Study with Copper Acetate(WSDTY) treated Hep G2 cell line demonstrated that mitochondrial toxicity is an intermediate-level event associated with copper toxicity to Hep G2 cells while lysosomal damage is the early event and plasma damage a late feature associated with copper toxicity. Considering that the copper-associated mitochondrial toxicity may have been delayed, we further explored the changes in the expression of skin irritation-related biomarkers at the genomic level. In response to chemical stress, keratinocytes produce and release inflammatory cytokines, chemokines and other signaling markers that rapidly generate cutaneous inflammation. Among the genes evaluated, expression levels of genes were not significantly different in GHK and GHK-Cu group as compared to control.
However, we found that four genes, IL-1α, IL8, HSPA1A and FOSL1, were significantly induced by Copper Acetate and Cu(OAc)2 without inhibiting the cell viability. The protein expression of the four genes in culture medium were further tested with ELISA kits. With the exception of FOSL1, which was undetectable in all of the samples in the ELISA test, the protein level regulation of IL-1α, IL8, HSPA1A by the copper compounds were similar with the gene level regulation. GHK and GHK-Cu didn’t cause any significant changes in the extracellular protein concentration of IL-1α, IL8, HSPA1A. However, Copper Acetate and Cu(OAc)2 significantly upregulated the extracellular protein expression of the three genes at concentrations (58μM and 580μM) without inhibiting the cell viability after 24?h.
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