Dose–Response Relationship between Environmental Exposure to Nickel and Pulmonary Function in the Korean General Population Aged 40 or Older

Nickel is a well-known skin allergen; however, few studies to date have investigated the association between nickel exposure and lung function impairment. The present study, therefore, evaluated the relationship between blood nickel concentrations and lung function profiles in the Korean general population (n = 1,098). Dose–response relationships between blood nickel quartiles and pulmonary function were assessed by sex in multivariate models, after adjustment for potentially confounding factors such as age, height, and smoking status. Quartiles of blood nickel concentrations were significantly associated with markers of pulmonary function in Korean men, such as forced expiratory volume in 1 second (FEV1) and forced expiratory flow 25–75% (FEF25–75%). Relative to the first quartile, the estimated coefficients (standard error (SE)) of blood nickel levels for FEV1 in the third and fourth quartiles of Korean men were −126.6 mL (59.1) and −138.5 mL (59.8), respectively (p < 0.05). Relative to the first quartile, the estimated coefficients (SE) of blood nickel levels for FEF25–75% in the second and fourth quartiles were −244.9 mL (109.5) and −266.8 mL (111.5), respectively (p < 0.05). Dose–response relationships were observed between quartiles of blood nickel concentrations and the pulmonary function markers FEV1 and FEF25–75% in Korean men aged 40 or older.

Physiological, Photochemical and Antioxidant Responses of Wild and Cultivated Carthamus Species Exposed to Nickel Toxicity and Evaluation of Their Usage Potential in Phytoremediation

The responses of growth, photochemical and antioxidant defence of safflower species (Carthamus oxyacantha M. Bieb. and Carthamus tinctorius L. exposed to nickel (Ni) toxicity were investigated in the study. Fourteen-day-old seedlings were treated with excessive Ni levels [control, 0.50, 0.75 and 1.00 mM] for 7 days. The results of chlorophyll a fluorescence indicated that toxic nickel exposure led to changes in specific, phenomenological energy fluxes and quantum yields in thylakoid membranes, and activities of donor and acceptor sides of photosystems. These changes resulted in a significant decrease in the photosynthetic performance of the species, but these negative effects of Ni were not in a level to destroy the functionality of the photosystems. At the same time, toxic Ni affected membrane integrity and the amount of photosynthetic pigments in the antenna and active reaction centers. Additionally, the accumulation of Ni was higher in roots than in stem and leaves for both species. Depending on Ni accumulation, a significant reduction in dry biomass of root and shoot was observed in both species. Two species could probably withstand deleterious Ni toxicity with better upregulating own protective defence systems such as antioxidant enzymes. Among of them, SOD and POD activities were increased with increasing Ni concentrations. The POD activities of both species were most prominent and consistently increased in toxic Ni levels and may be protected them from damaging effect of H2O2. When all results are evaluated as a whole, Carthamus species produced similar responses to toxicity and also both species have Bioconcentration (BCF) and Bioaccumulation factors (BF) > 1 and Translocation factor (TF) < 1 under Ni toxicity may be regarded a good indication of Ni tolerance. Consequently, it is possible to use the Carthamus species in the remediation (phytostabilization) of soils contaminated with nickel, because of their roots accumulating more nickel.

Intracellular nickel accumulation induces apoptosis and cell cycle arrest in human astrocytic cells

Nickel, a heavy metal found in electronic wastes and fume from electronic cigarettes, induces neuronal cell death and is associated with neurocognitive impairment. Astrocytes are the first line of defense against nickel after entering the brain; however, the effects of nickel on astrocytes remain unknown. Herein, we investigated the effect of nickel exposure on cell survival and proliferation and the underlying mechanisms in U-87 MG human astrocytoma cells and primary human astrocytes. Intracellular nickel levels were elevated in U-87 MG cells in both a dose- and time-dependent manner after exposure to nickel chloride. The median toxic concentrations of nickel in astrocytoma cells and primary human astrocytes were 600.60 μM and &gt; 1,000 μM at 48 h post-exposure, respectively. Nickel exposure triggered apoptosis in concomitant with the decreased expression of anti-apoptotic B-cell lymphoma protein (Bcl-2), and increased caspase-3/7 activity. Nickel induced reactive oxygen species formation. Additionally, nickel suppressed astrocyte proliferation in a dose- and time-dependent manner by delaying G2 to M phase transition through the upregulation of cyclin B1 and p27 protein expression. These results indicate that nickel-induced cytotoxicity of astrocytes is mediated by the activation of apoptotic pathway and disruption of cell cycle regulation.