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.

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.

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.