Nickel di(acetate)

Specific investigations: other studies

Additional information

A single study was identified characterizing events associated with lipid peroxidation following exposure to nickel acetate in mice. Misra et al. (1991) studied the lipid perioxidation potential (measured by LPO) of nickel acetate and its effect on various cellular enzymes in kidneys of multiple strains of mice. The impact of exposures to nickel on enzyme activities and GSH levels varied over time and consisted of transient inhibitions/enhancements of different amounts regardless of LPO, strain, or basal exposures. The authors concluded that this study emphasized the importance of specific enzymes (GSH and GSH-Px) in preventing oxidative cell damage induced by nickel

Cheng et al. (2003) conducted a genetic study evaluating acute impacts of nickel (II) acetate on gene expression in cultured human peripheral lung epithelial HPL1D cells using microarray analyses (~ 8,000 cDNAs per chip). The authors treated the cells with nickel acetate concentrations classified as nontoxic (50, 100, or 200 μM) or toxic (400, 800, or 1,600 μM) for 24 hours. mRNA from each nickel exposed cell culture was compared with the mRNA from the untreated control culture. Cluster analysis was then applied to the 868 genes having a 2-fold or greater change in gene expression at any of the six nickel acetate concentrations, as well as producing a signal at each concentration. Based on additional analyses, the authors concluded that for multiple genes, changes in expression at high, toxic concentrations are not consistent with changes occurring at low, nontoxic concentrations. At the three lower (nontoxic), concentrations, 113 genes displayed a 2-fold or greater change; the authors stated that these changes were most relevant to carcinogenesis in vivo and environmental nickel concentrations.