Toxicity Of Zn2 Research Articles

Eucalyptus Leaf Solution to Replace Metals in the Removal of Cyanobacteria in Wastewater from the Paper Mill Industry

The frequent occurrence of cyanobacterial blooms, caused by the eutrophication of water bodies, has triggered several ecological issues. Metal-controlled cyanobacteria are resulting in a series of secondary environmental problems and thus limiting environmental sustainability. Whether there is a more environmentally friendly way to replace metals in the removal of cyanobacteria is still unclear. To explore whether common heavy metals inhibit algal growth and whether Eucalyptus leaves (EL) can replace heavy metal ions in controlling algae outbreaks, here, we add Fe3+, Al3+, 3 mol/L of zinc (Zn3), 10 mol/L zinc (Zn10), and EL to a medium containing Cyanobacteria. We determine the medium’s color (456 nm), UV (254 nm), chlorophyll a, turbidity, temperature, pH, total dissolved solids, conductivity, and blue-green algae (BGA) at days 1, 4, 7, 11, 14, 19, and 21. We find that Fe3+, Al3+, Zn3, Zn10, and EL can inhibit chlorophyll synthesis, thereby impeding algae biomass growth due to metal ions’ disruption of the chlorophyll structure. The toxicity of Zn2+ may be higher than that of Fe3+ and Al3+ since it can completely destroy the structure of chlorophyll a. The damage of Zn (10) to chlorophyll a is stronger than that of Zn (3), indicating that high concentrations of metals have a stronger inhibitory effect on algae. The toxicity of EL to algae is lower than that of other metals, but it can significantly inhibit the growth of algae. We suggest the use of Eucalyptus leaves to inhibit algal growth in eutrophic water bodies. Our results provide a scientific basis for an environmentally friendly approach to controlling cyanobacteria outbreaks.

MT-like proteins: Potential bio-indicators of Chlorella vulgaris for zinc contamination in water environment

Chlorella vulgaris has been usually used to monitor the toxicity of Zn in water environment, but the biochemical responses of the algae to Zn2+ at different levels remain unknown to date. In the present study, the growth inhibition, the antioxidant enzymes, the subcellular Zn and the induced Zn-metallothionein-like (Zn-MT-like) proteins in C. vulgaris exposed to 0, 5, 10, 20, 50 and 100μmoll−1 of Zn2+ were investigated. Results showed that the growth of C. vulgaris was significantly inhibited (p<0.05) at Zn2+ level above 5μmoll−1. Compared with the control group, the activities of peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase mostly increased with the rises of Zn2+ concentrations ranging from 5 to 100μmoll−1, except for GSH-Px with a lower value in the 100μmoll−1 group compared with that of the 50μmoll−1 group, and SOD with no significant difference at the 5, 10 and 100μmoll−1 groups compared with that of the control group. Contrarily, the activities of guaiacol peroxidase significantly decreased (p<0.05) at Zn2+ concentrations from 5 to 100μmoll−1 compared with that of the control group. After 72h exposure, Zn in the algal cells was observed to mainly distribute in the form of heat stable fractions, in which Zn-binding metallothionein-like (MT-like) proteins were largely biosynthesized. In addition, the amounts of Zn-MT-like proteins induced in the algae significantly increased (p<0.05) with the rises of Zn2+ concentrations at the assay levels. The results indicated that the activities of antioxidant enzymes and the induction of Zn-MT-like proteins in C. vulgaris may play important roles in dealing with the toxicity of Zn2+ to the algal cells, and the induction of Zn-MT-like proteins in C. vulgaris can be used as a potential bio-indicator to monitor the contamination of Zn2+ in water environment.

Individual and joint toxicity of Zn2+ and Cd2+ during the early em-bryonic development of zebrafish (Danio rerio)

We evaluated the individual and joint toxicity of zinc and cadmium during the early embryonic devel-opment of the zebrafish(Danio rerio).Embryos were exposed to various concentrations of Zn2+ and Cd2+ 24 h post-fertilization(24 hpf).We monitored the number of embryonic coagulated eggs and the rhythm of the heart at 48 hpf and the number of embryonic coagulated eggs,hatching rate,and malfomation rate at 72 hpf.The effects of Zn2+ and Cd2+ differed among the stages of development.In general,Zn2+ was more toxic than Cd2+.The embryos were most sensitive to Zn2+ and Cd2+ toxicity at 72 hpf.Regardless of the ratio of Zn2+ and Cd2+ during joint ex-posure(1﹕1,1﹕2 or 2﹕1),the two chemicals tended to act synergistically.However,the joint toxicity was de-fendant on the endpoints and the ratio of each metal.For example,at equal concentrations of Zn2+ and Cd2+(1﹕1),the effect tended to be synergistic.However,at a ratio of 1﹕2(Zn2+:Cd2+) the effect was synergistic at 48 hpf but antagonistic at 72 hpf.Furthermore,at a ratio of 2﹕1(Zn2+:Cd2+) the effect on egg coagulation was synergistic whereas the effect on the rate of hatching was antagonistic.Thus,our results suggest that joint toxicity is affected by both the concentration of each chemical and the exposure time.

Acute ZnO nanoparticles exposure induces developmental toxicity, oxidative stress and DNA damage in embryo-larval zebrafish

Nano-scale zinc oxide (nano-ZnO) is widely used in various industrial and commercial applications. However, the available toxicological information was inadequate to assess the potential ecological risk of nano-ZnO to aquatic organisms and the publics. In this study, the developmental toxicity, oxidative stress and DNA damage of nano-ZnO embryos were investigated in the embryo-larval zebrafish, the toxicity of Zn2+ releasing from nano-ZnO were also investigated to ascertain the relationship between the nano-ZnO and corresponding Zn2+. Zebrafish embryos were exposed to 1, 5, 10, 20, 50, and 100mg/L nano-ZnO and 0.59, 2.15, 3.63, 4.07, 5.31, and 6.04mg/L Zn2+ for 144h post-fertilisation (hpf), respectively. Up to 144hpf, activities of superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx), and malondialdehyde (MDA) contents, the genes related to oxidative damage, reactive oxygen species (ROS) generation and DNA damage in zebrafish embryos were measured. The nano-ZnO was found to exert a dose-dependent toxicity to zebrafish embryos and larvae, reducing the hatching rate and inducing malformation and the acute toxicity to zebrafish embryos was greater than that of the Zn2+ solution. The generation of ROS was significantly increased at 50 and 100mg/L nano-ZnO. DNA damage of zebrafish embryo was evaluated by single-cell gel electrophoresis and was enhanced with increasing nano-ZnO concentration. Moreover, the transcriptional expression of mitochondrial inner membrane genes related to ROS production, such as Bcl-2, in response to oxidative damage, such as Nqo1, and related to antioxidant response element such as Gstp2 were significantly down-regulated in the nano-ZnO treatment groups. However, the nano-ZnO up-regulated the transcriptional expression of Ucp2-related to ROS production. In conclusion, nano-ZnO induces developmental toxicity, oxidative stress and DNA damage on zebrafish embryos and the dissolved Zn2+ only partially contributed to the toxicity of nano-ZnO. The adverse effects of nano-ZnO may be the important mechanisms of its toxicity to zebrafish embryos.

Energy-dependent zinc transport by escherichia coli.

The uptake of labelled Zn2+ by starved Escherichia coli has two main components. One is energy-independent, subject to quick reversal by exchange for inactive Zn2+ carrier and interpreted as adsorption. The second component appears to consist of carrier-mediated transport into the cell. It depends on metabolic energy and greatly exceeds the first component when exogenous fermentation (glucose + nitrogen), or, better, respiration (glucose + air) is possible. It has a large temperature coefficient and follows Michaelis-Menten kinetics. Energy-dependent uptake leads to a steady state with slow influx into, and efflux from, the cell. Under conditions of strong uptake into the cell, the toxicity of Zn2+ solutions for E. coli is enhanced.