-Vis spectra of ZnO NPs, which indicated that Ba might increase the colloidal stability of NPs. Taken together, the results of the present study indicated that the anti-oxidative phytochemical Ba might only modestly protected Caco-2 cells from the exposure to ZnO NPs associated with an insignificant reduction of the accumulation of intracellular Zn ions. These results also indicated that when assessing the combined effects of NPs and phytochemicals to cells lining gastrointestinal tract, it might be necessary to evaluate the changes of colloidal stability of NPs altered by phytochemicals.

Physiological effects and mode of action of ZnO nanoparticles against postharvest fungal contaminants.

Increasing concerns continue to be expressed about health hazards and environmental pollution resulting from the use of conventional fungicides for postharvest disease control. Nanoparticles represent an alternative solution for postharvest disease management. The objective of this work was to assess the physiological effects and the antifungal efficiency of ZnO nanoparticles (ZnO NPs) against a number of fungal contaminants. The efficacy of ZnO NPs was qualitatively and quantitatively assessed against: Penicillium expansum, Alternaria alternata, Botrytis cinerea and Rhizopus stolonifer. Mycelium growth diameters were measured onto Potato Dextrose Agar (PDA) plates loaded with different ZnO NPs concentrations (from 0mM to 15mM). Hereafter, the rate of the fungal diameter increase was quantified by linear regression modelling. Microscopic analysis was performed by scanning electron microscopy (SEM) images of agar plugs excised from plates with 0mM and 12mM ZnO. All the fungi were inhibited by ZnO NPs at concentrations higher than 6mM. SEM images showed clear morphological aberrations in the fungal structures of all the isolates grown in presence of ZnO. Additionally, knowing that the chelating agent EDTA sequesters metal ions, it was added to fungal inoculated PDA plates with ZnO to study the NPs' mode of action. Cultures where ZnO was mixed with EDTA showed a decrease in the antifungal effect of the nanoparticles. In conclusion, ZnO NPs are therefore a good candidate as an effective postharvest disease control antifungal agent.

Querectin Alleviates Zinc Oxide Nanoreprotoxicity in Male Albino Rats.

Zinc oxide nanopartciles (ZnONPs) involved in advanced technologies, and their wide-scale use in consumer market makes human beings more prone to the exposure to ZnONPs. The present study was undertaken to evaluate amelioration of ZnONP-induced toxicities with querectin in male albino rats. ZnONPs-treated rats showed a significant decrease in sperm cell count, sperm motility, live and normal sperms, as well as serum testosterone level. Severe histopathological damage with a significant increase in lipid peroxidation and a decrease in antioxidant enzymes activity and the GSH level were observed in the affected testis. Relative quantitative polymerase chain reaction results showed a significant decrease in antioxidant enzymes (superoxide dismutase and catalase) and a significant decrease in 3ß-HSD, 17ß-HSD, and Nr5A1 transcripts. Rats-administered querectin along with ZnONPs showed less toxic effects on all studied reproductive traits and mRNA transcripts. Our results suggest that querectin is beneficial for preventing or ameliorating ZnONP reproductive toxicities in males.

Zinc oxide nanoparticles induce apoptosis by enhancement of autophagy via PI3K/Akt/mTOR inhibition.

Zinc oxide nanoparticles (ZnO NPs) induced macrophage cell death and its mechanism remains to be solved. Herein, we report that ZnO NPs induced ROS generation by depleting antioxidant enzymes, increasing lipid peroxidation and protein carbonyl contents in macrophages. The oxidative stress was induced by the inhibition of Nrf2 transcription factor release. ZnO NPs also activated the cleavage of apoptosis markers like caspases 3, 8 and 9. γH2Ax activation and cleavage of poly (ADP-ribose) polymerase (PARP) that are known indicators of genotoxicity were found to be activated by following p53, p21/waf1 signaling. ZnO NPs increased the number of autophagosomes and autophagy marker proteins such as microtubule-associated protein 1 light chain 3-isoform II (MAP-LC3-II) and Beclin 1 after 0.5-24h of treatment. Phosphorylated Akt, PI3K and mTOR were significantly decreased on ZnO NPs exposure. Moreover, the apoptotic and autophagic cell death could be inhibited on blocking of ROS generation by N-acetylcysteine (NAC) which demonstrated the critical role of ROS in both types of cell death. In addition, inhibition of LC3-II by siRNA-dependent knockdown attenuated the cleavage of caspase 3. This study demonstrates autophagy supports apoptosis on ZnO NPs exposure.