Short-term effect of bisphenol-a on oxidative stress responses in Atlantic salmon kidney cell line: a transcriptional study

Abstract

Bisphenol A (BPA) is regularly detected in aquatic ecosystems due to increased use of products based on polycarbonate plastics and epoxy resins. It migrates from these products directly into rivers and marine waters or indirectly through effluents from wastewater treatment plants and landfilled sites. BPA can affect aquatic organisms both chronically and acutely at sensitive live stages. Despite reports indicating harmful effects of BPA, little is known about its role in oxidative stress responses in fish. In this study, we investigated the transcriptional effect of BPA (0, 1, 10, 100 μM) on an Atlantic salmon kidney (ASK) cell line for 6 h and 24 h by monitoring expression of 11 genes: elongation factor 1-alpha (ef1a), 18S ribosomal RNA (18s), gluthation (gsh), superoxide dismutase (sod), thioredoxin (txd), Salmo salar oxidative stress-responsive serine-rich 1 (oxr), glucose-regulated protein 78 (grp78), heat shock protein 70 (hsp70), sequestosome1 (p62), interleukin-1 beta (il-1beta) and toll-like receptor 8 (tlr8). In general, only the 100 μM concentration treatment altered the mRNA expression. BPA down-regulated the expression of gsh and sod genes for both exposure-times while txd gene was the only down-regulated after 6-h exposure. The up-regulation of genes in the ASK cell line exposed for 6 h was only observed in il-1beta, while the 24-h exposure resulted in the up-regulation of oxr, tlr8, hsp70, p62 and il-1beta genes. The last three genes increased several fold compared to the others. The results showed that BPA exposure at 100 μM imposed oxidative stress on the ASK cell line and longer exposure time involved transcriptional responses of immune-related genes. This may indicate the possible role of BPA-associated oxidative stress in induction of inflammatory response in this macrophage-like cell type.

Keywords:

• Atlantic salmon kidney cell line
• bisphenol A
• oxidative stress responses
• transcriptional changes

Disclosure statement

The authors report no conflicts of interest. The authors alone are responsible for the content and writing of this article.